Ocular disorders and Antiphospholipid syndrome

Antiphospholipid syndrome is an autoimmune disorder characterized by either a history of vascular thrombosis (one or more clinical episodes of arterial, venous, or small vessel thrombosis in any tissue or organ) or pregnancy morbidity in association with the presence of antiphospholipid antibodies. The systemic features of the syndrome are characterized by large variability depending on the affected organ(s). Among them, neurological and behavioural disturbances, dermatological features as livedo reticularis and renal, ocular, liver or valvular heart manifestations have been reported in antiphospholipid syndrome patients. However, studies on the frequency and clinical presentation of the ocular manifestations as the prevailing (first) sign of antiphospholipid syndrome in patients suffering from “unexplained” ocular disease are missing.

There is unexplained ocular features from the anterior or posterior segment and unexplained neuro-ophthalmologic symptoms. Sign and symptom bilateral retinal occlusive disease, unilateral nonarteritic anterior ischemic optic neuropathy with macular oedema. Moderate to high levels of antiphospholipid antibodies were detected in all of them at baseline as well as 6 to 12 weeks after initial testing confirming the presence of antiphospholipid antibodies. Anticoagulant treatment with acenocoumarol was instituted resulting in stabilization and/or improvement of ocular signs in all of them.
Due to the important diagnostic and therapeutic implications of antiphospholipid syndrome, the possibility of ocular features as the first clinical manifestation of antiphospholipid syndrome should be kept in mind of the physicians particularly in patients with no evident risk factors for ocular disease. Anticoagulant treatment and close follow-up seem to be essential for vision salvation and stabilization

Antiphospholipid syndrome
Antiphospholipid syndrome or

antiphospholipid antibody syndrome (APS or APLS or), often also Hughes syndrome, is an autoimmune, hypercoagulable state caused by antibodies against cell-membrane phospholipids that provokes blood clots (thrombosis) in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, or severe preeclampsia. The syndrome occurs due to the autoimmune production of antibodies against phospholipid (aPL), a cell membrane substance. In particular, the disease is characterised by antibodies against cardiolipin (anti-cardiolipin antibodies) and β2 glycoprotein I. The term “primary antiphospholipid syndrome” is used when APS occurs in the absence of any other related disease. APS however also occurs in the context of other autoimmune diseases, such as systemic lupus erythematosus (SLE), in which case the term “secondary antiphospholipid syndrome” is used. In rare cases, APS leads to rapid organ failure due to generalised thrombosis; this is termed “catastrophic antiphospholipid syndrome” (CAPS) and is associated with a high risk of death.

Antiphospholipid syndrome is diagnosed with blood tests. It often requires treatment with anticoagulant medication such as warfarin or heparin to reduce the risk of further episodes of thrombosis and improve the prognosis of pregnancy.

Signs and symptoms

The presence of antiphospholipid antibodies (aPL) in the absence of blood clots or pregnancy-related complications does not indicate APS (see below for the diagnosis of APS).

Antiphospholipid syndrome can cause (arterial/venous) blood clots (in any organ system) or pregnancy-related complications. In APS patients, the most common venous event is deep vein thrombosis of the lower extremities (blood clot of the deep veins of the legs) and the most common arterial event is stroke. In pregnant women affected by APS, miscarriage can occur prior to 20 week of gestation, while pre-eclampsia is reported to occur after that time. Placental infarctions, early deliveries and stillbirth are also reported in women with APS. In some cases, APS seems to be the leading cause of mental and/or development retardation in the newborn, due to an aPL-induced inhibition of trophoblast differentiation. The antiphospholipid syndrome responsible for most of the miscarriages in later trimesters seen in concomitant systemic lupus erythematosus and pregnancy.[1]

Other common findings, although not part of the APS classification criteria, are thrombocytopenia (low platelet count), heart valve disease, and livedo reticularis (a skin condition). Some patients report headaches, migraines, and oscillopsia.[2]

Very few patients with primary APS go on to develop SLE.

Risk factors

Risk factors for developing antiphospholipid syndrome include:[citation needed]

Primary APS
genetic marker HLA-DR7
Secondary APS
SLE or other autoimmune disorders
Genetic markers: HLA-B8, HLA-DR2, HLA-DR3
Race: Blacks, Hispanics, Asians, and Native Americans
Mechanism

Antiphospholipid syndrome is an autoimmune disease, in which “antiphospholipid antibodies” (anticardiolipin antibodies and lupus anticoagulant) react against proteins that bind to anionic phospholipids on plasma membranes. Like many autoimmune diseases, it is more common in women than in men. The exact cause is not known, but activation of the system of coagulation is evident. Clinically important antiphospholipid antibodies (those that arise as a result of the autoimmune process) are associated with thrombosis and vascular disease. The syndrome can be divided into primary (no underlying disease state) and secondary (in association with an underlying disease state) forms.

Anti-ApoH and a subset of anti-cardiolipin antibodies bind to ApoH, which in turn inhibits Protein C, a glycoprotein with regulatory function upon the common pathway of coagulation (by degradating activated factor V).

LAC antibodies bind to prothrombin, thus increasing its cleavage to thrombin, its active form.

In APS there are also antibodies binding to: Protein S, which is a co-factor of protein C. Thus, anti-protein S antibodies decrease protein C efficiency;

Annexin A5, which forms a shield around negatively-charged phospholipid molecules, thus reducing their availability for coagulation. Thus, anti-annexin A5 antibodies increase phospholipid-dependent coagulation steps.

The Lupus anticoagulant antibodies are those that show the closest association with thrombosis, those that target β2glycoprotein 1 have a greater association with thrombosis than those that target prothrombin. Anticardiolipin antibodies are associated with thrombosis at moderate to high titres (>40 GPLU or MPLU). Patients with both Lupus anticoagulant antibodies and moderate/high titre anticardiolipin antibodies show a greater risk of thrombosis than with one alone.

Diagnosis

Antiphospholipid syndrome is tested for in the laboratory using both liquid phase coagulation assays (lupus anticoagulant) and solid phase ELISA assays (anti-cardiolipin antibodies).

Genetic thrombophilia is part of the differential diagnosis of APS and can coexist in some APS patients. Presence of genetic thrombophilia may determine the need for anticoagulation therapy. Thus genetic thrombophilia screening can consist of:

Further studies for Factor V Leiden variant and the prothrombin mutation, Factor VIII levels, MTHFR mutation.
Levels of protein C, free and total protein S, Factor VIII, antithrombin, plasminogen, tissue plasminogen activator (TPA) and plasminogen activator inhibitor-1 (PAI-1)
The testing of antibodies to the possible individual targets of aPL such as β2 glycoprotein 1 and antiphosphatidyl serine is currently under debate as testing for anticardiolipin appears to be currently sensitive and specific for diagnosis of APS even though cardiolipin is not considered an in vivo target for antiphospholipid antibodies.

Lupus anticoagulant

This is tested for by using a minimum of two coagulation tests that are phospholipid sensitive, due to the heterogeneous nature of the lupus anticoagulant antibodies. The patient on initial screening will typically have been found to have a prolonged APTT that does not correct in an 80:20 mixture with normal human plasma (50:50 mixes with normal plasma are insensitive to all but the highest antibody levels). The APTT (plus 80:20 mix), dilute Russell’s viper venom time (DRVVT), the kaolin clotting time (KCT), dilute thromboplastin time (TDT/DTT) or prothrombin time (using a lupus sensitive thromboplastin) are the principal tests used for the detection of lupus anticoagulant. These tests must be carried out on a minimum of two occasions at least 6 weeks apart and be positive on each occasion demonstrating persistent positivity to allow a diagnosis of antiphospholipid syndrome. This is to prevent patients with transient positive tests (due to infection etc.) being diagnosed as positive.

Distinguishing a lupus antibody from a specific coagulation factor inhibitor (e.g.: Factor VIII). This is normally achieved by differentiating the effects of a lupus anticoagulant on factor assays from the effects of a specific coagulation factor antibody. The lupus anticoagulant will inhibit all the contact activation pathway factors (Factor VIII, Factor IX, Factor XI and Factor XII). Lupus anticoagulant will also rarely cause a factor assay to give a result lower than 35 iu/dl (35%) whereas a specific factor antibody will rarely give a result higher than 10 iu/dl (10%). Monitoring IV anticoagulant therapy by the APTT ratio is compromised due to the effects of the lupus anticoagulant and in these situations is generally best performed using a chromogenic assay based on the inhibition of Factor Xa by antithrombin in the presence of heparin.

Anticardiolipin antibodies

These can be detected using an enzyme-linked immunosorbent assay (ELISA) immunological test, which screens for the presence of β2glycoprotein 1 dependent anticardiolipin antibodies (ACA).

A Low platelet count and positivity for antibodies against β2-glycoprotein 1 or phosphatidylserine may also be observed in a positive diagnosis.

Criteria

Classification with APS requires evidence of both one or more specific, documented clinical events (either a vascular thrombosis and/or adverse obstetric event) and the confirmed presence of a repeated aPL. The Sapporo APS classification criteria (1998, published in 1999) were replaced by the Sydney criteria in 2006.[3] Based on the most recent criteria, classification with APS requires one clinical and one laboratory manifestation:

Clinical:
A documented episode of arterial, venous, or small vessel thrombosis—other than superficial venous thrombosis in any tissue or organ by objective validated criteria with no significant evidence of inflammation in the vessel wall and/or
1 or more unexplained deaths of a morphologically normal fetus (documented by ultrasound or direct examination of the fetus) at or beyond the 10th week of gestation and/or 3 or more unexplained consecutive spontaneous abortions before the 10th week of gestation, with maternal anatomic or hormonal abnormalities and paternal and maternal chromosomal causes excluded or at least 1 premature birth of a morphologically normal neonate before the 34th week of gestation due to eclampsia or severe pre-eclampsia according to standard definitions, or recognized features of placental insufficiency plus
Laboratory:
Anti-cardiolipin IgG and/or IgM measured by standardized, non-cofactor dependent ELISA on 2 or more occasions, not less than 12 weeks apart; medium or high titre (i.e., > 40 GPL or MPL, or > the 99th percentile) and/or
Anti-β2 glycoprotein I IgG and/or IgM measured by standardized ELISA on 2 or more occasions, not less than 12 weeks apart; medium or high titre (> the 99th percentile) and/or
Lupus anticoagulant detected on 2 occasions not less than 12 weeks apart according to the guidelines of the International Society of Thrombosis and Hemostasis.
There are 3 distinct APS disease entities: primary (the absence of any comorbidity), secondary (when there is a pre-existing autoimmune condition, most frequently systemic lupus erythematosus, SLE), and catastrophic (when there is simultaneous multi-organ failure with small vessel occlusion).

According to a 2006 consensus statement,[4] it is advisable to classify APS into one of the following categories for research purposes:

I: more than one laboratory criterion present in any combination;
IIa: lupus anticoagulant present alone
IIb: anti-cardiolipin IgG and/or IgM present alone in medium or high titers
IIc: anti-β2 glycoprotein I IgG and/or IgM present alone in a titer greater than 99th percentile
The International Consensus Statement is commonly used for Catastrophic APS diagnosis.[5] Based on this statement, Definite CAPS diagnosis requires:

a) Vascular thrombosis in three or more organs or tissues and
b) Development of manifestations simultaneously or in less than a week ‘and
c) Evidence of small vessel thrombosis in at least one organ or tissue and
d) Laboratory confirmation of the presence of aPL.
Some serological tests for syphilis may be positive in aPL-positive patients (aPL bind to the lipids in the test and make it come out positive) although the more specific tests for syphilis that use recombinant antigens will be negative.

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CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation htpp://www.allergyclinic.wordpress.com/

WORKING TOGETHER FOR STRONGER, SMARTER AND HEALTHIER CHILDREN BY EDUCATION, CLINICAL INTERVENTION, RESEARCH AND INFORMATION NETWORKING. Advancing of the future pediatric and future parenting to optimalized physical, mental and social health and well being for fetal, newborn, infant, children, adolescents and young adult

LAYANAN KLINIK KHUSUS “CHILDREN GRoW UP CLINIC”

PROFESIONAL MEDIS “CHILDREN GRoW UP CLINIC”

  • Dr Narulita Dewi SpKFR, Physical Medicine & Rehabilitation
  • Dr Widodo Judarwanto SpA, Pediatrician
  • Fisioterapis

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Ophthalmology Problems and Autoimmune Diseases

The immune system protects us from disease and is amazingly complex.  Like other complex systems in our body, the immune system can malfunction.  When the immune system malfunctions and acts on our own body’s tissues, that is autoimmune disease Autoimmune disease can affect any part of the body.  The most well known is rheumatoid arthritis of the joints, for which people may see a rheumatologist or orthopedic doctor.  Autoimmune diseases can also affect the brain, eyes, ears, liver, kidneys, lungs, heart,  stomach and intestines, muscles, and peripheral nerves.  Essentially any part of the body, including the eye, can be affected by autoimmune disease.

Autoimmune disease of the eye is known as uveitis.  Immune cells enter the eye, become active, and exert their effects (“inflammation”).  The normal eye does not have significant inflammation at any one time.

Dry eye  syndrome is a common complaint in a number of different autoimmune  disorders. In dry eye syndrome, the eyes are unable to produce adequate tears,  which leads to eye dryness, irritation and inflammation. Symptoms of dry eye  include stinging, burning, eye irritation, and a feeling of grittiness. Dry eyes  are often seen in thyroid eye  disease, which is a feature of autoimmune thyroid disease, and also  myasthenia gravis, Sjogren’s syndrome, uveitis, multiple sclerosis, Cogan’s  syndrome, and many other autoimmune conditions. In patients with diabetes,  immune system changes can lead to corneal abrasions and poor wound healing.

 

Ophtalmology Problems and Autoimmune Diseases


Disease Ocular manifestations
Rheumatoid arthritis Keratoconjunctivitis sicca, scleritis, episcleritis, keratitis, ulcerative keratitis, choroiditis, retinal vasculitis, episcleral nodules, retinal detachments, macular edema
Juvenile rheumatoid arthritis Uveitis
Sjögren’s syndrome Keratoconjunctivitis sicca
Ankylosing spondylitis Uveitis
Reiter’s syndrome Conjunctivitis, uveitis, keratitis
Enteropathic arthritis Uveitis, episcleritis, peripheral ulcerative keratitis
Psoriatic arthritis Uveitis, conjunctivitis, keratitis
Systemic lupus erythematosus Keratoconjunctivitis sicca, conjunctivitis, uveitis, episcleritis, scleritis, keratitis, retinal hemorrhages, retinal vasculitis, proliferative retinopathy, optic neuritis, ischemic optic neuropathy, hemianopia, amaurosis, internuclear ophthalmoplegia, pupillary abnormalities, oculomotor abnormalities, visual hallucinations
Multiple sclerosis Afferent: optic neuritis, retrobulbar neuritis, visual field defects
Efferent: internuclear ophthalmoplegia, dysmetria, nystagmus, cranial nerve palsies
Giant cell arteritis Amaurosis fugax, diplopia, vision loss
Graves’ disease Proptosis/exophthalmos, lid lag and retraction, keratitis, decreased visual acuity, reduced visual fields, relative afferent pupillary defect, loss of color vision
Myasthenia gravis Diplopia, eyelid ptosis
Sarcoidosis Uveitis, conjunctival nodules, cranial nerve palsies, enlarged lacrimal glands, optic neuropathy
Wegener’s granulomatosis Proptosis/exophthalmos, orbital cellulitis, uveitis, corneal ulcers, optic neuropathy
Behçet’s syndrome Uveitis, hypopyon
Antiphospholipid syndrome Vaso-occlusive retinopathy, ischemic optic neuropathy
Polyarteritis nodosa Episcleritis, scleritis, optic neuropathy
Takayasu’s arteritis Vaso-occlusive retinopathy, ischemic optic neuropathy, cataracts
Dermatomyositis Eyelid/conjunctival edema, retinopathy, uveitis

Manifestation Clinical of Ocular and Autoimmune Disease


Condition Symptoms Signs Treatment
Keratitis Pain with photophobia, foreign body sensation, tearing, red eye, decreased vision Inflammatory cell infiltrate, corneal opacification, corneal vascularization, corneal ulceration NSAIDs, topical/oral/IV steroids, immunosuppressives, surgery
Keratoconjunctivitis sicca Dry eye, burning, pain, blurred vision, pruritus, foreign-body sensation, mucous threads and crusting about the eyelids Diminished corneal tear meniscus, abnormal Schirmer’s test Sunglasses, room humidifiers, tear substitutes, surgery
Scleritis Gradual onset; deep, boring pain may radiate into cheek, eyebrows, and temples blurred vision; photophobia Decreased visual acuity; bluish appearance with engorged blood vessels; may have immovable, tender nodules over the sclera, general tenderness on palpation; engorged blood vessels do not blanch with phenylephrine (Neo-Synephrine); avascular areas over the sclera NSAIDs, topical/oral/IV steroids, immunosuppressives, surgery
Episcleritis Sudden onset; mild ache may radiate into cheek, eyebrows, and temples; no blurred vision; photophobia No change in visual acuity; bright red appearance with engorged blood vessels; may have movable, nontender nodules over the episclera; no tenderness on palpation; engorged blood vessels blanch with phenylephrine NSAIDs, topical/oral steroids
Uveitis Red eye, pain, photophobia, blurred vision Decreased visual acuity, inflammatory infiltrate in the anterior chamber, synechiae, pupillary miosis Cycloplegics, topical steroids, immunosuppressives
Optic neuritis Visual loss, pain with eye movement, photophobia Decreased visual acuity, loss of color vision, central scotoma, afferent pupillary defect, swollen optic nerve IV steroids with positive MRI findings
Exophthalmos Irritable and gritty eyes, double or blurred vision, photophobia, increased tearing, orbital pressure Protruding globe, widened palpebral fissures, conjunctival injection and chemosis, lid lag and retraction, exposure keratitis Lubricating eye drops, sleeping with head elevated, sunglasses, eyelid taping at night, steroids, radiotherapy, surgery

NSAIDs = nonsteroidal anti-inflammatory drugs; IV = intravenous; MRI = magnetic resonance imaging.

Sjögren’s Syndrome

The primary ocular manifestation of Sjögren’s syndrome is keratoconjunctivitis sicca. The signs and symptoms are similar to those of keratoconjunctivitis sicca associated with RA. In addition to the treatment noted above, 5 mg of oral pilocarpine (Salagen) four times daily may improve the symptoms of dry eyes and dry mouth. Patients should be cautioned that the side effects of diaphoresis and poor night vision may occur.

Spondyloarthropathies

Among the seronegative spondyloarthropathies, uveitis in ankylosing spondylitis is the most common ocular manifestation. It occurs in approximately 25 percent of patients with ankylosing spondylitis, in up to 37 percent of patients with Reiter’s syndrome, in approximately 20 percent of patients with psoriatic arthritis, and in up to 9 percent of patients with enteropathic arthritis (arthritis associated with Crohn’s disease or ulcerative colitis). Ocular symptoms can be unilateral or bilateral, and pain is caused by ciliary spasm in response to anterior chamber inflammation. As noted earlier, patients suspected of having uveitis should be referred to an ophthalmologist. Complications include glaucoma, cataracts, or blindness.

Systemic Lupus Erythematosus

Ocular disease occurs in 20 percent of patients with systemic lupus erythematosus (SLE). In some cases, ocular disease may indicate reactivation of SLE that was thought to be in remission. External ocular manifestations include keratoconjunctivitis sicca, conjunctivitis, uveitis, episcleritis, scleritis, keratitis, and a discoid lupus rash over the eyelids that is often confused with blepharitis. Neuroophthalmic involvement in SLE is primarily caused by microinfarction, hemorrhage, or vasculitis in various locations of the eye and along the visual pathway. Typical complications include optic neuritis, ischemic optic neuropathy, hemianopia, amaurosis, internuclear ophthalmoplegia, pupillary abnormalities, oculomotor abnormalities, pseudotumor cerebri, and visual hallucinations. Retinal disease primarily occurs in patients with active SLE and may include cotton-wool spots , retinal hemorrhages, retinal vasculitis, or proliferative retinopathy. Treatment of ocular disease is based on specific pathology and underlying disease. Keratoconjunctivitis sicca is thought to be the most common manifestation and can be treated as noted above

Retinal disease has a high morbidity and should be treated aggressively by an ophthalmologist. Ophthalmic screening programs in SLE are controversial. Most physicians agree that patients on antimalarial or steroid regimens should receive a full dilated-eye examination on initiation of therapy then with routine examinations in low-risk patients and yearly for high-risk patients. High risk is defined by medication dosage (>6.5 mg per kg hydroxychloroquine or >3 mg per kg chloroquine), duration of use (more than five years), high body fat level, presence of renal or liver disease, presence of concomitant retinal disease, and age greater than 60 years

Uveitis

Uveitis can reduce vision in may ways.  Going from “front to back,” the cornea, the very front window into the eye, may develop calcium deposits that block vision.  The lens of the eye may develop clouding, known as cataract.  The front colored portion of the eye, the iris, may develop adhesions.  The vitreous gel of the eye may develop cloudiness (“haze”) and floaters.  The center of the retina, the macula, may develop swelling (macular edema).  If the RPE-choroid underneath the retina thins or atrophies with chronic inflammation the retina itself will lose visual function.  The cells in the retina can degenerate with chronic inflammation.

Classify uveitis as:

  • anterior if it affects the front part of the eye.
  • intermediate if it affects the middle or vitreous gel portion of the eye.
  • posterior if it affects the retina and/or choroid.
  • ”pan” as in “panuveitis” if all three compartments of the eye are affected.

Uveitis is treated with medicines that damp down the activity of the immune system. Steroids are are first  line of treatment.  Steroid eye drops may treat uveitis in the front portion of the eye.  For intermediate or posterior uveitis affecting the vitreous gel or retina and choroid, steroid eye drops alone are insufficient.  We recommend steroids taken by mouth and/or injections of steroids underneath the skin layer of the eye (“subTenons” injection).   Steroids are generally used for one to three months to quiet the inflammation and the dosage is then tapered.  Steroids are not continued indefinitely as long term steroid use has significant side effects, both on the eye itself and on the rest of the body (when the steroids are taken by mouth). In some patients, uveitis treated in this fashion will “stay quiet” for months to years after the steroids are stopped.  In other patients with more severe disease, the inflammation will return quickly.  In these patients, therapy may be needed for months to years.  In this case, we recommend alternative non-steroid medications that can be taken for longer time periods without the side effects of steroids.  These medications are borrowed from the field of organ transplantation and include methotrexate, azathioprine (Imuran), mycophenolate (Cellcept), cyclosporine, infliximab (Remicade), daclizumab (Zenapax), and others.

Rheumatoid Arthritis

Approximately 25 percent of patients with rheumatoid arthritis (RA) will have ocular manifestations. These may include keratoconjunctivitis sicca, scleritis, episcleritis, keratitis, peripheral corneal ulceration, and less common entities such as choroiditis, retinal vasculitis, episcleral nodules, retinal detachments, and macular edema.

Keratoconjunctivitis sicca, or dry eye syndrome, is the most common ocular manifestation of RA and has a reported prevalence of 15 to 25 percent.  Symptoms are historically more prominent during the latter part of the day because of the evaporation of the tear film. A simple and easy-to-perform test assessing the function of the lacrimal glands is the Schirmer’s test. It is performed by first drying the tear film, then inserting a Schirmer strip into the lower conjunctival cul-de-sac toward the temporal aspect of the lower lid. No anesthetic should be used. After five minutes, if the strip measures less than 10 mm of wetting, the lacrimal glands are not functioning correctly. If a slit lamp is available, corneal examination may reveal punctate erosive keratopathy or filaments

Juvenile Rheumatoid Arthritis

Juvenile rheumatoid arthritis accounts for approximately 80 percent of cases of uveitis in children.  Delay in diagnosis can lead to cataracts, glaucoma, and blindness. Although uveitis can be found in all forms of juvenile RA, it is most commonly found in the pauciarticular subtype. Most patients will be symptom-free or have blurred vision. On examination, the patient may have decreased visual acuity, band keratopathy, synechiae, cataracts, or elevated ocular pressure. Diagnosis or suspicion of juvenile RA should prompt a referral to a pediatric ophthalmologist. Recommendations for ocular screening examinations are based on the risk of developing uveitis. Therapy involves close monitoring by an ophthalmologist, with the use of cycloplegic agents, steroids, NSAIDs, or immunosuppressive agents

Multiple Sclerosis

The ocular manifestations of multiple sclerosis (MS) can be divided into afferent and efferent disorders. Optic neuritis is diagnosed in 75 percent of patients with MS and is the presenting symptom in 14 to 25 per cent of cases. Visual field defects in patients with MS are a result of demyelination along the visual pathway. Bilateral internuclear ophthalmoplegia is almost always caused by a demyelinating disorder. Dysmetria, nystagmus, and cranial nerve palsies, especially involving the sixth and third nerves, may result from lesions of the brain stem and cerebellum.

Nystagmus, which may be the first neurologic finding in patients with MS, is commonly horizontal but may also be rotary or vertical. Patients with suspected ocular involvement should receive magnetic resonance imaging (MRI), a full dilated-eye examination, and treatment with intravenous corticosteroids if the MRI is positive. Periodic follow-up evaluations should be done to monitor the progression of disease.

Giant Cell Arteritis

Up to 50 percent of patients with giant cell arteritis present with ocular symptoms that include pain, diplopia, visual loss, and amaurosis fugax, in addition to headache, jaw claudication, and neck pain. It is important to note that ocular involvement is common in the absence of systemic signs and symptoms. Patients may have temporal artery tenderness or a decreased temporal artery pulse, but diagnosis is confirmed with biopsy of the artery and elevated titers of erythrocyte sedimentation rate and C-reactive protein. Biopsy will remain positive for up to two weeks after the initiation of corticosteroid therapy. Intravenous corticosteroids should be used in patients with visual symptoms. Immediate therapy can be dramatic in effect and prevent further vasculitic complications, permanent blindness, or death.

Graves’ Disease

Exophthalmos occurs in approximately 50 percent of patients with thyroid disease. It is strongly associated with smoking and may also be found in patients who are euthyroid or hypothyroid. If signs of optic nerve compression, such as decreased visual acuity, reduced visual fields, relative afferent pupillary defect, and loss of color vision are present, computed tomography or MRI of the orbit is recommended.

REFERENCES

  • Nguyen QD, Foster CS. Systemic lupus erythematosus and the eye. Int Ophthalmol Clin. 1998;38:33–60.
  • Soo MP, Chow SK, Tan CT, Nadior N, Yeap SS, Hoh HB. The spectrum of ocular involvement in patients with systemic lupus erythematosus without ocular symptoms. Lupus. 2000;9:511–4.
  • Davis EA, Rizzo JF. Ocular manifestations of multiple sclerosis. Int Ophthalmol Clin. 1998;38:129–39.
  • Neff AG, Greifenstein EM. Giant cell arteritis update. Semin Ophthalmol. 1999;14:109–12.
  • Hayreh SS, Podhajsky PA, Zimmerman B. Ocular manifestations of giant cell arteritis. Am J Ophthalmol. 1998;125:509–20.
  • Adam A, Mishriki YY. The painful, protruding eye. Unilateral euthyroid Graves’ ophthalmopathy. Postgrad Med. 1999;105:81–4.
  • Coday MP, Dallow RL. Managing Graves’ orbitopathy. Int Ophthalmol Clin. 1998;38:103–15.
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  • Friedlaender MH. Ocular manifestations of Sjögren’s syndrome: keratoconjunctivitis sicca. Rheum Dis Clin North Am. 1992;18:591–608.
  • McGavin DD, Williamson J, Forrester JV, Foulds WS, Buchanan WW, Dick WC, et al. Episcleritis and scleritis. A study of their clinical manifestations and association with rheumatoid arthritis. Br J Ophthalmol. 1976;60:192–226.
  • Watson PG, Hayreh SS. Scleritis and episcleritis. Br J Ophthalmol. 1976;60:163–91.
  • Messmer EM, Foster CS. Destructive corneal and scleral disease associated with rheumatoid arthritis. Medical and surgical management. Cornea. 1995;14:408–17.
  • Waheed NK, Miserocchi E, Foster CS. Ocular concerns in juvenile rheumatoid arthritis. Int Ophthalmol Clin. 2001;41:223–34.
  • Rosenbaum JT. Acute anterior uveitis and spondyloarthropathies. Rheum Dis Clin North Am. 1992;18:143–51.
  • Bañares A, Hernández-García C, Fernández-Gutiérrez B, Jover JA. Eye involvement in the spondyloarthropathies. Rheum Dis Clin North Am. 1998;24:771–84.
  • Lyons JL, Rosenbaum JT. Uveitis associated with inflammatory bowel disease compared with uveitis associated with spondyloarthropathy. Arch Ophthalmol. 1997;115:61–4.

Provided by

CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation htpp://www.allergyclinic.wordpress.com/

WORKING TOGETHER FOR STRONGER, SMARTER AND HEALTHIER CHILDREN BY EDUCATION, CLINICAL INTERVENTION, RESEARCH AND INFORMATION NETWORKING. Advancing of the future pediatric and future parenting to optimalized physical, mental and social health and well being for fetal, newborn, infant, children, adolescents and young adult

LAYANAN KLINIK KHUSUS “CHILDREN GRoW UP CLINIC”

PROFESIONAL MEDIS “CHILDREN GRoW UP CLINIC”

  • Dr Narulita Dewi SpKFR, Physical Medicine & Rehabilitation
  • Dr Widodo Judarwanto SpA, Pediatrician
  • Fisioterapis

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Allergy March, Perbedaan Perjalanan Alamiah Setiap Usia dan Setiap Individu

“PADA PENDERITA ALERGI SETIAP INDIVIDU DAN SETIAP USIA ORGAN TUBUH YANG  SENSITIF BERBEDA KARENA ALERGI BERPINDAH ORAGAN TARGET SASARAN, BUKAN BERARTI ALERGI SEMBUH PADA USIA TERTENTU TETAPI BERPINDAH KE SENSITIF ORGAN LAINNYA: Widodo judarwanto 2004

allergy-march1

PERJALANAN ALAMIAH PENYAKIT ALERGI :

Berbagai pendapat dan teori baik dari kalangan awam dan para ahli tentang perjalanan alergi sangat beragam. Sebagian orang awam meyakini dahulu dirinya mengalami asma pada saat usia anak, tetapi setelah rajin olahraga dan berenang asmanya hilang. Orang lain berkesaksian setelah minum vitamin, atau darah ular asmanya hilang. Sedangkan orangtua lain menceritakan setelah sering bermain di pantai asmanya hilang. Sedangkan dokter berpendapat lain, setelah memberikan pasiennya obat pencegahan asma golongan ketotifen, gejala asma pasiennya menghilang setelah usia 12 tahun. Benarkah berbagai hal tersebut dapat menghilangkan penyakit asma? Ternyata berbagai penelitian mengungkapkan bahwa terdapat Allergy March atau perjalanan alamiah penyakit alergi yang timbul sesuai dengan perkembangan usia. Perjalanan alamiah alergi tersebut menunjukkan bahwa pada usia tertentu manifestasi klinisatau organ tubuh yang terganggu tampak berbeda.

Meskipun banyak variasi Allergy March yang terjadi tetapi secara umum digambarkan setiap usia manifestasi organ yang terganggu berbeda. Pada usia sejak lahir hingga usia 5-7 tahun organ tubuh yang sangat sensitif adalah kulit dan saluran cerna. Setelah itu saluran napas termasuk asma dan hidung mulai sering terganggu. Pada usia remaja setalah memasuli usia dewasa asma berkurang tetapi gangguan hidung masih berkepanjangan. Tampaknya fenomena perjalanan alamiah alergi inilah yang menunjukkan pada usia tertentu asma akan menghilang. Hal inilah yang sering dikaitkan dengan intervensi upaya pengobatan pada penyakit asma dan tingkat keberhasilannya. Contohnya, gangguan kulit, saluran cerna dan asma dianggap hilang saat usia tertentu karena olah raga renang, bermain dipantai, minum darah ular, atau binatang ”tokek”. Tetapi orangtua jangan berharap senang, karena ternyata setelah gangguan kulit, gangguan saluran cerna dan asmanya menghilang orag tubuh yang terganggu adalah hidung. Jadi, sebenarnya alegi tidak membaik, hanya organ tubuh yang terganggu berpindah tempat dari kulit, ke asma dan berikutnya ke hidung. Perjalanan alamiah alergi setiap individu berbeda tergantung karakteristik fenotip tiap orang. Ternyata karakteristik perjalanan alamiah alergi orangtua atau saudara kandung yang wajahnya sama dengan anak dapat dijadikan pedoman krakteristik perjalanan alamian anak di masa depan.

Setiap individu dengan fenotipe berbeda dan setiap periode usia mempunyai karakter alergi yang berbeda. Seringkali alergi menganggu berabagai organ tubuh sevcara bersamaan seperti kulit, saluran cerna, saluran napas, tetapi setiap anak berbeda dominasi yang sensitif. Anak yang satu lebih dominan sensitif saluran cerna anak lainnya lebih dominan sensitif kulit sedangkan anak lainnya lebih dominan sensitif saluran napas. Pada individu tertentu pada satu keluarga atau bayi kembar, sama sensitif kulitnynya tetapi anak satu kulitnya lebih sensitif tetapi anak lainnya manifestasinya lebih ringan. Begitu juga dengan gangguan sensitif lainnya , sama-sama mempunyai sensitif saluran cerna tetapi anak yang satu sulit BAB tetapi anak lainnya sering muntah. Demikian juga sensitif saluran napas, anak yang satu kalau flu lebih dominan gangguan hidung sedangkan anak lainnya gangguan batuk atau dahaknya lebih banyak sehingga harus diinhalasi atau diuap.

Begitu juga dengan periode usia yang terganggu setiap usia berbeda sesuai denga perjalanan alamiah penyakit alergi atau “Allergy march”. Anak tertentu sesak usia sebelum prasekolah tetapi anak lainnya baru sesak usia SD atau SMP. Pada usia 0-5 tahun kulit dan pencernaan lebih sensitif tetapi masuk usia SD dan SMP pencernaannya membaik tetapi berpindah ke saluran napas berupa sesak dan asma dan saat dewasa sesak hilang tetapi berpindah ke hidung sensitif dan disertai sinusitis

Karakteristrik alergi sesuai fenotip atau tipikal tertentu pada setiap individu berbeda

Tanda dan gejala alergi setiap individu seringkali berbeda organ tubuh yang sensitif. Pada hampir semua penderita alergi pada umumnya mengalami  menifestasi sensitif pada hampir semua organ tubuh khususnya saluran cerna, saluran napas, hidung dan kulit secara bersamaan. Tetapi setiap kelompak anak yang satu dan yang lainnya berbeda yang lebih dominan, pada anak tertentu lebih dominan sensitif saluran napas batuk atau hidung sensitif , anak lainnya lebih dominan kulit sedangkan anak lainnya lebih dominan saluran cerna yang sensitif.

Adapun beberapa manifestasi klinis alergi sesuai dengan fenotip tertentu adalah sebagai berikut

TIPE A (TIPE RINITIS):  Dominan sensitif saluran napas hidung

  • Mudah terkena flu, hidung buntu dan sering bersin.  Beresiko terjadi sinusitis terutama setelah usia 5 tahun.
  • Sebagaian besar kasus disertai sensitif kulit di lengan atas sering bruntusan kecil-kecil
  • Sebagian besar kasus disertai gangguan sensitif saluran cerna khusus nyeri perut dan sulit BAB.

TIPE B (TIPE ASMATIK):  Dominan sensitif saluran napas batuk

  • Pada usia 0 – 6 tahun napas berbunyi grok-grok atau hipersekresi bronkus dan mudah bersin. Saluran napas khususnya bronkitis alergi dan asma dengan  gejala  sesak dan batuk berulang. Bila sakit infeksi saluran napas dahaknya berlebihan sehingga seringkali memerlukan inbhalasi.
  • Terdapat dua kelompok besar, Tipikal asmatik pra sekolah dan Tipikal Asmatik murni
  • Terdapat dua kelompok besar, Tipikal asmatik pra sekolah. Sebagian kelompok terjadi sesak, timbul wheezing atau mengi sebelum pra sekolah. Pada kasus ini bila batuk sering dahaknya berlebihan dan sering dilakukan inhalasi saat batuk. Setelah usia 5-7 tahun sebagian besar kasus sesak membaik, tetapi sebagian kecil kasus menteap tetapi sesak sangat ringan sekakil tetapi hidung lebih sensitif.
  • Tipikal Asmatik murni: pada kelompok ini sesak, timbul wheezing atau mengi justru timbul setelah usia 5 – 12 tahun. Setelah usia SMP sesak berkurang tetapi mulai terjadi sensitif hidung atau rinitis alergi
  • Disertai saluran cerna sensitif : sering muntah, nyeri perut dan gangguan buang air besar , bisa konstipasi atau sering BAB. Sensitif kulit sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya.

 

TIPE C (SALURAN CERNA):  Dominan sensitif saluran cerna

  • Saluran Cerna sensitif : Gastrooesepageal refluks, sering muntah, nyeri perut dan gangguan buang air besar , bisa konstipasi atau sering BAB.
  • Sensitif kulit sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya.
  • Daya tahan tubuh tidak baik, mudah sakit batuk dan pilek, dan disertai sulit makan dan gangguan mengunyah menelan.
  • Sebagioan besar kasus berat badan sangat gemuk dan sebagian terjadi kegemukan. sebagian kecil terjadi gangguankenaikkan berat badan pada usia sebelum 3-5 tahun.
  • Beberapa kasus disertai gangguan keterlambatan bicara yang sebagian besar  membaik setelah usia 2 tahun. Tetapi berganti sensitif hidung atau rinitis alergi tetapi terjadi lebih ringan dibandingkan tipe 2 (rinitis). Sebagian besar kasus mudah mengalami minisan atau hidung berdarah

 

TIPE D (SENSITIF KULIT): Dominan sensitif kulit

  •  Sensitif kulit sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya. Pada usia 0-9 bulan terjadi dermatitis atopi pada pipi dan daerah popok sering kemerahan. Pada usia 1-5 tahun kulit sensitif berpindah ke tangan dan kaki seperti digigit nyamuk dan kulit kering.
  • Saluran Cerna sedikit sensitif : sering konstipasi atau sulit buang air besar atau sebagian kecil lainnya sering BAB.
  • Daya tahan tubuh relatif baik jarang mengalami batuk dan pilek. Tetapi sebagian kecil kasus daya tahan tubuh tidak baik mudah batuk dan pilek teruitama kelompok anak kulit sensitif disertai gangguan muntah dan mual. Anak tidak bisa diam , sangat lincah dan emosi sangat tinggi

TIPE E (GANGGUAN BERAT BADAN): Dominan sensitif  saluran cerna

  •  Sensitif kulit sering gatal, tangan dan kaki seperti digigit nyamuk dan kulit kering.
  • Saluran Cerna sedikit sensitif : sering konstipasi atau sulit buang air besar atau sebagian kecil lainnya sering BAB.
  • Daya tahan tubuh relatif baik jarang mengalami batuk dan pilek. Tetapi sebagian kecil kasus daya tahan tubuh tidak baik mudah batuk dan pilek teruitama kelompok anak kulit sensitif disertai gangguan muntah dan mual. Anak tidak bisa diam , sangat lincah dan emosi sangat tinggi

PERJALANAN ALAMIAH ALERGI BEBERAPA KELOMPOK FENOTIP TERTENTU

Tanda dan gejala alergi setiap usia seringkali berbeda organ tubuh yang sensitif. Pada hampir semua penderita alergi pada umumnya mengalami  menifestasi sensitif pada hampir semua organ tubuh khususnya saluran cerna, saluran napas, hidung dan kulit secara bersamaan. Tetapi setiap kelompak usia yang sensitif , pada anak tertentu lebih dominan sensitif saluran napas batuk atau hidung sensitif , anak lainnya lebih dominan kulit sedangkan anak lainnya lebih dominan saluran cerna yang sensitif.

Adapun beberapa manifestasi klinis alergi sesuai dengan fenotip tertentu adalah sebagai berikut

TIPE A (TIPE ASMATIK):  Dominan sensitif saluran napas batuk

  • Usia 0-5 tahun : Saluran Cerna sensitif : sering muntah, nyeri perut dan gangguan buang air besar , bisa konstipasi atau sering BAB. Sensitif kulit sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya. Pada usia 0 – 6 tahun napas berbunyi grok-grok atau hipersekresi bronkus.
  • Usia 6 – 12 tahun : Saluran napas khususnya bronkitis alergi dan asma dengan  gejala  sesak dan batuk berulang. Sudah mulai terjadi sensitif hidung atau rinitis alergi
  • Usia 13 tahun hingga dewasa: Asma berkurang tetapi berganti hidung lebih sensitif sering bersin, sinustis. Saluran cerna dan kulit gangguan berkurang

TIPE B (TIPE RINITIS):  Dominan sensitif saluran napas hidung

    • Usia 0-5 tahun : Hidung sensitif biasanya sering bersin, kotoran hidung berlebihan , mudah mimisan atau hidung berdarah. Juga disertai saluran cerna sensitif : sering muntah, nyeri perut dan gangguan buang air besar , bisa konstipasi atau sering BAB. Sensitif kulit: sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya.
    • Usia 6 – 12 tahun : Sensitif kulit dan saluran cerna berkurang tetapi berganti lebih dominan sensitif hidung atau rinitis alergi. Mudah terkena flu, hidung buntu dan sering bersin. Beresiko terjadi sinusitis. Terjadi sensitif kulit di lengan atas sering bruntusan kecil-kecil.
    • Usia 13 tahun hingga dewasa:  Hidung sensitif sedikit berkurang tetapi sebagian kelompok kasus menetap hingga dewasa. Saluran cerna dan kulit gangguan berkurang. Tetapi sebagian besar kasus mengalami jerawat ringan saat usia setelah 12 tahun dan sensitif kulit di lengan atas bagian luar sering bruntusan kecil-kecil.

TIPE C (SALURAN CERNA):  Dominan sensitif saluran cerna

  • Usia 0-5 tahun : Saluran Cerna sensitif : sering muntah, nyeri perut dan gangguan buang air besar , bisa konstipasi atau sering BAB. Sensitif kulit sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya. Daya tahan tubuh tidak baik, mudah sakit batuk dan pilek, dan disertai sulit makan dan gangguan mengunyah menelan. Beberapa kasus disertai gangguan keterlambatan bicara yang sebagian besar  membaik setelah usia 2 tahun.
  • Usia 6 – 12 tahun : Saluran cerna masih sensitif tetapi sudah jauh membaik, gangguan muntah jauh membaik  tetapi kadangkala masih timbul gangguan nyeri perut dan mual khususnya pada pagi hari. Keluhan mual akan membaik saat usia 7-8 tahun.  Daya tahan tubuh membaik dan gangguan kesulitan makan dan gangguan mengunyah menelan sudah semakin membaik. Pada usia ini mulai sering disertai gangguan sakit kepala dan gangguan konsentrasi sekolah. Tetapi berganti sensitif hidung atau rinitis alergi tetapi terjadi lebih ringan dibandingkan tipe 2 (rinitis)
  • Usia 13 tahun hingga dewasa: Gangguan pencernaan sebagian besar kasus menetap hingga dewasa, Sebagian besar kasus mengalami jerawat ringan saat usia setelah 12 tahun. Jerawat ringan akan menetap pada usia dewasa dan sering terjadi peri oral dermatitis jerawat atau sensitif kulit khususnya sekitar mulut terutama di bawah bibir bawah atau dagu. Sebagia kasus hidung sensitif mudah bersin tetapi lebih ringan dibandingkan tipe 2 (rinitis)

TIPE D (SENSITIF KULIT): Dominan sensitif saluran napas hidung

  • Usia 0-5 tahun : Sensitif kulit sering gatal, merah seperti digigit nyamuk dan gangguan sensitif kulit lainnya. Pada usia 0-9 bulan terjadi dermatitis atopi pada pipi dan daerah popok sering kemerahan. Pada usia 1-5 tahun kulit sensitif berpindah ke tangan dan kaki seperti digigit nyamuk dan kulit kering. Saluran Cerna sedikit sensitif : sering konstipasi atau sulit buang air besar atau sebagian kecil lainnya sering BAB.  Daya tahan tubuh relatif baik jarang mengalami batuk dan pilek. Tetapi sebagian kecil kasus daya tahan tubuh tidak baik mudah batuk dan pilek teruitama kelompok anak kulit sensitif disertai gangguanmuntah dan mual. Anak tidak bisa diam , sangat lincah dan emosi sangat tinggi
  • Usia 6 – 12 tahun : Pada usia ini sebagian kasus gangguan kulit berpindah ke paha bagian belakang, lipatan tangan dan lipatan kaki. Tetapi berganti sensitif hidung atau rinitis alergi tetapi terjadi lebih ringan dibandingkan tipe 2 (rinitis)
  • Usia 13 tahun hingga dewasa: Pada usia ini sebagian kasus gangguan kulit berpindah ke paha bagian belakang, lipatan tangan dan lipatan kaki. Timbul jerawat berlebihan pada muka di sekitar mulut. Tetapi sebagian besar kasus kulitnya membaik tetapi sebagian kecil kasus menetap hingga dewasa.

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MENGAPA TERJADI ALERGI MARCH

Terdapat 3 faktor penyebab terjadinya alergi makanan, yaitu faktor genetik, imaturitas usus, pajanan alergi yang kadang memerlukan faktor pencetus. Alergi bersifat genetik dan dapat diturunkan dari orang tua atau kakek/nenek pada penderita . Faktor penyebab terjadi alergi yang lain adalah factor imaturitas saluran cerna atau ketidakmatangan saluran cerna. Secara mekanik integritas mukosa usus dan peristaltik merupakan pelindung masuknya alergen ke dalam tubuh. Secara kimiawi asam lambung dan enzim pencernaan menyebabkan denaturasi allergen. Secara imunologik sIgA pada permukaan mukosa dan limfosit pada lamina propia dapat menangkal allergen masuk ke dalam tubuh. Pada usus imatur sistem pertahanan tubuh tersebut masih lemah dan gagal berfungsi sehingga memudahkan alergen masuk ke dalam tubuh. Faktor pajanan alergi yang merangsang produksi IgE spesifik sudah dapat terjadi sejak bayi dalam kandungan. Faktor imaturitas saluran cerna inilah tampaknya yang bnerperanan dalam perjalanan alamiah alergi seseorang. Saat usia sejak lahir ketidak matangan saluran cerna sangat berat pada bayi tertentu seperti sering muntah, kolik, dan gangguan kulit. Seiring dengan pertambahan usia, setelah 3 bulan kolik berangsur berkurang, usia 6 hingga 2 tahun keluhan muntah berkurang.

PERIODE JANIN

Alergi adalah penyakit dengan pola Th2. Pada orang normal yang non atopi, pola sitokin Th1 dan Th2 dalam keadaan seimbang. Sedangkan pada penderita atopi, keseimbangan lebih berat pada pola sitokin Th2 . Pada masa kehamilan dominasi juga pada pola sitokin Th2. Sawar darah placenta masih transparan terhadap alergen dalam lingkungan ibu. Faktor lingkungan dapat bekerja sebelum dan sesudah lahir. Faktor lingkungan sebelum lahir dapat mempengaruhi diferensiasi sel T yang allergen spesifik menjadi fenotipe Th2, sehingga alergi atopi sudah bekerja sebelum lahir. Kehamilan yang berhasil ditandai dengan pergeseran Th1 ke Th2 di fase antar fetomaternal untuk mengurangi reaktifitas sistem imun maternal terhadap allograft janin. Setelah kelahiran sistem imán menjadi matang, kesimbangan bergeser ke arah Th1, sehingga profil sitokin Th1 daTh2 menjadi seimbang. Pada bayi yang punya bakat atopi keseimbangan ini tidak pernah tercapai sehingga dominasi Th2 terus terjadi, mengakibatkan sensitisasi dan timbulnya gangguan alergi. Dalam perkembangan terakhir ditemukan T regulator, sehingga ada peluang terjadi supresi imun toleran. Fenomena ini dapat digunakan upaya pencegahan primer.

PERIODE BAYI 0-7 TAHUN

Pada periode ini gangguan organ tubuh yang paling sering terjadi adalah gangguan kulit dan saluran cerna. Karena imaturitas saluran pencernaan inilah maka gangguan pencernaan yang disebabkan karena alergi paling sering ditemukan pada anak usia di bawah 2 tahun, yang paling sensitif di bawah 3 bulan. Pada bayi baru lahir hingga usia 3 tahun biasanya ditandai sering rewel, colic/menangis terus menerus tanpa sebab pada malam hari, hiccups (cegukan), sering “ngeden”, sering mulet, meteorismus, muntah, sering flatus, berak berwarna hitam atau hijau, berak timbul warna darah. Pada lidah sering ditemukan berwarna putih. Gangguan buang air besar dapat berupa sulit buang air besar (tidak setiap hari) atau malahan sering buang air besar . Pada yang lebih besar dapat berupa nyeri perut berulang, sering buang air besar (>3 kali/perhari), gangguan buang air besar (kotoran keras, berak, tidak setiap hari, berak di celana, berak berwarna hitam atau hijau, berak ngeden) kembung, muntah, sulit berak, sering flatus, sariawan, mulut berbau dan lidah sering kotor (geographic tongue). Gangguan pada saluran cerna biasanya sering disertai oleh gangguan kulit dan rhinitis. Biasanya keluhan gangguan saluran cerna bersamaan dengan gangguan kulit. Mulut adalah termasuk salah satu bagian dari sistem saluran cerna. Bila saluran cerna terganggu karena alergi makanan biasanya tampak juga gangguan pada organ tubuh di daerah mulut di antaranya lidah, gigi dan bagian di rongga mulut lainnya. Pada bayi lidah sering tampak kotor berwarna putih, gejala ini mirip gangguan moniliasis (like moniliasis symptoms) sejenis jamur pada mulut. Bedanya pada alergi warna putih hanya tipis dan tidak terlalu tebal, namun pada moniliasis tampak lebih tebal. Bila gangguan tersebut karena jamur biasanya dengan obat tetes mulut jamur akan cepat membaik, namun bila karena alergi biasanya diberi obat jamur tetap tidak akan membaik dan tetap sering timbul. Bila karena alergi sebaiknya tidak perlu diberi obat jamur, namun cukup dibersihkan dengan kasa basah. Pada anak yang lebih besar gangguan alergi bisa menimbulkan sariawan atau luka (aphtous ulcer) pada lidah dan mulut yang sering berulang. Biasanya juga disertai lidah kotor mirip gambaran pulau-pulau (geographic tounge). Gangguan lain adalah timbulnya nyeri gigi atau gusi yang bukan di sebabkan karena infeksi atau gigi berlubang. Gangguan ini biasanya sering dianggap sebagai impacted tooth (gigi yang tumbuhnya miring). Tanda dan gejala alergi pada kulit biasanya sudah dapat di deteksi sejak lahir. Bayi yang baru lahir apabila sejak dalam kandungan sudah terpapar oleh pencetus alergi tampak terdapat bintil dan bercak kemerahan dan kusam pada kulit dahi dan wajah, kadang disertai timbulnya beberapa papul warna putih di hidung. Apabila pencetus alergi tersebut berlangsung terus maka sering. Pada bayi sering timbul dermatitis atopi di pipi, daerah popok (dermatitis diapers) dan telinga, kadang dijumpai dermatitis seboroikum atau timbul kerak di kulit kepala. Sering juga timbul bintik kemerahan di sekitar mulut. Kadang timbul furunkel di kepala dan badan. Sering urticaria, miliaria, bengkak di bibir, lebam biru kehitaman seperti bekas terbentur, bercak ke hitam seperti bekas digigit nyamuk. Perbedaan lokasi alergi kulit sesuai dengan usia tertentu. Pada bayi sering lokasi alergi sekitar wajah dan daerah popok, pada usia anak lokasi tersebut biasanya berpindah pada darerah lengan dan tungkai. Sedangkan pada anak yang lebih besar atau usia dewasa lokasi alergi kulit biasanya pada pelipatan dalam antara lengan atas dan bawah atau pelipatan dalam antara tungkai atas dan bawah. Ternyata saat gangguan hipersensitif pada saluran cerna inilah sering timbul berbagai masalah pada penderita alergi. Saat saluran cerna terganggu atau sensitif akan mengakibatkan daya tahan tubuh seorang anak memburuk. Hal ini terjadi karena merkanisme pertahanan tubuh seseorang hampir sebagian besar atau sekitar 70% dibentuk di saluran cerna.

Selama masa usia 0-5 tahun gangguan saluran cerna seperti sering muntah, neyri perut dan sulit BAB adalah fase dimana anak sangat vrentan atau mudah terserang infeksi seperti demam, batuk dan pilek. Hal inilah juga menunjukkan bahwa banyak gangguan perilaku pada anak terjadi sebelum usia 5-7 tahun lebih berat atau berkurang setelah usia 5-7 tahun. Gangguan perilaku tersebut meliputi gangguan bicara, gangguan emosi, gangguan konsentrasi, gangguan tidur, gangguan motorik dan sebagainya.

PERIODE 7-12 TAHUN

Setelah usia 5-7 tahun gangguan kulit dan saluran cerna cenderung membaik. Pada periode ini organ tubuh yang terganggu berpeindah pada saluran napas yang paling sering ditemukan. Manifestasi klinisnya berupa keluhan batuk, pilek, tanpa,atau dengan disertai sesak atau asma. Keluhan tersebut biasanya terjadi pada malam atau pagi hari. Biasanya keluhan tersebut lama sembuhnya meskipun sudah diobati.

PERIODE 12 TAHUN DEWASA

Setelah usia 12 tahun biasanya asma jauh berkurang meskipun pada sebagian kecil menetap hingga usia dewasa. Pada usia ini organ tubuuh yang sensitive berpindah pada hgidung. Manifestasi klinis alergi pada Telinga Hidung Tenggorok berupa rinitis, hidung gatal, bersin dan sinusitis. Kadang dijumpai tenggorokan atau palatum terasa gatal dan post nasal drip. Bila keluhan sering terjadi dan berlanjut akan menyebabkan komplikasi sinusitis, epistaksis, deviasi septum nasi, tonsillitis kronis atau faringitis kronis. Ciri khas pada anak biasanya dijumpai tanda hidung kelinci (rabbit nose) yaitu anak sering menggerak-gerakkan hidung, sering menggosok-gosok hidung (salam alergi), mata sering gatal, belekan dan sering berair, di bawah kelopak mata tampak tanda kehitaman (allergic shiner). Bila tidur sering ngorok, atau napas dengan mulut, kadang juga timbul suara serak atau parau. Sering timbul benjolan kelenjar di leher dan belakang kepala.

  • Fenomena perjalanan alamiah alergi ini ternyata sangat penting untuk pertimbangan pencegahan penyakit alergi dikemudian hari. Misalnya, penderita bayi dengan gangguan kulit, saluran cerna yang mempunyai riwayat orangtua alergi akan beresiko mengalami asma dikemudian hari. Kejadian asma dikemudian hari inilah yang dapat dicegah bila manifestasi alergi saat usia bayi dan anak dapat diminimalkan. Demikian juga gangguan rinitis dan sinbusitis di masa dewasa dapat dicegah bila manifesasi alergi sejak dini diminmalkan. Sehingga gejala dan manifestasi alergi saat usia bayi dan anak harus diwaspadai dan diminmalkan karena dapat meminimalkan perjalanan alamiah penyakit alergi di kemudian hari.
  • Bila terdapat riwayat keluarga baik saudara kandung, orangtua, kakek, nenek atau saudara dekat lainnya yang alergi atau asma. Dan bila anak sudah terdapat ciri-ciri alergi sejak lahir atau bahkan bila mungkin deteksi sejak kehamilan maka harus dilakukan pencegahan sejak dini. Resiko alergi pada anak dikemudian hari dapat dihindarkan bila kita dapat mendeteksi dan mencegah sejak dini.

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CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation htpp://www.allergyclinic.wordpress.com/

WORKING TOGETHER FOR STRONGER, SMARTER AND HEALTHIER CHILDREN BY EDUCATION, CLINICAL INTERVENTION, RESEARCH AND INFORMATION NETWORKING. Advancing of the future pediatric and future parenting to optimalized physical, mental and social health and well being for fetal, newborn, infant, children, adolescents and young adult

LAYANAN KLINIK KHUSUS “CHILDREN GRoW UP CLINIC”

PROFESIONAL MEDIS “CHILDREN GRoW UP CLINIC”

  • Dr Narulita Dewi SpKFR, Physical Medicine & Rehabilitation
  • Dr Widodo Judarwanto SpA, Pediatrician
  • Fisioterapis

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Abstract References Update: The Future Research Management Ocular Allergies

About 30% of people suffer from allergic symptoms, and 40% to 80% of them have eye symptoms. Atopic conjunctivitis is divided into seasonal allergic conjunctivitis and perennial allergic conjunctivitis. The treatment of seasonal allergic conjunctivitis is simple: antihistamines, anti-inflammatory agents, or cromoglycate. Perennial allergic conjunctivitis needs longer therapy with mast cell stabilizers and sometimes local steroids. Atopic keratoconjunctivitis requires long-term treatment of the lid eczema and keratoconjunctivitis. Vernal keratoconjunctivitis mainly affects children and young people. It commonly calms down after puberty. It demands intensive therapy, often for many years, to avoid serious complicating corneal ulcers. Giant papillary conjunctivitis is a foreign body reaction in contact lens users or patients with sutures following ocular surgery. Nonallergic eosinophilic conjunctivitis affects mostly middle-aged and older women with eosinophilic conjunctivitis and dry eye. Contact allergic blepharoconjunctivitis is often caused by cosmetics and eye medication. Work-related ocular allergies should be considered as a cause of resistant ocular symptoms in workplaces

Abstract References Update: The Future Research Management Ocular Allergies

Diagnostics and New Developments in the Treatment of Ocular Allergies.
Kari O, et al. Curr Allergy Asthma Rep. 2012

Images in clinical medicine. Vernal keratoconjunctivitis.
Homme J, et al. N Engl J Med. 2012

An open label, active controlled, multicentric clinical trial to assess the efficacy and safety of fluticasone furoate nasal spray in adult Indian patients suffering from allergic rhinitis.
Kubavat AH, et al. J Assoc Physicians India. 2011

Stevens-Johnson syndrome in Thai children: a 29-year study.
Singalavanija S, et al. J Med Assoc Thai. 2011

Oral acyclovir suppression and neurodevelopment after neonatal herpes.
Kimberlin DW, et al. N Engl J Med. 2011

Clinical relevance of non-grass pollens respiratory allergies in Italy and effects of specific sublingual immunotherapy: The Rainbow Trial, a multicentre 3-year prospective observational study.
Milani M, et al. Eur Ann Allergy Clin Immunol. 2011

Vernal keratoconjunctivitis in school children in Rwanda and its association with socio-economic status: a population-based survey.
Smedt SD, et al. Am J Trop Med Hyg. 2011

Growth suppression caused by corticosteroid eye drops.
Wolthers OD, et al. J Pediatr Endocrinol Metab. 2011

Epidemiology of allergic conjunctivitis.
Rosario N, et al. Curr Opin Allergy Clin Immunol. 2011

A prospective, observational, all-prescribed-patients study of cyclosporine 0.1% ophthalmic solution in the treatment of vernal keratoconjunctivitis].
Takamura E, et al. Nihon Ganka Gakkai Zasshi. 2011.

Case-control study of IL13 polymorphisms, smoking, and rhinoconjunctivitis in Japanese women: the Kyushu Okinawa Maternal and Child Health Study.
Miyake Y, et al. BMC Med Genet. 2011

Prevalence and risk factors for early presentation of asthma among preschool children in Taiwan.
Yeh KW, et al. Asian Pac J Allergy Immunol. 2011

Vernal keratoconjunctivitis in school children in Rwanda and its association with socio-economic status: a population-based survey.
Smedt SD, et al. Am J Trop Med Hyg. 2011

Prevalence of allergy in patients with severe motor and intellectual disabilities (SMID)].
Hosoki K, et al. Arerugi. 2011.

Topical cyclosporine prevents seasonal recurrences of vernal keratoconjunctivitis in a randomized, double-masked, controlled 2-year study.
Lambiase A, et al. J Allergy Clin Immunol. 2011

Serum IgE reactivity profiling in an asthma affected cohort.
Dottorini T, et al. PLoS One. 2011

Specific tear IgE in patients with moderate-to-severe autumnal allergic conjunctivitis.
Mimura T, et al. Int Arch Allergy Immunol. 2011

Growth suppression caused by corticosteroid eye drops.
Wolthers OD, et al. J Pediatr Endocrinol Metab. 2011

Global analysis of breast feeding and risk of symptoms of asthma, rhinoconjunctivitis and eczema in 6-7 year old children: ISAAC Phase Three.
Björkstén B, et al. Allergol Immunopathol (Madr). 2011

Organochlorine concentrations in breast milk and prevalence of allergic disorders in Japanese women.
Miyake Y, et al. Chemosphere. 2011

Oralair®: sublingual immunotherapy for the treatment of grass pollen allergic rhinoconjunctivitis.
Hong J, et al. Expert Rev Clin Immunol. 2011

Epidemiology of allergic conjunctivitis.
Rosario N, et al. Curr Opin Allergy Clin Immunol. 2011

Age-related prevalence of allergic diseases in Tokyo schoolchildren.
Futamura M, et al. Allergol Int. 2011

Allergic mediators in tear from children with seasonal and perennial allergic conjunctivitis].
Martínez R, et al. Arch Soc Esp Oftalmol. 2011. Article in Spanish.

Sibling number and prevalence of allergic disorders in pregnant Japanese women: baseline data from the Kyushu Okinawa Maternal and Child Health Study.
Miyake Y, et al. BMC Public Health. 2011

Disparity of innate immunity-related gene effects on asthma and allergy on Karelia.
Zhang G, et al. Pediatr Allergy Immunol. 2011

Severe pepper allergy in a young child.
Gimenez L, et al. WMJ. 2011

A prospective, observational, all-prescribed-patients study of cyclosporine 0.1% ophthalmic solution in the treatment of vernal keratoconjunctivitis].
Takamura E, et al. Nihon Ganka Gakkai Zasshi. 2011.

Enhanced diagnosis of pollen allergy using specific immunoglobulin E determination to detect major allergens and panallergens.
Orovitg A, et al. J Investig Allergol Clin Immunol. 2011

Ocular symptoms in nonspecific conjunctival hyperreactivity.
Mourão EM, et al. Ann Allergy Asthma Immunol. 2011

Prolonged effectiveness of bepotastine besilate ophthalmic solution for the treatment of ocular symptoms of allergic conjunctivitis.
Williams JI, et al. J Ocul Pharmacol Ther. 2011

Cluster immunotherapy in allergic rhinoconjunctivitis].
Klimek L, et al. MMW Fortschr Med. 2011.

Polyunsaturated fatty acid intake and prevalence of eczema and rhinoconjunctivitis in Japanese children: the Ryukyus Child Health Study.
Miyake Y, et al. BMC Public Health. 2011

Vernal keratoconjunctivitis with limbal stem cell deficiency.
Sangwan VS, et al. Cornea. 2011

Association between allergic sensitization and attention deficit hyperactivity disorder (ADHD).
Suwan P, et al. Asian Pac J Allergy Immunol. 2011

Rupatadine improves nasal symptoms, quality of life (ESPRINT-15) and severity in a subanalysis of a cohort of Spanish allergic rhinitis patients.
Valero A, et al. J Investig Allergol Clin Immunol. 2011

Histamine H4 receptors in normal conjunctiva and in vernal keratoconjunctivitis.
Leonardi A, et al. Allergy. 2011

Eosinophil cationic protein as a marker for assessing the efficacy of tacrolimus ophthalmic solution in the treatment of atopic keratoconjunctivitis.
Wakamatsu TH, et al. Mol Vis. 2011

Risk factors for wheezing, eczema and rhinoconjunctivitis in the previous 12 months among six-year-old children in Himeji City, Japan: food allergy, older siblings, day-care attendance and parental allergy history.
Kurosaka F, et al. Allergol Int. 2011

Atopic diseases and intestinal helminth infections].
Rîpă C, et al. Rev Med Chir Soc Med Nat Iasi. 2010.

Association of hemopexin in tear film and conjunctival macrophages with vernal keratoconjunctivitis.
Pong JC, et al. Arch Ophthalmol. 2011

Topical 0.005% tacrolimus eye drop for refractory vernal keratoconjunctivitis.
Kheirkhah A, et al. Eye (Lond). 2011
Pediatric allergy and immunology in Italy.
Tozzi AE, et al. Pediatr Allergy Immunol. 2011

Causes and management of red eye in pediatric ophthalmology.
Seth D, et al. Curr Allergy Asthma Rep. 2011

Cedar pollen aggravates atopic dermatitis in childhood monozygotic twin patients with allergic rhino conjunctivitis.
Murakami Y, et al. Allergol Int. 2011

Boston type 1 keratoprosthesis for severe blinding vernal keratoconjunctivitis and Mooren’s ulcer.
Basu S, et al. Int Ophthalmol. 2011

Provided by

CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation htpp://www.allergyclinic.wordpress.com/

WORKING TOGETHER FOR STRONGER, SMARTER AND HEALTHIER CHILDREN BY EDUCATION, CLINICAL INTERVENTION, RESEARCH AND INFORMATION NETWORKING. Advancing of the future pediatric and future parenting to optimalized physical, mental and social health and well being for fetal, newborn, infant, children, adolescents and young adult

LAYANAN KLINIK KHUSUS “CHILDREN GRoW UP CLINIC”

PROFESIONAL MEDIS “CHILDREN GRoW UP CLINIC”

  • Dr Narulita Dewi SpKFR, Physical Medicine & Rehabilitation
  • Dr Widodo Judarwanto SpA, Pediatrician
  • Fisioterapis

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Obstruksi Ductus Nasolacrimalis, Gangguan Mata dan Alergi Pada Bayi

Orangtua sering mengeluhkan gangguan mata bayinya yang tak klunjung sembuh berupa mata belekan dan air mata berlebihan yang lebih sering pada satu sisi. Bayi yang baru lahir dan bayi yang lebih muda umumnya memiliki beberapa gangguan pada mata yang sering masih belum jelas penyebabnya. Gangguan mata pada bayi tersebut adalah Sumbatan Ductus Nasolacrimalis, Epiphora, Hordeolum dan Pink Eye.  Sampai saat ini masih banyak kontroversi yang terjadi antara beberapa dokter dalam memastikan penyebabnya. Selama ini sumbatan tersebut sering dianggap karena infeksi dan harus diberi antibiotika tetes mata. Ternyata berbagai laporan ilmiah kasus menunjukkan bahwa gangguan tersebut berkaitan dengan alergi. Saat dilakukan terapi dengan pemijatan, obat tetes antibiotika dan bahkan dengan operasi juga tidak membaik. Tetapi saat dilakukan penanganan alergi dengan melakukan eliminasi provokasi gangguan tersebut dapat membaik dengan cepat tanpa dilakukan pengobatan atau operasi.

Gangguan Mata Yang Sering Dikaitkan Dengan Alergi pada Bayi

  • Sumbatan Ductus Nasolacrimalis Mata bayi tampak selalu berair (belekan), karena saluran air mata dari mata ke hidung tersumbat. Meskipun sering sulit dibedakan dengan Pink Eye, lebih sering disebabkan oleh saluran air mata tersumbat atau dacryostenosis.   Saluran air mata tersumbat terjadi ketika saluran nasolacrimal yang mengeluarkan air mata dari mata ke dalam hidung, tersumbat karena berbagai hal mekanisme inflamasi seperti allergi, infeksi  dan trauma. Diperkirakan hingga 30 persen bayi baru lahir dilahirkan dengan saluran air mata tersumbat. Beberapa dokter biasanya memberi obat tetes antibiotik untuk menjaga agar tidak terjadi infeksi, dan orang tua diajari memijit-mijit pangkal hidung secara rutin setiap hari untuk membantu ‘membuka’ sumbatan. Jika masih tersumbat juga, kemungkinan dilakukan operasi kecil untuk membuka sumbatan tersebut. Apabila setelah dilakukan pijatan sumbatan menetap hingga anak berusia 12-18 bulan, perlu dilakukan tindakan yang lebih invasif menggunakan selang logam untuk mendorong sumbatan, atau dengan implan saluran air mata buatan yang disebut “Jonas tube”. Ternyata gangguan mata  tersebut tidak banyak perbaikan dan manfaat pemberian antibiotika tetes mata dan pemijatan tidak terlalu bermakna. Bahkan setelah pemberian antibiotika dan pemijatan tidak membaik dilakukan operasi. Tetapi setelah dilakukan operasi gangguan membaik sesaat tetapi beberapa saat kemudian gangguan tersebut timbul lagi. Tetapi setelah dilakukan pengamatan bayi dengan gangguan tersebut juga mempunyai tanda dan gejala alergi lainnya. Saat dilakukan intervensi eliminasi provokasi makanan ternyata gangguan tersebut dapat hilang tanpa operasi.
  • Epiphora, dimana mata terus berair akibat air mata yang keluar berlebihan. Berkat adanya sistem lakrimal, kedua mata kita mata dipertahankan untuk selalu basah, tetapi bagaimana bila mata menjadi terlalu basah sehingga tidak henti-hentinya mengeluarkan air mata. Sistem lakrimal terdiri atas kelenjar lakrimal dan saluran lakrimal. Kelenjar lakrimal terletak di antara alis dan sudut mata bagian luar, sedangkan saluran lakrimal ditemukan di sudut mata dalam dekat hidung. Epiphora juga dapat terjadi pada 5-6% anak. Namun 60-90% nya dapat sembuh spontan dalam satu tahun kehidupan
  • Pink Eye. Gangguan lain berupa mata sedikit merah dan belekan paling sering dialami oleh bayi sering disebut Pink Eye. Pink eye atau conjungtivitis adalah kemerahan dan bengkak pada selaput mata yang menutupi putih mata dan selaput pada bagian dalam kelopak mata.  Pink Eye seringkali disebabkan karena virus, alergi atau iritasi. Paling kasus infeksi virus, sering gangguan ini disertai infeksi saluran napas atas lainnya seperti Common Cold, Flu atau Influenza. Pada penyakit flu yang sering mengalami tampilan gangguan mata seperti ini sering disebabkan karena virus berjenis norovirus. Ketika mata bayi  atau anak belekan dan sedikit merah di ujungnya, meski ringan serigkali membuat orangtua panik. Tidak tanggung-tanggung selain dokter anak juga dikonsultasikan ke dokter ahli mata. Akhirnya ke dua dokter memberi obat yang berbeda. Sedangkan orangtua yang memperhitungkan biaya dalam menangani kesehatan anak, hanya membeli obat tetes mata antibiotika sendiri langsung ke apotik. Padahal sebagian besar kasus infeksi mata tersebut adalah “Pink Eye” yang bisa disebabkan alergi, iritasi atau virus flu yang menyertai gangguan saluran napas dan tidak memerlukan pengobatan khusus seperti antibiotika tetes mata atau antibiotika minum per oral. Penanganan Pink Eye pada umumnya cukup dibersihkan kapas atau kain basah hangat yang bersih bila timbul kotoran mata.
  • Hordeolum ( stye ) (bintitan atau timbilan). Hordeolum selamai ini masih dianggap karena infeksi atau peradangan pada kelenjar di tepi kelopak mata bagian atas maupun bagian bawah yang disebabkan oleh bakteri, biasanya oleh kuman Stafilokokus (Staphylococcus aureus). Hordeolum dapat timbul pada 1 kelenjar kelopak mata atau lebih. Kelenjar kelopak mata tersebut meliputi kelenjar Meibom, kelenjar Zeis dan Moll. Berdasarkan tempatnya, hordeolum terbagi menjadi 2 jenis, (1) Hordeolum interna, terjadi pada kelenjar Meibom. Pada hordeolum interna ini benjolan mengarah ke konjungtiva (selaput kelopak mata bagian dalam). (2)Hordeolum eksterna, terjadi pada kelenjar Zeis dan kelenjar Moll. Benjolan nampak dari luar pada kulit kelopak mata bagian luar (palpebra). Tanda-tanda hordeolum sangat mudah dikenali, yakni nampak adanya benjolan pada kelopak mata bagian atas atau bawah, berwarna kemerahan. Adakalanya  nampak bintik berwarna keputihan atau kekuningan disertai dengan pembengkakan kelopak mata. Pada hordeolum interna, benjolan akan nampak lebih jelas dengan membuka kelopak mata. Keluhan yang kerap dirasakan oleh penderita hordeolum diantaranya rasa mengganjal pada kelopak mata, nyeri takan dan makin nyeri saat menunduk. Kadang mata berair dan peka terhadap sinar. Hordeolum dapat membentuk abses di kelopak mata dan pecah dengan mengeluarkan nanah. Pada penelitian Judarwanto W, pada 33 kasus penderita hordeolum yang datang ke Children Allergy Clinic telah mengalami keluhan lebih dari 2 minggu. Dari sebagian penderita tersebut sebelum datang ke klinik 60%  sudah diberikan antibiotika tetes dan salep mata, 10% dioperasi dan 30 % belum diobati. Pada pasien yang dioperasi semua penderita mengalami kekambuhan hordolum tempat yang sama atau di sekitarnya, bahkan terdapat 2 pasien yang sudah dioperasi 2 kali. Setelah dilakukan pemeriksaan fisik dan mengetahui riwayat kesehatan sebelumnya ternyata semua pasien mengalami gejala dan tanda alergi. Saat dilakukan penanganan alergi dengan melelaui eliminasi provokasi makanan tanpa pemberian obat 88% atau 29 penderita terdapat perbaikkan tanpa pemberian obat dan operasi selama 3 minggu. Sedangkan 5 penderita keluar dari penelitian karena tidak dapat memtuhi prosedur eliminasi provokasi makanan dengan disiplin.

Gangguan Mata dan Alergi

Gejala alergi yang menimbulkan gangguan mata pada bayi sering dicetuskan dan disebabkan karena banyak faktor. Tetapi yang paling sering terjadi justru dipicu atau diperberat karena infeksi virus ringan yang tidak terdeteksi. Sedangkan faktor lainnya dengan manifestasi lebih ringan disebabkan karena  diet ibu bila minum ASI dan makanan yang dikonsumsi termasuk susu sapi. Bila karena alergi makanan biasanya gangguan keluarnya air mata berlebihan atau kotoran mata hanya satu sisi dan lebih ringan. Tetapi bila terkena infeksi virus saluran napas atas maka gangguan sumbatan lebih berat berupa, gangguan kotoran mata atau pink eye bisa terjadi pada ke dua mata dengan kotoran mata lebih banyak

Deteksi Alergi

Melihat demikian luas dan banyaknya pengaruh alergi yang mungkin bisa terjadi, maka deteksi dan pencegahan alergi sejak dini sebaiknya dilakukan. Gejala serta faktor resiko alergi dapat dideteksi sejak lahir, bahkan mungkin sejak dalam kandungan. Alergi makanan tidak terjadi pada semua orang, tetapi sebagian besar orang mempunyai potensi menjadi alergi. Tampaknya sebagian besar orang bila dicermati pernah mengalami reaksi alergi. Namun sebagian lainnya tidak pernah mengalami reaksi alergi. Terdapat 3 faktor penyebab terjadinya alergi makanan, yaitu faktor genetik, imaturitas usus, pajanan alergi yang kadang memerlukan faktor pencetus.

Alergi dapat diturunkan dari orang tua atau kakek dan nenek pada penderita. Bila ada orang tua menderita alergi kita harus mewaspadai tanda alergi pada anak sejak dini. Bila ada salah satu orang tua yang menderita gejala alergi maka dapat menurunkan resiko pada anak sekitar 20 – 40%, ke dua orang tua alergi resiko meningkat menjadi 40 – 80%. Sedangtkan bila tidak ada riwayat alergi pada kedua orang tua maka resikonya adalah 5 – 15%. Pada kasus terakhir ini bisa saja terjadi bila nenek, kakek atau saudara dekat orang tuanya mengalami alergi.

Manifestasi klinis lain yang sering menyertai penderita Obstruksi Ductus Nasolacrimalis, Gangguan Mata dan Alergi pada bayi.

  • GANGGUAN SALURAN CERNA : Sering muntah/gumoh, kembung,“cegukan”, sering buang angin, sering “ngeden /mulet”, sering REWEL / GELISAH/COLIK terutama malam hari), Sering buang air besar (> 3 kali perhari), tidak BAB tiap hari, BERAK DARAH. Feses cair, hijau, bau tajam, kadang seperti biji cabe. Hernia Umbilikalis (pusar menonjol), Scrotalis, inguinalis (benjolan di selangkangan, daerah buah zakar atau pusar atau “turun berok”) karena sering ngeden sehingga tekanan di dalam perut meningkat.
  • Kulit sensitif. Sering timbul bintik atau bisul kemerahan terutama di pipi, telinga dan daerah yang tertutup popok. Kerak di daerah rambut.Timbul bekas hitam seperti tergigit nyamuk. Mata, telinga dan daerah sekitar rambut sering gatal, disertai pembesaran kelenjar di kepala belakang. Kotoran telinga berlebihan kadang sedikit berbau.
  • Kuning Timbul kuning tinggi atau kuning bayi baru lahir berkepanjangan seharusnya setelah 2 minggu menghilang sering disebut Breastfeeding Jaundice (kuning karena ASI mengandung hormon pregnandiol).  Seringkali jadi pertanyaan mengapa sebagian besar bayi dengan ASI tidak mengalami kuning berkepanjangan. Setelah usia 6 telapak tangan dan kaki kadang berwarna kuning, sampai saat ini seringkali dianggap karena terlalu banyak makan wortel atau kelebihan vitamin A padahal selama ini hipotesa itu hanya sekedar dugaaan dan belum pernah dibuktikan dengan pemeriksaan darah. Kuning berkepanjangan meningkat pada bayi bisa sering terjadi pada bayi dengan gangguan saluran cerna dengan keluhan obstipasi (sering ngeden/mulet) dan konstipasi. Bila dicermati saat gangguan saluran cerna meningkat kuning semkai terlihat jelas dan sebaliknya saat saluran cerna membaik kuning menghilang.
  • Mulut hipersensitif. Lidah sering timbul putih kadang sulit dibedakan dengan jamur (candidiasis) atau memang kadang juga disertai infeksi jamur. Bibir tampak kering atau kadang pada beberapa bayi bibir bagian tengah berwarna lebih gelap atau biru. Produksi air liur meningkat, sehingga sering “ngeces (“drooling”) biasanya disertai bayi sering menjulurkan lidah keluar atau menyembur-nyemburkan ludah dari mulut.
  • Sesak Saat Baru lahir. Sesak segera setelah lahir. Sesak bayi baru lahir hingga saat usia 3 hari, biasanya akan membaik paling lama 7-10 hari. Disertai kelenjar thimus membesar (TRDN (Transient respiratory ditress Syndrome) /TTNB). BILA BERAT SEPERTI PARU-PARU TIDAK MENGEMBANG (LIKE RDS). Bayi usia cukup bulan (9 bulan) secara teori tidak mungkin terjadi paru2 yang belum mengembang. Paru tidak mengembang hanya terjadi pada bayi usia kehamilan < 35 minggu) Bayi seperti ini menurut penelitian beresiko asma (sering batuk/bila batuk sering dahak berlebihan )sebelum usia prasekolah. Keluhan ini sering dianggap infeksi paru atau terminum air ketuban.
  • Hidung Sensitif. Sering bersin, pilek, kotoran hidung banyak, kepala sering miring ke salah satu sisi (Sehingga beresiko kepala “peyang”) karena hidung buntu, atau minum dominan hanya satu sisi bagian payudara. Karena hidung buntu dan bernapas dengan mulut waktu minum ASI sering tersedak  
  • Keringat Berlebihan. Sering berkeringat berlebihan, meski menggunakan AC keringat tetap banyak terutama di dahi
  • Berat Badan Berlebihan atau kurang. Karena minum yang berlebihan atau sering minta minum berakibat berat badan lebih dan kegemukan (umur <1tahun). Sebaliknya terjadi berat badan turun setelah usia 4-6 bulan, karena makan dan minum berkurang
  • Saluran kencing. Kencing warna merah atau oranye (orange) denagna sedikit bentukan kristal yang menempel di papok atau diapers . Hal ini sering dianggap inmfeksi saluran kencing, saat diperiksa urine seringkali normal bukan disebabkan karena darah.
  • Kepala, telapak tangan atau telapak kaki sering teraba sumer/hangat.
  • Gangguan Hormonal. Mempengaruhi gangguan hormonal berupa keputihan/keluar darah dari vagina, timbul jerawat warna putih. timbul bintil merah bernanah, pembesaran payudara, rambut rontok, timbul banyak bintil kemerahan dengan cairan putih (eritema toksikum) atau papula warna putih
  • Gangguan Sulit Makan dan Gangguan Kenaikkan Berat Badan. Pada bayi berusia di atas 6 bulan dengan keluhan sering mual, BAB ngeden atau sulit, BAB > 3 kali seringkali mengakibatkan kesulitan makan atau makan hanya sedikit yang mengakibatkan gangguan kenaikkan berat badan dan sering mengalami daya tahan tubuh menurun sejak usia 6 bulan. Pada usia sebelum 6 bulan kenaikkan pesat tetapi setelah usia 6 bulan kenaikkan relatif datar. Pada penderita hipersensitifitas non alergi (non atopi) biasa nya ghangguan berat badan dan sulit makan lebih tidak ringan dan timbul sejak usia sebelum 6 bulan tetapi setelah 6 bulan lebih buruk
  • PROBLEM MINUM ASI : minum berlebihan, berat berlebihan karena bayi sering menangis dianggap haus. Haus palsu adalah tampilan bayi sering menangis, mulutnya sering seperti mau ngempeng atau mencari puting tampak sucking refleks berlebihan dirangsang pipinya sedikit sudah seperti mencari puting. Hal itu belum tentu karena haus atau bukan karena ASI kurang. Pada bayi alergi yang sering rewel seringkali saluran cernanya sedikit sakit sehingga bila ada perasaan tidak nyaman bayi akan sering seperti ngempeng atau minta digendong. Sering menggigit puting sehingga luka. Minum ASI sering tersedak, karena hidung buntu dan napas dengan mulut. Minum ASI lebih sebentar pada satu sisi,`karena satu sisi hidung buntu, jangka panjang bisa berakibat payudara besar sebelah.

PERILAKU YANG SERING MENYERTAI PENDERITA ALERGI PADA BAYI

  • GANGGUAN NEURO ANATOMIS : Mudah kaget bila ada suara yang mengganggu. Gerakan tangan, kaki dan bibir sering gemetar. Kaki sering dijulurkan lurus dan kaku. Breath Holding spell : bila menangis napas berhenti beberapa detik kadang disertai sikter bibir biru dan tangan kaku. Mata sering juling (strabismus). Kejang tanpa disertai ganggguan EEG (EEG normal)
  • GERAKAN MOTORIK BERLEBIHAN Usia < 1 bulan sudah bisa miring atau membalikkan badan. Usia < 6 bulan: mata/kepala bayi sering melihat ke atas. Tangan dan kaki bergerak berlebihan, tidak bisa diselimuti (“dibedong”). Kepala sering digerakkan secara kaku ke belakang, sehingga posisi badan bayi “mlengkung” ke luar. Bila digendomg tidak senang dalam posisi tidur, tetapi lebih suka posisi berdiri.Usia > 6 bulan bila digendong sering minta turun atau sering bergerak/sering menggerakkan kepala dan badan atas ke belakang, memukul dan membentur benturkan kepala. Kadang timbul kepala sering bergoyang atau mengeleng-gelengkan kepala. Sering kebentur kepala atau jatuh dari tempat tidur.
  • GANGGUAN TIDUR (biasanya MALAM-PAGI) gelisah,bolak-balik ujung ke ujung; bila tidur posisi “nungging” atau tengkurap; berbicara, tertawa, berteriak dalam tidur; sulit tidur atau mata sering terbuka pada malam hari tetapi siang hari tidur terus; usia lebih 9 bulan malam sering terbangun atau tba-tiba duduk dan tidur lagi,
  • AGRESIF MENINGKAT, pada usia lebih 6 bulan sering memukul muka atau menarik rambut orang yang menggendong. Sering menarik puting susu ibu dengan gusi atau gigi, menggigit, menjilat tangan atau punggung orang yang menggendong. Sering menggigit puting susu ibu bagi bayi yang minum ASI, Setelah usia 4 bulan sering secara berlebihan memasukkan sesuatu ke mulut. Tampak anak sering memasukkan ke dua tangan atau kaki ke dalam mulut. Tampak gampang seperti gemes atau menggeram
  • GANGGUAN KONSENTRASI : cepat bosan terhadap sesuatu aktifitas bermain, memainkan mainan, bila diberi cerita bergambar sering tidak bisa lama memperhatikan. Bila minum susu sering terhenti dan teralih perhatiannya dengan sesuatu yang menarik tetapi hanya sebentar
  • EMOSI MENINGKAT, sering menangis, berteriak dan bila minta minum susu sering terburu-buru tidak sabaran. Sering berteriak dibandingkan mengiceh terutama saat usia 6 bulan
  • GANGGUAN MOTORIK KASAR, GANGGUAN KESEIMBANGAN DAN KOORDINASI : Pada POLA PERKEMBANGAN NORMAL adalah BOLAK-BALIK, DUDUK, MERANGKAK, BERDIRI DAN BERJALAN sesuai usia. Pada gangguan keterlambatan motorik biasanya bolak balik pada usia lebih 5 bulan, usia 6 – 8 bulan tidak duduk dan merangkak, setelah usia 8 bulan langsung berdiri dan berjalan.
  • GANGGUAN ORAL MOTOR: KETERLAMBATAN BICARA: Kemampuan bicara atau ngoceh-ngoceh hilang dari yang sebelumnya bisa. Bila tidak ada gangguan kontak mata, gangguan pendengaran, dan gangguan intelektual biasanya usia lebih 2 tahun membaik. GANGGUAN MENGUNYAH DAN MENELAN: Gangguan makan makanan padat, biasanya bayi pilih-pilih makanan hanya bisa makanan cair dan menolak makanan yang berserat. Pada usia di atas 9 bulan yang seharusnya dicoba makanan tanpa disaring tidak bisa harus di blender terus sampai usia di atas 2 tahun.
  • IMPULSIF : banyak tersenyum dan tertawa berlebihan, lebih dominan berteriak daripada mengoceh.
  • Memperberat ADHD dab Autis. Jangka panjang akan memperberat gangguan perilaku tertentu bila anak mengalami bakat genetik seperti ADHD (hiperaktif) dan AUTIS (hiperaktif, keterlambatan bicara, gangguan sosialisasi). Tetapi alergi bukan penyebab Autis tetapi hanya memperberat. Penderita alergi dengan otak yang normal atau tidak punya bakat Autis tidak akan pernah menjadi Autis.
Gejala alergi pada bayi selain makanan justru paling sering seringkali diperberat saat sakit atau terjadi oleh infeksi  berupa infeksi virus, bakteri atau infeksi lainnya. Paling sering di antaranya adalah infeksi virus. Pada bayi tanda dan gejala infeksi virus ringan ini lebih sulit dikenali. Biasanya hanya berupa badan sumer teraba hangat hanya di kepala, telapak tangan dan badan bila diukur suhu normal. Biasanya disertai bersin, batuk sekali-sekali dan pada anak bayi tertentu nafas bunyi grok-grokFlu pada bayi jarang sekali menimbulkan hidung meler biasanya hanya basah sedikit di sekitar hidung atau batuk sekali-sekali karena refleks batuk pada bayi basih belum sempurna.  Bahkan sebagian dokter menilai gejala infeksi virus tersebut dianggap sebagai gejala alergi.Pada keadaan sakit seperti itu biasanya ada kontak yang sakit flu, demam, batuk atau infeksi virus ringan lainnya di dalam di rumah. Sayangnya orangtua juga sering tidak menyadari bahwa selama ini sering terkena infeksi virus yang gejalanya tidak khas tersebut. Gejala infeksi virus yang ringan yang dialami oleh penderita dewasa berupa badan ngilu, terasa pegal,nyeri tenggorokan atau kadang disertai  sakit kepala. Gejala ringan, tidak khas dan cepat membaik ini sering dianggap “gejala mau flu tidak jadi”, masuk angin, kurang tidur, panas dalam atau kecapekan

PENYEBAB ALERGI MAKANAN PADA BAYI

Alergi makanan lebih sering terjadi pada usia bayi atau anak dibandingkan pada usia dewasa. Hal itu terjadi karena belum sempurnanya saluran cerna pada anak. Secara mekanik integritas mukosa usus dan peristaltik merupakan pelindung masuknya alergen ke dalam tubuh. Secara kimiawi asam lambung dan enzim pencernaan menyebabkan denaturasi allergen. Secara imunologik sIgA pada permukaan mukosa dan limfosit pada lamina propia dapat menangkal allergen masuk ke dalam tubuh. Pada usus imatur sistem pertahanan tubuh tersebut masih lemah dan gagal berfungsi sehingga memudahkan alergen, virus dan bakteri masuk ke dalam tubuh. Dengan pertambahan usia, ketidakmatangan saluran cerna tersebut semakin membaik. Biasanya setelah 2 tahun saluran cerna tersebut berangsur membaik. Hal ini juga yang mengakibatkan penderita alergi sering sakit pada usia sebelum 2 tahun. Fenomena tersebut juga menunjukkan bahwa sewaktu bayi atau usia anak mengalami alergi makanan tetapi dalam pertambahan usia membaik.

Gejala dan tanda karena reaksi alergi pada anak dapat ditimbulkan oleh adanya alergen dari beberapa makanan tertentu yang dikonsumsi bayi. Penyebab alergi di dalam makanan adalah protein, glikoprotein atau polipeptida dengan berat molekul lebih dari 18.000 dalton, tahan panas dan tahan ensim proteolitik. Sebagian besar alergen pada makanan adalah glikoprotein dan berkisar antara 14.000 sampai 40.000 dalton. Molekul-molekul kecil lainnya juga dapat menimbulkan kepekaan (sensitisasi) baik secara langsung atau melalui mekanisme hapten-carrier.

Susu sapi dianggap sebagai penyebab alergi makanan pada bayi yang paling sering. Beberapa penelitian di beberapa negara di dunia prevalensi alergi susu sapi pada anak dalam tahun pertama kehidupan sekitar 2%. Alergi susu sapi adalah suatu kumpulan gejala yang mengenai banyak organ dan system tubuh yang ditimbulkan oleh alergi terhadap susu sapi. Reaksi hipersensitif terhadap protein susu sapi dengan keterlibatan mekanisme sistem imun. Reaksi simpang makanan yang tidak melibatkan mekanisme sistem imun dikenal sebagai intoleransi susu. Sekitar 1-7% bayi pada umumnya menderita alergi terhadap protein yang terdapat dalam susu sapi. Sedangkan sekitar 80% susu formula bayi yang beredar di pasaran ternyata menggunakan bahan dasar susu sapi. Alergi susu sapi adalah suatu kumpulan gejala yang mengenai banyak organ dan system tubuh yang ditimbulkan oleh alergi terhadap susu sapi. Reaksi hipersensitif terhadap protein susu sapi dengan keterlibatan mekanisme sistem imun. Alergi terhadap protein susu sapi atau alergi terhadap susu formula yang mengandung protein susu sapi merupakan suatu keadaan dimana seseorang memiliki sistem reaksi kekebalan tubuh yang abnormal terhadap protein yang terdapat dalam susu sapi. Sistem kekebalan tubuh bayi akan melawan protein yang terdapat dalam susu sapi sehingga gejala-gejala reaksi alergi pun akan muncul.

Pada bayi yang hanya mendapatkan ASI eksklusif maka diet yang dikonsumsi ibu sangat berpotensi menimbulkan gangguan alergi. Diet ibu yang sangat berpotensi menimbulkan gangguan pada bayi yang paling sering adalah ikan laut (terutama yang kecil seperti udang, kerang, cumi dan sebagainya), kacang tanah dan buah-buahan (tomat, melon, semangka).

Saat pemberian makanan tambahan usia 4-6 bulan, gejala alergi pada bayi sering timbal. Jenis makanan yang sering diberikan dan menimbulkan gangguan adalah pemberian buah-buahan (jeruk, dan pisang), bubur susu (kacang hijau), nasi tim (tomat, ayam, telor, ikan laut (udang, cumi,teri), keju, dan sebagainya. Sehingga penundaan pemberian makanan tertentu dapat mengurangi resiko gangguan alergi pada anak. Menurut beberapa penelitian pemberian multivitamin pada bayi beresiko alergi ternyata meningkatkan gangguan penyakit alergi di kemudian hari.

Referensi:

Kumpulan Artikel: Segala Permasalahan Alergi pada Bayi

Kumpulan Artikel: Segala Permasalahan Alergi pada Bayi

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We are guilty of many errors and many faults. But our worst crime is abandoning the children, neglecting the fountain of life.
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Adipokines and hormones of obesity in childhood asthma.

Role of adipokines and hormones of obesity in childhood asthma.

Yuksel H, et al.

Allergy Asthma Immunol Res. 2012 Mar;4(2):98-103. Epub 2011 Nov 29.

Abstract
PURPOSE: The aim of this study was to evaluate serum levels of leptin, ghrelin, and adiponectin in obese and non-obese children with asthma and in healthy non-asthmatic children, and analyze their relationships with clinical outcomes.

METHODS: This study enrolled 40 obese and 51 non-obese children with asthma and 20 healthy children. Body mass index and serum leptin, ghrelin, and adiponectin levels were determined in all children. Asthma symptom scores and lung function test results were recorded for subjects with asthma.

RESULTS: Serum leptin levels (11.8±7.9, 5.3±6.8, and 2.1±2.4 ng/mL in the obese asthmatic, non-obese asthmatic, and control groups, respectively) and adiponectin levels (12,586.2±3,724.1; 18,089.3±6,452.3; and 20,297.5±3,680.7 ng/mL, respectively) differed significantly among the groups (P<0.001 for all). Mean ghrelin levels were 196.1±96.8 and 311.9±352.8 pg/mL in the obese and non-obese asthmatic groups, respectively, and 348.8±146.4 pg/mL in the control group (P=0.001). The asthma symptom score was significantly higher in the obese children with asthma than in the non-obese children with asthma (P<0.001). Leptin and adiponectin levels were correlated with the asthma symptom score in non-obese children with asthma (r=0.34 and r=-0.62, respectively).

CONCLUSIONS: Obesity leads to more severe asthma symptoms in children. Moreover, leptin, adiponectin, and ghrelin may play important roles in the inflammatory pathogenesis of asthma and obesity co-morbidity.

Kumpulan Artikel Permasalahan Alergi dan Imunologi Anak, Dr Widodo Judarwanto, pediatrician

Current Allergy Immunology by Widodo Judarwanto

The prevalence of allergic diseases and asthma is increasing worldwide, particularly in low and middle-income countries. Moreover, the complexity and severity of allergic diseases, including asthma, continue to increase especially in children and young adults, who are bearing the greatest burden of these trends. In order to address this major global challenge that threatens health and economies alike, it is important to have a global action plan that includes partnerships involving different stakeholders from low-income, middle-income, and high-income countries. Immunology is a branch of biomedical science that covers the study of all aspects of the immune system in all organisms.It deals with the physiological functioning of the immune system in states of both health and diseases; malfunctions of the immune system in immunological disorders (autoimmune diseases, hypersensitivities, immune deficiency, transplant rejection); the physical, chemical and physiological characteristics of the components of the immune system in vitro, in situ, and in vivo. Immunology has applications in several disciplines of science, and as such is further divided

Special Articles Children Allergy and Immunology

by Dr Widodo Judarwanto SpA (Pediatrician)

INDONESIA

ALERGI PADA BAYI

PERMASALAHAN ALERGI PADA ANAK

FOR PROFESSIONAL

MEDIKAMENTOSA ALERGI

CLINICAL IMMUNOLOGY

BASIC IMMUNOLOGY

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The Future Concept and New Insight

PARENTING FOOD ALLERGY AND ASSOCIATED DISEASES

KUMPULAN ARTIKEL PENTING TENTANG ALERGI MAKANAN

Allergy Immunology Care

Allergic diseases include life-threatening anaphylaxis, food allergies, certain forms of asthma, rhinitis, conjunctivitis, angioedema, urticaria, eczema, eosinophilic disorders, including eosinophilic esophagitis, and drug and insect allergies. Globally, 300 million people suffer from asthma and about 200–250 million people suffer from food allergies. One-tenth of the population suffers from drug allergies and 400 million from rhinitis. Moreover, allergic diseases commonly occur together in the same individual, one disease with the other. This requires an integrated approach to diagnosis and treatment and greater awareness of the underlying causes among family physicians, patients as well as specialists.

A recent report from the World Allergy Organization, the WAO White Book on Allergy, summarizes the burden of allergic diseases worldwide, the risk factors, impact on quality of life of patients, morbidity, mortality, their socio-economic consequences, recommended treatment strategies, future therapies, and the cost–benefit analyses of care services. For instance, asthma prevalence is rising in several high as well as low-income and middle-income countries, and the prevalence and impact of allergic diseases continue to grow. According to the World Health Organization, the number of patients having asthma is 300 million and with the rising trends it is expected to increase to 400 million by 2025. Patients with asthma and allergic diseases have a reduced quality of life. According to the World Health Organization, asthma causes 250 000 deaths annually. Moreover, asthma in infancy often goes unrecognized and thus untreated. In the United States, 23 million people including 7 million children suffer from asthma and the prevalence is increasing. The economic costs of asthma are high both in terms of direct and indirect costs, especially in severe or uncontrolled asthma. In the United States, pediatric asthma results in 14 million missed days of school each year, which in turn result in lost workdays – and lost wages – for caregivers. As asthma continues to affect more children in lower-income countries, this will lead to long-term consequences for their education and perpetuation of their poverty. The ways to control indoor and outdoor air pollution, to train healthcare professionals to diagnose and treat asthma in children, and to ensure that asthma medications are affordable for all who need them. Educational programs for self-management of asthma and national efforts to tackle asthma as a public health problem have produced remarkable benefits resulting in dramatic reductions in deaths and hospital admissions.

The upsurge in the prevalence of allergies is observed as societies become more affluent and urbanized. An increase in environmental risk factors like outdoor and indoor pollution like tobacco smoke combined with reduced biodiversity also contributes to this rise in prevalence. In many low-income and middle-income countries, including rural areas in India, people rely on solid fuel (wood, cow dung, or crop residues) that they burn in simple stoves or open fires for domestic energy. Secondhand smoke has become more common as parents become affluent enough to buy cigarettes. Together, these factors generate indoor air pollution that is estimated to be as much as five times as severe in poor countries as in rich ones. In rural Bangladesh, the prevalence of wheezing in rural children over a 12-month period was 16%The White Bookhighlights data from China that reports outdoor pollution as a cause of 300 000 deaths annually. Moreover, climate change, change in ambient temperatures, and changes in weather during pollen seasons can cause both biological and chemical changes to pollens and have direct adverse consequences on human health by inducing disease exacerbations especially in urban and polluted regions. Appropriate environmental control measures of risk factors like indoor tobacco smoke, outdoor pollution, and biomass fuel can have huge health benefits. There are also other complex, but measurable, associations between early life circumstances like maternal and childhood nutrition. Such evidences indicate early life opportunities for interventions targeted towards the prevention of allergies and asthma. (source Current Opinion in Allergy & Clinical Immunology: February 2012)

Immunology

Immunology is a branch of biomedical science that covers the study of all aspects of the immune system in all organisms.It deals with the physiological functioning of the immune system in states of both health and diseases; malfunctions of the immune system in immunological disorders (autoimmune diseases, hypersensitivities, immune deficiency, transplant rejection); the physical, chemical and physiological characteristics of the components of the immune system in vitro, in situ, and in vivo. Immunology has applications in several disciplines of science, and as such is further divided.

Classical immunology ties in with the fields of epidemiology and medicine. It studies the relationship between the body systems, pathogens, and immunity. The earliest written mention of immunity can be traced back to the plague of Athens in 430 BCE. Thucydides noted that people who had recovered from a previous bout of the disease could nurse the sick without contracting the illness a second time. Many other ancient societies have references to this phenomenon, but it was not until the 19th and 20th centuries before the concept developed into scientific theory.

The study of the molecular and cellular components that comprise the immune system, including their function and interaction, is the central science of immunology. The immune system has been divided into a more primitive innate immune system, and acquired or adaptive immune system of vertebrates, the latter of which is further divided into humoral and cellular components.

The humoral (antibody) response is defined as the interaction between antibodies and antigens. Antibodies are specific proteins released from a certain class of immune cells (B lymphocytes). Antigens are defined as anything that elicits generation of antibodies, hence they are Antibody Generators. Immunology itself rests on an understanding of the properties of these two biological entities. However, equally important is the cellular response, which can not only kill infected cells in its own right, but is also crucial in controlling the antibody response. Put simply, both systems are highly interdependent.

In the 21st century, immunology has broadened its horizons with much research being performed in the more specialized niches of immunology. This includes the immunological function of cells, organs and systems not normally associated with the immune system, as well as the function of the immune system outside classical models of immunity

Clinical immunology

Clinical immunology is the study of diseases caused by disorders of the immune system (failure, aberrant action, and malignant growth of the cellular elements of the system). It also involves diseases of other systems, where immune reactions play a part in the pathology and clinical features.

The diseases caused by disorders of the immune system fall into two broad categories: immunodeficiency, in which parts of the immune system fail to provide an adequate response (examples include chronic granulomatous disease), and autoimmunity, in which the immune system attacks its own host’s body (examples include systemic lupus erythematosus, rheumatoid arthritis, Hashimoto’s disease and myasthenia gravis). Other immune system disorders include different hypersensitivities, in which the system responds inappropriately to harmless compounds (asthma and other allergies) or responds too intensely.

The doctor of the future will give no medicine, but will instruct his patient in the care of the human frame, in diet and in the cause and prevention of disease.

Jangan Remehkan Alergi Pada Bayi. Alergi pada bayi adalah awal perjalanan panjang gangguan alergi di masa depan

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Current Allergy Immunology by Widodo Judarwanto

Gejala Alergi pada bayi dan anak justru paling sering dipicu oleh adanya infeksi khususnya infeksi virus. Tetapi sebaliknya saat itu sering dianggap karena alergi susu atau alergi makanan. Gejala infeksi virus pada bayi khususnya sulit dikenali karena mirip gejala alergi. Reaksi terhadap alergi susu atau alergi makanan biasanya relatif ringan, namun begitu dipicu infeksi manifestasinya lebih berat. Pemicu alergi tidak akan berarti bila penyebab alergi dihindari. Widodo Judarwanto 2012
The doctor of the future will give no medicine, but will instruct his patient in the care of the human frame, in diet and in the cause and prevention of disease.

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ALLERGY ONLINE CLINIC FOR CHILDREN, TEEN AND ADULT Yudhasmara Foundation www.allergyclinic.me   http://www.growupclinic.com GROW UP CLINIC I JL Taman Bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021)  5703646 – 44466102 GROW UP CLINIC II  MENTENG SQUARE Jl Matraman 30 Jakarta Pusat 10430 phone 44466103 www.growupclinic.com   Creating-hashtag-on-twitter@growupclinic http://www.facebook.com/GrowUpClinic

 

“GRoW UP CLINIC” Jakarta Focus and Interest on: *** Allergy Clinic Online *** Picky Eaters and Growup Clinic For Children, Teen and Adult (Klinik Khusus Gangguan Sulit Makan dan Gangguan Kenaikkan Berat Badan)*** Children Foot Clinic *** Physical Medicine and Rehabilitation Clinic *** Oral Motor Disorders and Speech Clinic *** Children Sleep Clinic *** Pain Management Clinic Jakarta *** Autism Clinic *** Children Behaviour Clinic *** Motoric & Sensory Processing Disorders Clinic *** NICU – Premature Follow up Clinic *** Lactation and Breastfeeding Clinic *** Swimming Spa Baby & Medicine Massage Therapy For Baby, Children and Teen ***
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Curriculum Vitae Widodo Judarwanto

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Pemakaian Kacamata, Kelainan Refraksi dan Riwayat Alergi Pada Anak

Kelainan Refraksi Mata Pada Anak dan Alergi

Sebagian Besar Pemakai Kacamata Pada Anak Mempunyai Riwayat Alergi

Abstract

Many study was to determine if atopy is a risk factor for keratoconus, myopia and astigmatismus.  The association of keratoconus, myopia or astigmatismus and atopic disease has been reported on several occasions but the only controlled clinical study that has so far been published found no evidence to support this view. Atopy may contribute to keratoconus, myopia and astigmatismus, but most probably via eye rubbing associated with the itch of atopy. No other variable measured was significantly associated with the aetiology of keratoconus. Since it is now known that atopy is often associated with changes in various immunoglobulins, particularly IgE, it was considered desirable to determine the immunological profiles of a large series of keratoconus cases in order to seek evidence for coexistence of the two conditions in one individual

Banyak penelitian menunjukkan bahwa alergi atau atopi merupakan faktor risiko untuk keratoconus, miopia dan astigmatismus. Hubuhngan  keratoconus, miopia atau astigmatismus dan penyakit atopik telah dilaporkan pada beberapa studi klinis. Atopi dapat menyebabkan keratoconus, miopia dan astigmatismus, tapi kemungkinan besar melalui mata menggosok terkait dengan gatal atopi. Tidak ada variabel lain yang diukur secara bermakna dikaitkan dengan etiologi keratoconus. Karena sekarang diketahui bahwa atopi sering dikaitkan dengan perubahan berbagai imunoglobulin, terutama IgE, untuk menentukan profil imunologi dari serangkaian gangguan mata dalam rangka mencari bukti koeksistensi dua kondisi dalam satu individu

Dalam waktu terakhir ini angka kejadian anak-anak memakai kaca mata sejak dini tampaknya meningkat. Sampai saat ini masih belum diketahui secara pasti penyebab pemakaian kacamata sejak dini. Dalam penelitian Judarwanto W didapatkan bahwa penderita myopia (kaca mata minus) atau astigmatismus (kaca mata silinder) sebagian besar mengalami riwayat alergi.

Beberapa penelitian juga menunjukkan bahwa penderita rabun jauh atau mipoia ternyata memang berkaitan dengan alergi. Hanya saja masih belum dapat dipastikan mekanisme terjadinya kejadian tersebut. Untuk memastikan sebab akibat atau hubungan antara alergi dan pemakaian kacamata perlu dilakukan penelitian lebih jauh. Bila hal ini terbukti maka biasa saja nantinya dalam upaya pencegahan alergi akan merupakan pencegahan pemakaian kacamata sejak dini pula.

Dari pengamatan awal pada 125 anak pengguna kaca mata minus atau penderita kelainan refraksi miopia dan kelainan astimagtismus (kcamata silinder) ternyata sebagian besar atau hampir 85% ternyata mengalami riwayat alergi. Tanda dan gejala alergi yang dialami adalah dermatitis, rinitis dan asthma. Kelompok anak yang diteliti adalah anak usia 6 tahun hingga 12 tahun. Hampir sepertiganya atau sekitar 20% dari kelompok tersebut ternyata diadviskan oleh dokter memakai kacamata sejak usia 6-8 tahun.

Miopia atau astimagtismus umumnya merupakan kelainan yang diturunkan oleh orangtua atau bersifat genetik sehingga banyak dijumpai pada anak-anak usia dini sekolah. Dalam penelitian tersebut di atas ternyata sebagian besar hampir 94% salah satu orangtuanya adalah penderita kelainan refraksi pula. yang menarik orang tua yang mempunyai kelainan yang sama dengan orang tua biasanya sebagian besar hampir 96% berwajah sama dengan anaknya. Dan lebih menarik lagi orangtua dengan karakteristik sama tersebut juga sebagian besar mempunyai riwayat alergi sebelumnya.

Pemakaian Kaca Mata (Kelainan Refraksi)

Penderita yang memakai kacamata  dalam istilah kedokteran sering disebut orang yang mengalami kelainan refraksi mata. Kelainan Refraksi adalah keadaan dimana mata tidak mampu membiaskan atau memfokuskan cahaya ke retina sehingga bayangan benda yang dilihat menjadi kabur. Keadaan seperti ini disebabkan oleh kelengkungan kornea atau daya bias kornea yang abnormal, daya bias lensa dan badan kaca (korpus vitreus) yang abnormal atau sumbu bola mata yang abnormal (axial).

Jenis kelainan refraksi meliputi banyak istilah yang dipakai, berdasarkan gangguan penglihatan yang dialami rabun jauh dan rabun dekat. Ada pula yang menyebutkan berdasar lensa koreksi yang dipakai yaitu mata minus untuk myopia atau rabun jauh karena dapat dikoreksi dengan pemberian lensa kacamata minus. Sedangkan lensa kaca mata plus untuk hipermetropia atau rabun dekat karena dapat dikoreksi dengan kacamata plus dan silinder untuk astimagtismus karena dapat dikoreksi dengan kacamata silinder.

Rabun jauh (miopia/kaca mata minus)

Myopia (Rabun Jauh), keluhan yang sering timbul adalah keadaan kabur bila melihat obyek jauh. Kata myopia berasal dari kata yunani yang  berarti “memidingkan mata” karena penderiata kelainainan ini selalu memicingkan matanya untuk bisa melihat dengan jelas. Myopia paling banyak dijumpai pada anak-anak dan umumnya ada faktor keturunan dari orang tua. Lazimnya myopia terjadi karena memanjangnya sumbu bola mata, pemanjangan sumbu ini menyebabkan bekas cahaya yang dibiaskan tidak mencapai retina sehingga terfokus di depan retina. Sejalan dengan memanjangnya sumbu bola mata, derajat myopiapun akan bertambah. Pada usia anak-anak proses ini merupakan bagian dari pertumbuhan, sehingga ukuran kaca matapun terus bertanbah. Karenan itu pada anak-anak dianjurkan untuk pemeriksaan ulang setiap 6 bulan sekali. Pada golongan usia 20 – 30 tahun pertambahanya mulia lambat. Walaupun agak jarang myopia dapat pula disebabkan perubahan daya bias lensa mata atau kornea.

Astimagtismus (kaca mata silinder)

Astimagtismus (silinder), pada keadaan ini berkas cahaya dibiaskan tidak pada satu titik fokus, melainkan pada beberapa titik fokus sehingga bayangan terbentuk menjadai kabur (tidak fokus). Untuk mengatasi hal ini sipakai lensa silinder. Dalam hal ini Atimagtismua dabagi dua yaitu pertama Astimagtismus Irregular (tidak teratur) dimana banyak titik fokus dan tidak terletak pada sumbu penglihatan, keadaan ini disebabkan karena permukaan retina tidak rata atau akibat kekeruhan yan tidak merata pada lensa. Kedua Astimagtismus Regular, dimana banyak titik fokus tetapi masih terletak pada sumbu penglihatan. Pada jenis ini terdapat 2 bidang utama dengan daya bias terkuat dan terlemah.

Berdasarkan letak titik fokus terhadap retina dibedakan pula astigmatismus myopi dan astigmatismua hipermetropi. Ini penting untuk menentukan jenis lensa silinder yang dipakai, apakah silinder minus ataukah silinder plus. Karakteristik penderita astigmatism selain kabur adalah pusing bila berada di kerumunan orang banyak, atau melihat garis-garis yang rapat. Hal ini karena sumbu garis-garis tersebut tidak sesuai dengan sumbuh astigmatismnya sehingga mata berusaha untuk memfokuskan.

Gangguan Mata yang sering terjadi pada penderita alergi :

  • Pada bayi mata sering timbul kotoran atau belekan pada salah satu bagian sisi mata. Hal ini terjadi karena gangguan obstruksi duktus lakrimalis. Gagguan ini sering disertai bayi sering bersin dan tidur sering miring ke salah satu sisi karena hidung buntu. Mata dan hidung dihubungkan dengan saluran, biasanya kalau hidung terganggu mata juga terpengaruh. Selama ini gangguan seperti ini diberi obat tetas mata atau salep mata tidak akan pernah membaik. pada beberapa kasus dilakukan operasi berulang kali juga akan tetap hilang timbul. tetapi saat dilakukan penanganan alergi gangguan tersebut membaik tanpa obat.
  • Kelopak mata bagian bawah berwarna gelap atau kehitaman.
  • Mata gatal sering digaruk atau “kucek-kucek mata”. Selama ini gangguan gatal mata ini sering dianggap karena ngantuk. Pada keadaan seperti ini mata bagian bawah tampak berwarna kehitaman. Kadang mata juga berwarna merah timbul biasanya satu sisi atau ke dua sisi.
  • Hordeolum atau bintitan. Timbul bintil di kelopak mata. Berbagai kasus tersebut selama ini masih kontroversi. Selama ini teori yang dianut penyebabnya adalah karena tangan kotor yang mengusap mata sehingga timbul infeksi. Dalam penelitian biasanya tidak didapatkan kelainan atau tanda infeksi saat dilakukan kultur pada jaringannya. Penulis selama ini tidak pernah memberikan antiobitotyika pada kasus ini tetapi membaik dengan sendirinya saat dilakukan penatalaksanaan alergi. Sebaliknya banyak kasus setelah diberi antibiotika jangka keluhan tersebut tetap timbul juga.
  • Keratokonus. Keratokonus adalah perubahan bentuk (penipisan) kornea yang terjadi secara bertahap, sehingga bentuknya menyerupai kerucut. Keratokonus mulai terjadi pada usia 10-20 tahun. Keratokonus terjadi jika bagian tengah kornea menipis dan secara bertahap menonjol ke arah luar sehingga bentuknya menyerupai kerucut.  Kelainan kelengkungan ini menyebabkan perubahan pada kekuatan pembiasan kornea. Sebagai akibatnya terjadi astigmata sedang sampai berat dan rabun dekat.  Keratokonus juga bisa menyebabkan pembengkakan dan pembentukan jaringan parut yang menghalangi penglihatan.
  • Konyungtivitis alergik. Penyakit alergi pada mata yang paling sering didapat adalah konyungtivitis alergik  (hay fever), konyungtivitis vernalis, keratokonyungtivitis atopik, dan konyungtivitis giant papilar. Keadaan penyakit dapat mulai dari konyungtivitis ringan sampai yang berat seperti keratokonyungtivitis atopik yang dapat menyebabkan kebutaan. Konyungtiva adalah mukosa permukaan bola mata, setara dengan epitel usus dan bronkus, yang berhubungan dengan sel dan berfungsi sebagai pertahanan terhadap antigen dan mikroorganisme dari luar. Konyungtiva dan jaringan limfoid di daerah tersebut akan memproses antigen sehingga timbul sel T dan sel B yang sudah tersentisasi, yang telah siap dengan respons imunnya bila timbul rangsangan dari luar. Mata merah alergi yang musiman dan mata merah alergi yang berkelanjutan adalah jenis yang paling sering dari reaksi alergi pada mata. Mata merah alergi yang musiman sering disebabkan oleh serbuk sari pohon atau rumput, oleh karenanya jenis ini timbul khususnya pada musim semi atau awala musim panas. Serbuk sari gulma bertanggung jawab pada gejala alergi mata merah pada musim panas dan awal musim gugur. Alergi mata merah yang berkelanjutan terjadi sepanjang tahun; paling sering disebabkan oleh tungau debu, bulu hewan, dan bulu unggas.  Mata merah Vernal adalah bentuk alergi mata merah yang lebih serius dimana penyebabnya tidak diketahui. Kondisi paling sering terjadi pada anak laki-laki, khususnya yang berumur kurang dari 10 tahun yang memiliki eksema, asma, atau alergi musiman. Mata merah Vernal biasanya kambuh setiap musim semi dan hilang pada musim gugur dan musim dingin. Banyak anak tidak mengalaminya lagi pada umur dewasa muda.
  • Gangguan sensoris biasanya anak mengalami mata yang mudah silau dan tidak suka cahaya yang terang seperti sinar matahari atau lampu yang sangat terang. Gangguan sensoris mata ini sering disertai gangguan sensoris pada raba dan ensitif terhadap suara (frekuensi tinggi), perabaan telapak kaki dan tangan sensitif  (jalan jinjit, flat foot, mudah geli, mudah jijik, tidak suka memegang bulu, boneka dan bianatang berbulu)
  • Gangguan TICK atau mata sering berkedip. Selama ini gangguan ini sering dianggap mata lelah karena seiing melihat televisi atau main game. Sampai saat ini penyebab gangguan Tick ini belum diketahui

Amati Tanda dan gejala gangguan saluran cerna karena alergi dan hipersensitif makanan (Gastrointestinal Hipersensitivity) (Gejala Gangguan Fungsi saluran cerna yang ada selama ini sering dianggap normal)

  • Pada Bayi  : GASTROOESEPHAGEAL REFLUKS ATAU GER, Sering MUNTAH/gumoh, kembung,“cegukan”, buang angin keras dan sering, sering rewel gelisah (kolik) terutama malam hari, BAB > 3 kali perhari, BAB tidak tiap hari. Feses warna hijau,hitam dan berbau.  Sering “ngeden & beresiko Hernia Umbilikalis (pusar), Scrotalis, inguinalis. Air liur berlebihan. Lidah/mulut sering timbul putih, bibir kering
  • Pada anak yang lebih besar :
  1. Mudah MUNTAH bila menangis, berlari atau makan banyak. MUAL pagi hari.
  2. Sering Buang Air Besar (BAB)  3 kali/hari atau lebih, sulit BAB sering ngeden kesakitan saat BAB (obstipasi). Kotoran bulat kecil hitam seperti kotoran kambing, keras, warna hitam, hijau dan bau tajam. sering buang angin, berak di celana. Sering KEMBUNG, sering buang angin dan bau tajam. Sering NYERI PERUT, tidur malam nungging (biasanya karena perut tidak nyaman)
  3. Nyeri gigi, gigi berwarna kuning kecoklatan, gigi rusak, gusi mudah bengkak/berdarah. Bibir kering dan mudah berdarah, sering SARIAWAN, lidah putih & berpulau, mulut berbau, air liur berlebihan.
MANIFESTASI KLINIS YANG SERING MENYERTAI ALERGI DAN HIPERSENSITIFITAS MAKANAN PADA BAYI :
  • KULIT : sering timbul bintik kemerahan terutama di pipi, telinga dan daerah yang tertutup popok. Kerak di daerah rambut. Timbul bekas hitam seperti tergigit nyamuk. Kotoran telinga berlebihan & berbau. Bekas suntikan BCG bengkak dan bernanah. Timbul bisul.
  • SALURAN NAPAS : Napas grok-grok, kadang disertai batuk ringan. Sesak pada bayi baru lahir disertai kelenjar thimus membesar (TRDN/TTNB)
  • HIDUNG : Bersin, hidung berbunyi, kotoran hidung banyak, kepala sering miring ke salah satu sisi karena salah satu sisi hidung buntu, sehingga beresiko ”KEPALA PEYANG”.
  • MATA : Mata berair atau timbul kotoran mata (belekan) salah satu sisi.
  • KELENJAR : Pembesaran kelenjar di leher dan kepala belakang bawah.
  • PEMBULUH DARAH :  telapak tangan dan kaki seperti pucat, sering terba dingin
  • GANGGUAN HORMONAL : keputihan/keluar darah dari vagina, timbul bintil merah bernanah, pembesaran payudara, rambut rontok.
  • PERSARAFAN : Mudah kaget bila ada suara keras. Saat menangis : tangan, kaki dan bibir sering gemetar atau napas tertahan/berhenti sesaat (breath holding spells)
  • PROBLEM MINUM ASI : minum berlebihan, berat berlebihan krn bayi sering menangis dianggap haus (haus palsu : sering menangis belum tentu karena haus atau bukan karena ASI kurang.). Sering menggigit puting sehingga luka. Minum ASI sering tersedak, karena hidung buntu & napas dengan mulut. Minum ASI lebih sebentar pada satu sisi,`karena satu sisi hidung buntu, jangka panjang bisa berakibat payudara besar sebelah.
MANIFESTASI KLINIS YANG SERING MENYERTAI ALERGI DAN HIPERSENSITIFITAS MAKANAN PADA ANAK
  • SALURAN NAPAS DAN HIDUNG : Batuk / pilek lama (>2 minggu), ASMA, bersin, hidung buntu, terutama malam dan pagi hari. MIMISAN, suara serak, SINUSITIS, sering menarik napas dalam atau tidur ngorok.
  • KULIT : Kulit timbul BISUL, kemerahan, bercak putih dan bekas hitam seperti tergigit nyamuk. Warna putih pada kulit seperti ”panu”. Sering menggosok mata, hidung, telinga, sering menarik atau memegang alat kelamin karena gatal. Kotoran telinga berlebihan, sedikit berbau, sakit telinga bila ditekan (otitis eksterna).
  • SALURAN CERNA : Mudah MUNTAH bila menangis, berlari atau makan banyak. MUAL pagi hari. Sering Buang Air Besar (BAB)  3 kali/hari atau lebih, sulit BAB (obstipasi), kotoran bulat kecil hitam seperti kotoran kambing, keras, sering buang angin, berak di celana. Sering KEMBUNG, sering buang angin dan bau tajam. Sering NYERI PERUT.
  • PEMBULUH DARAH Vaskulitis (pembuluh darah kecil pecah) : sering LEBAM KEBIRUAN pada tulang kering kaki atau pipi atas seperti bekas terbentur. Berdebar-debar, mudah pingsan, tekanan darah rendah.
  • OTOT DAN TULANG : nyeri kaki atau kadang  tangan, sering minta dipijat terutama saat malam hari. Kadang nyeri dada
  • SALURAN KENCING : Sering minta kencing, BED WETTING (semalam  ngompol 2-3 kali)
  • HORMONAL : rambut berlebihan di kaki atau tangan, keputihan, gangguan pertumbuhan tinggi badan.
  • Kepala,telapak kaki/tangan sering teraba hangat. Berkeringat berlebihan meski dingin (malam/ac). Keringat  berbau.
  • FATIQUE :  mudah lelah, sering minta gendong
 
GANGGUAN PERILAKU YANG SERING MENYERTAI PENDERITA ALERGI DAN HIPERSENSITIFITAS MAKANAN PADA ANAK
  • SUSUNAN SARAF PUSAT : sakit kepala, MIGRAIN, TICS (gerakan mata sering berkedip), , KEJANG NONSPESIFIK (kejang tanpa demam & EEG normal).
  • GERAKAN MOTORIK BERLEBIHAN Mata bayi sering melihat ke atas. Tangan dan kaki bergerak terus tidak bisa dibedong/diselimuti. Senang posisi berdiri bila digendong, sering minta turun atau sering menggerakkan kepala ke belakang, membentur benturkan kepala. Sering bergulung-gulung di kasur, menjatuhkan badan di kasur (“smackdown”}. ”Tomboy” pada anak perempuan : main bola, memanjat dll.
  • AGRESIF MENINGKAT sering memukul kepala sendiri, orang lain. Sering menggigit, menjilat, mencubit, menjambak (spt “gemes”)
  • GANGGUAN KONSENTRASI: cepat bosan sesuatu aktifitas kecuali menonton televisi,main game, baca komik, belajar. Mengerjakan sesuatu  tidak bisa lama, tidak teliti, sering kehilangan barang, tidak mau antri, pelupa, suka “bengong”, TAPI ANAK TAMPAK CERDAS
  • EMOSI TINGGI (mudah marah, sering berteriak /mengamuk/tantrum), keras kepala, negatifisme
  • GANGGUAN KESEIMBANGAN KOORDINASI DAN MOTORIK : Terlambat bolak-balik, duduk, merangkak dan berjalan. Jalan terburu-buru, mudah terjatuh/ menabrak, duduk leter ”W”.
  • GANGGUAN SENSORIS : sensitif terhadap suara (frekuensi tinggi) , cahaya (mudah silau), perabaan telapak kaki dan tangan sensitif  (jalan jinjit, flat foot, mudah geli, mudah jijik, tidak suka memegang bulu, boneka dan bianatang berbulu)
  • GANGGUAN ORAL MOTOR : TERLAMBAT BICARA, bicara terburu-buru, cadel, gagap. Gangguanmengunyah menelan
  • IMPULSIF : banyak bicara,tertawa berlebihan, sering memotong pembicaraan orang lain
  • Memperberat gejala AUTIS dan ADHD (Alergi dan hipersensititas makanan bukan penyebab Autis atau ADHD tetapi hanya memperberat gejalanya)
KOMPLIKASI SERING MENYERTAI ALERGI DAN HIPERSENSITIFITAS MAKANAN PADA ANAK
  • Daya tahan menurun sering sakit demam, batuk, pilek setiap bulan bahkan sebulan 2 kali. (normal sakit seharusnya 2-3 bulan sekali)
  • Karena sering sakit berakibat Tonsilitis kronis (AMANDEL MEMBESAR) hindari operasi amandel yang tidak perlu atau mengalami Infeksi Telinga
  • Waspadai dan hindari efek samping PEMAKAIAN OBAT TERLALU SERING.
  • Mudah mengalami INFEKSI SALURAN KENCING.  Kulit di sekitar kelamin sering kemerahan
  • SERING TERJADI OVERDIAGNOSIS TBC  (MINUM OBAT JANGKA PANJANG PADAHAL BELUM TENTU MENDERITA TBC / ”FLEK ”)  KARENA GEJALA ALERGI MIRIP PENYAKIT TBC. BATUK LAMA BUKAN GEJALA TBC PADA ANAK BILA DIAGNOSIS TBC MERAGUKAN SEBAIKNYA ”SECOND OPINION” DENGAN DOKTER LAINNYA
  • Sering megalami Gizi Ganda : satu kelompok sulit makan terdapat kelompok lain makan berlebihan sehingga beresiko kegemukan
  • GANGGUAN SULIT MAKAN : nafsu makan menurun bahkan kadang tidak mau makan sama sekali, gangguan mengunyah menelan, tidak bisa  makan makanan berserat (daging sapi, sayur tertentu, nasi). Hanya mau makanan yang crispy atau renyah seperti : krupuk, biskuit dan sebagainya.  Disertai keterlambatan pertumbuhan gigi.
  • MAKAN BERLEBIHAN KEGEMUKAN atau OBESITAS
  • INFEKSI JAMUR (HIPERSENSITIF CANDIDIASIS) di lidah, selangkangan, di leher, perut atau dada, KEPUTIHAN
 
 

Daftar Pustaka

  • Mimura T, Yamagami S, Usui T, Funatsu H, Noma H, Honda N, Amano S. Relationship between myopia and allergen-specific serum IgE levels in patients with allergic conjunctivitis. Clin Experiment Ophthalmol. 2009 Sep;37(7):670-7.
  • T Mimura, Y Mimura, A Arimoto, S Amano, S Yamagami, H Funatsu, T Usui, H Noma, N Honda and S Okamoto. Relationship between refraction and allergic conjunctivitis Refraction and allergic conjunctivitis. Eye 23, 63-66 (January 2009)
  • M G Kerr Muir,  E G Woodward,  T J Leonard. Corneal thickness, astigmatism, and atopy. Br J Ophthalmol 1987;71:207-211 doi:10.1136/bjo.71.3.207
  • Peter A. Gardiner, Griffith James.ASSOCIATION BETWEEN MATERNAL DISEASE DURING PREGNANCY AND MYOPIA IN THE CHILD    Br J Ophthalmol 1960;44:172-178
  • Reider N. Sublingual immunotherapy for allergic rhinoconjunctivitis–the seeming and the real. Int Arch Allergy Immunol. Jul 2005;137(3):181-6. [Medline].
  • I Toda,  J Shimazaki,  K Tsubota. Allergic conjunctivitis and dry eye. H Fujishima,  Br J Ophthalmol 1996;80:994-997
  • Shuhei Imayama,  Shigeru Sugai,  Yoh-Ichi Kawano,  Tatsuro Ishibashi. Increased number of IgE positive Langerhans cells in the conjunctiva of patients with atopic dermatitis Ayako Yoshida.  Br J Ophthalmol 1997;81:402-406
  • Shearer WT, Fleisher TA. The Immune System. In: Middleton E, Reed CE, Ellis EF, eds. Allergy: Principles and Practice. St Louis: Mosby; 1998:1-13.
  • William G Hodge. Atopy and keratoconus: a multivariate analysis Ahmed M Bawazeer. B LorimerBr J Ophthalmol 2000;84:834-836 doi:10.1136/bjo.84.8.834
  • P T Klouda, D L Easty, M Manku, J Charles, C M Stewart. Association between keratoconus and atopy. R J Harrison,   Br J Ophthalmol 1989;73:816-822
  • Bonini S. Advances and gaps in ocular allergies. Arch Soc Esp Oftalmol. Apr 2005;80(4):205-7.
  • Braude LS, Chandler JW. Atopic corneal disease. Int Ophthalmol Clin. 1984;24(2):145-56.
  • Brauninger GE, Centifanto YM. Immunoglobulin E in human tears. Am J Ophthalmol. Sep 1971;72(3):558-61.
  • Brunsting LA, Reed WB, Bair HL. Occurrence of cataracts and keratoconus with atopic dermatitis. Arch Dermatol. 1955;72:237.
  • Friedlaender MH. Allergy and Immunology of the Eye. New York: Harper & Row; 1979.
  • Friedlaender MH. Conjunctival provocation tests: a model of human ocular allergy. Trans Am Ophthalmol Soc. 1990;87:577.
  • Garrity JA, Liesegang TJ. Ocular complications of atopic dermatitis. Can J Ophthalmol. Feb 1984;19(1):21-4.
  • Treumer H. Reversible irregular corneal astigmation in disseminated neurodermatitis  Klin Monbl Augenheilkd. 1978 Aug;173(2):253-6. German. PMID: 703151
  • CARTER JH. Residual astigmatism of the human eye. Optom Wkly. 1963 Jul 4;54:1271-2. No abstract available.
  • WILLIAMS OA. Latent astigmatism in practice. Am J Optom Arch Am Acad Optom. 1963 Mar;40:143-7.
  • HIRSCH MJ. Changes in astigmatism during the first eight years of school–an interim report from the Ojai longitudinal study.  Am J Optom Arch Am Acad Optom. 1963 Mar;40:127-32. No abstract available.
  • YUN WS. Astigmatism. Chosen Ibo. 1962 Oct;7:762-4. Korean. No abstract available. PMID: 14002914
  • Kornerup T, Lodin A. Ocular changes in 100 cases of Besnier’s prurigo (atopic dermatitis). Acta Ophthalmol (Kbh) 1959; 37:508-21.
  • Davies PD, Lobascher D, Menon JA, Rahi AHS, Ruben M. Immunological studies in keratoconus. Trans Ophthalmol Soc UK 1976;9:173-8.
  • Marechal-Courtois C. Topographic study of the cornea at different stages of  the development of keratoconus. Bull Soc Belge Ophtalmol 1967;147: 495-505.
  • Troutman RC, Meltzer M. Astigmatism and myopia inkeratoconus. Trans Am Ophthalmol Soc 1972; 70: 265-77.
  • Woodward EG. Keratoconus-the disease and its progression. Doctoral thesis. London: City University, 1980: 11.
  • Copeman, P. W. M. (1965). Eczema and Keratoconus. British Medical Journal, 2, 977-979.
  • Brunsting LA, Reed WB, Blair HL(1955) Occurrence of cataract and keratoconus with atopic dermatitis. Arch Dermatol 72:237–241.[Abstract/FREE Full text]
  • Galin MA, Berger R(1958) Atopy and keratoconus. Am J Ophthalmol 45:904–906
  • Spencer WH, Fisher JJ. (1959) The association of keratoconus with atopic dermatitis. Am J Ophthalmol 47:332–334.[Medline]
  • Roth HL, Kierland RR. (1964) The natural history of atopic dermatitis. Arch Dermatol 89:209–214.[Medline]
  • Lowell FC, Carroll JM. (1970) A study of the occurrence of atopic traits in patients with keratoconus. J Allergy Clin Immunol 46:32–39.
  • Copeman PWM (1965) Eczema and keratoconus. BMJ 2:977–979.
  • Davies PD, Lobascher D, Menon JA, et al.(1976) Immunological studies in keratoconus. Trans Ophthalmol Soc UK 96:173–178.[Medline][Web of Science]
  • Rah A, Davies P, Ruben M, et al.(1977) Keratoconus and coexisting atopic disease. Br J Ophthalmol 61:761–764
  • Gasset AR, Hinson WA, Frias JL(1978) Keratoconus and atopic disease. Ann Ophthalmol 10:991–994
  • Harrison RJ, Klouda PT, Easty DL, et al.(1089) Association between keratoconus and atopy. Br J Ophthalmol 73:816–822
  • Rabinowitz YS, Nesburn AB, McDonnell PJ(1993) Videokeratography of the fellow eye in unilateral keratoconus. Ophthalmology 100:181–186.[Medline][Web of Science]
  • Williams HC, Burney PGJ, Pembroke AC, et al. (1994) The UK working party’s diagnostic criteria for atopic dermatitis. III. Independent hospital validation. Br J Dermatol 131:406–416.[CrossRef][Medline][Web of Science]
  • Karseras AG, Ruben M(1976) Aetiology of keratoconus. Br J Ophthalmol 60:522–524
  • Coyle JT (1984) Keratoconus and eye rubbing. Am J Ophthalmol 97:527–528
  • A Rahi, P Davies, M Ruben, D Lobascher. Keratoconus and coexisting atopic disease. J MenonBr J Ophthalmol 1977;61:761-764 doi:10.1136/bjo.61.12.761
  • Davies, P. D., Lobascher, D., Menon, J. A., Rahi, A. H. S.,and Ruben, M. (1976). Immunological studies in keratotoconus. Transactions of the Ophthalmological Societies of the United Kingdom, 96, 173-178.
  • Easty, D., Entwistle, C., Funk, A., and Witcher, J. (1975). Herpes simplex keratitis and keratoconus in atopic patient: A clinical and immunological study. Transactions of the Ophthalmological Societies of the United Kingdom,95,267-276.
  • Galin, M. A., and Berger, R. (1958). Atopy and keratoconus. American Journal of Ophthalmology, 45, 904-906. Goodfriend, L., Lapkoff, C. B., and Marsh, D. D. (1973). Ragweed pollen allergen Ra5: Isolation, chemical properties and genetic basis for its cutaneous activity in man (Abst.) Journal of Allergy and Clinical Immunology,51,81-82.
  • Hamburger, R. N., and Bazaral, M. (1972). IgE levels  in twins confirm genetic control in human beings (Abst.) Journal of Allergy and Clinical Immunology, 49, 91.
  • Iaufman,H. S., and Hobbs, J. R. (1970). Immunological defects in an atopic population. Lancet, 2, 1061-1063.
  • Longmore, L. (1970). Atopic dermatitis, cataract and keratoconus. Australian Journal of Dermatology, 11, 139-141.
  • Lowell, F. C., and Carroll, J. M. (1970). A study  of the occurrence of atopic traits in patients  with keratoconus. Journal of Allergy, 46,  32-39.
  • Manfridi, M. L. R., and Romel, L. (1966). The electrophoreticprotein picture of keratoconus. Minerva  oftalmologica, 220-221.
  • Porteous, J. R., Fisher, J. M., Lewin, K. J., and Taylor, K. B. (1974). Induction of autoallergic gastritis in dogs.  Journal ofPathology, 112, 139-146.
  • Pouliquen, Y., Graf, B., Frouin, M. A., Faure, J. P.,Robert,L.,and Junqua, S. (1972). An attempt at  interpretation of the histological and ultrastructural lesions of thecornea in keratoconus (in French) Berichte der deutschen ophthalmologischen Gesellschaft, 71, 52-57.
  • Rahi, A. H. S., Holborow, E. J., Perkins, E. S., Gungen,Y.Y., and Dinning,  W. J. (1976). Immunological investigations in uveitis. Transaction of the Ophthalmological Societies of the United Kingdom,  96, 113-122.
  • Ridley, F. (1956). Contact lenses in treatment  of keratoconus. British Journal of Ophthalmology,  40, 295-304.
  • Spencer, W. H., and Fisher, J. J. (1959). The association of keratoconus with atopic dermatitis. American Journal  of Ophthalmology, 47, 332-334.
  • Taylor, B., Norman, A. P., Orgel, H. A., Stokes, C. R., Turner, M. W., and Soothill, J. F. (1973). Transient IgA deficiency and pathogenesis of infantile atopy. Lancet, 2, 111-113.
  • Turner, M. W., Brostoff, J., Wells, R. S., Stokes, C. R., and Soothill, J. F. (1977). HLA in Eczema and Hay Fever.Clinical and

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Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider

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Signs and symptoms Eyes Allergy in Children

Signs and symptoms Eyes Allegy in children

Allergic conjunctivitis is commonly referred along with allergic rhinitis as “allergic rhinoconjunctivitis” due to the high-frequency of co-existence with allergic rhinitis and allergic asthma.

Despite the fact that allergic patients often present with other manifestations such as rhinitis, asthma, urticaria or eczema, ocular symptoms may be the initial and the most prominent indication of the allergic response.

In general, it is estimated that ocular allergies affect 5-22% of the population . Especially in the USA, ocular allergy is estimated to affect 15-20% of the general population. The eye is a common site and target for the development of an allergic inflammatory disorder, in spite of the fact that tears may prevent the impact of allergens, such as pollens, on its surface . Red eye is the most common sign of allergic conjunctivitis. Other common symptoms are watery eyes (88%), itching (88%), redness (78%), soreness (75%), swelling (72%) or stinging (65%) .

Ocular allergy, as an inflammatory disorder, consists of variable allergic manifestations with different presentations such as: a) seasonal allergic conjunctivitis (SAC), which is the most common one, b) perennial allergic conjunctivitis (PAC), c) giant papillary conjunctivitis (GPC), d) vernal keratoconjunctivitis (VKC) and e) atopic keratoconjunctivitis (AKC) . GPC is usually associated with the use of contact lenses or caused by physical trauma. The most common types of ocular allergy are SAC and PAC . AKC and VKC are characterized by chronic immune inflammation with T cell infiltration and may be sight threatening. On the contrary, SAC and PAC remain self-limited .

In practice, approximately 6% of consultations of general practitioners concern inflamed or red eye, half of which are caused by ocular allergy . However, the allergic background of conjunctivitis is usually overlooked. Hence, allergic conjunctivitis is often under diagnosed and consequently under treated except when it is severe and the chief complaint of a consultation in a specialty clinic. Pharmacological treatment mainly includes the prescription of topical ocular mast cell stabilizers or antihistamines and in more severe cases corticosteroids, immunosuppressant drugs and immunotherapy . The evaluation of the patients with skin prick tests (SPTs) is usually overlooked. SPTs represent an immediate IgE mediated allergic reaction and may provide clear evidence for the diagnosis of every specific allergic manifestation

The aforementioned facts justify the need to identify the prevalence of allergic conjunctivitis in allergic populations and the common co existence of allergic conjunctivitis with other allergic manifestations, thereby enabling doctors to manage ocular allergies more effectively. In addition, the identification of the proportional frequencies of sensitization to the most common allergens provides a useful insight to exacerbating factors of allergic conjunctivitis.

The eyes are the windows to the soul because they reflect our state of mind. This certainly can’t be true if our eyes are red, swollen, watery, and itchy from an allergic reaction. Severe allergic eye symptoms can be very distressing and are a common reason for visits to the allergist, ophthalmologist, and even the emergency room. Occasionally, severe eye allergies cause serious damage that can threaten eyesight.

If your children eyes itch, are red, tearing or burning, pay attention to what they may be telling you. You may have eye allergies, or allergic conjunctivitis, a condition that affects millions of Americans. It is a condition that can occur alone, but often accompanies nasal allergy symptoms, such as sneezing, sniffling and a stuffy nose. And, while most people treat nasal allergy symptoms, they often ignore their itchy, red, watery eyes. Here you will find answers to common questions and information on eye allergy treatment.

Eye allergies usually are associated with other allergic conditions, particularly hay fever (allergic rhinitis) and atopic eczema (dermatitis). The causes of eye allergies are similar to those of allergic asthma and hay fever. Medications and cosmetics can play a significant role in causing eye allergies. Reactions to eye irritants and other eye conditions (for  example, infections such as pinkeye) are often confused with eye allergy. Any kind of irritant, whether environmental, infectious, or manmade, can cause symptoms consistent with eye allergies.  

The symptoms that a child displays will vary depending upon the underlying condition afflicting the eye. However, there are several general signs and symptoms typically associated with eye-related disorders. They include:

  • Watery eyes. Eyes can water either because tear ducts are blocked, or because something is irritating them, such as an allergy.
  • Itchiness and burning. Histamine and other chemicals released during an allergic cascade produce these symptoms.
  • Redness. A healthy eye should have red blood vessels that are visible. However, chronic and excessive redness is a sign that the eyes are irritated, possibly by an allergy. Other factors, such as excessive coughing, also can cause this symptom.
  • Black circles around the eyes. Sometimes known as allergic shiners, they are the result of constant rubbing and scratching of the skin, which causes a darkening effect. This can be seen in children with allergic rhinitis (hay fever), as well as with other conditions.
  • Sensation that something is in the eye.
  • Cobblestone pattern of lesions on the conjunctiva under the eyelids.
  • Light sensitivity (photophobia).
  • Discharge. The characteristics of the discharge will vary based on the type of condition.
  • Swelling of the eyelid.

Symptoms of allergy-related eye conditions may occur alone or can appear in combination with nasal (e.g., sneezing, sniffling, stuffy nose).Children may not always indicate that their eyes are bothering them. For this reason, parents should watch for certain physical or behavioral indicators of an underlying eye problem . General signs of eye-related problems in children that require medical attention include:

  • Abnormal alignment of the eyes, or unusual eye movement after 6 months of age
  • Red-rimmed, crusted or swollen eyelids
  • Watery or red eyes

Children can also reveal potential eye problems through their behavior. Parents should watch to see if their child:

  • Rubs eyes often
  • Closes or covers one eye
  • Tilts head, or thrusts head forward
  • Struggles with reading or other work that involves close-up vision
  • Blinks more often than normal
  • Mentions that things are blurry or hard to see
  • Squints or frowns a lot while trying to see things
  • Has difficulty following (tracking) objects visually

Allergic conjunctivitis

Allergic conjunctivitis, also called “allergic rhinoconjunctivitis,” is the most common allergic eye disorder. The condition is usually seasonal and is associated with hay fever. The main cause is pollens, although indoor allergens such as dust mites, molds, and dander from household pets such as cats and dogs may affect the eyes year-round. Typical complaints include itching, redness, tearing, burning, watery discharge, and eyelid swelling. To a large degree, the acute (initial) symptoms appear related to histamine release.

Vernal keratoconjunctivitis
Vernal keratoconjunctivitis is an uncommon condition that tends to occur in  preadolescent boys (3:1 male to female ratio) and is usually outgrown during the  late teens  or early adulthood.  (Vernal is another term for “spring.”)  Vernal keratoconjunctivitis usually appears in the late  spring and particularly occurs in rural areas where dry,  dusty, windy, and warm conditions prevail.  The eyes become  intensely itchy, sensitive to light, and the lids feel  uncomfortable and droopy.  The eyes produce a “stringy”  discharge and, when examined, the surface under the upper  eyelids appears “cobblestoned.”  A closer examination of  the eye reveals severe inflammation due to the vast number  of mast cells and accumulated eosinophils  (a type of white blood cell involved in the allergic response), producing so-called  called “Trantas dots.”

Giant papillary conjunctivitis (GPC)
This condition is named for its typical feature, large  papillae, or bumps, on the conjunctiva under the upper  eyelid.  These bumps are likely the result of irritation  from a foreign substance, such as contact lenses.  Hard,  soft, and rigid gas-permeable lenses are all associated  with the condition.  The reaction is possibly linked to the  protein buildup on the contact lens surface.  This condition is believed, in part, to be due to an allergic reaction to either the contact lens itself, protein deposits on the contact lens, or the preservative in the solution for the contact lenses.  Redness and  itching of the eye develop, along with a thick  discharge.

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Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

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Keratokonus Mata dan Alergi

Keratokonus Disebabkan Karena Alergi ?

Abstract

Many study was to determine if atopy is a risk factor for keratoconus. Other potential risk factors were also studied and included age, sex, race, eye rubbing, mitral valve prolapse, handedness, collagen vascular disease, ocular trauma, pigmentary retinopathy, Marfan’s syndrome, Down’s syndrome, and a history of contact lens wear. Atopy was less common in patients with unilateral keratoconus, and keratoconus occurred more frequently on the side of the dominant hand. There was a significantly lower frequency of HLA B7 in the keratoconus group than in the controls. No abnormalities of essential fatty acid metabolism were found in keratoconus patients with or without atopy.  Atopy may contribute to keratoconus but most probably via eye rubbing associated with the itch of atopy. No other variable measured was significantly associated with the aetiology of keratoconus.

Keratokonus

Keratokonus adalah perubahan bentuk (penipisan) kornea yang terjadi secara bertahap, sehingga bentuknya menyerupai kerucut.  Keratokonus mulai terjadi pada usia 10-20 tahun. Sampai saat ini penyebab pasti kelainan ini belum diketahui.  Tetapi beberapa penelitian terakhir menunjukkan bahwa keratokonus sering berkaitan dengan alergi.

Keratokonus lebih sering ditemukan pada pemakai lensa kontak dan penderita rabun dekat.  Penelitian menunjukkan bahwa keratokonus kemungkinan terjadi karena beberapa hal berikut: Kelainan kornea bawaan. Cedera mata (misalnya menggisik-gisik mata atau memakai lensa kontak yang keras selama bertahun-tahun) Penyakit mata tertentu (misalnya retinitis pigmentosa, retinopati, konjungtivitis vernal). Penyakit sistemik (misalnya amorosis kongenitalis Leber, sindroma Ehlers-Danlos, sindroma Down dan osteogenesis imperfekta).

Keratokonus terjadi jika bagian tengah kornea menipis dan secara bertahap menonjol ke arah luar sehingga bentuknya menyerupai kerucut. Kelainan kelengkungan ini menyebabkan perubahan pada kekuatan pembiasan kornea. Sebagai akibatnya terjadi astigmata sedang sampai berat dan rabun dekat.  Keratokonus juga bisa menyebabkan pembengkakan dan pembentukan jaringan parut yang menghalangi penglihatan.  Diagnosis ditegakkan berdasarkan gejala dan hasil pemeriksaan kornea dengan slit lamp  Untuk mengetahui kelengkungan kornea bisa dilakukan topografi kornea. Pada keratokonus stadium lanjut, penipisan kornea bisa diukur dengan pakimetri.

Keratokonus dan Alergi

Enam puluh tujuh pasien dengan keratoconus dikelompokkan berdasarkan status atopik. Keratoconus pasien dengan dan tanpa atopi tidak berbeda secara signifikan berkaitan dengan jenis kelamin, umur onset, atau tingkat keratoplasty, tetapi pasien dengan tingkat IgE yang sangat tinggi lebih rentan terhadap penolakan jaringan. Pengaruh atopy tidak biasa pada pasien dengan keratoconus unilateral, dan keratoconus terjadi lebih sering pada sisi tangan yang dominan. Terdapat kecenderungan  HLA B7 secara signifikan lebih rendah pada kelompok keratoconus daripada di kontrol. Tidak ada kelainan metabolisme asam lemak esensial ditemukan pada pasien keratoconus dengan atau tanpa atopi. Tidak ada bias kelas sosial dalam kelompok. Studi ini termasuk sibling dengan keratoconus dan atopi, dan pasien non-atopik yang kembar identik tidak memiliki keratoconus.

Penanganan Keratokonus biasanya menyerang kedua mata. Pada awalnya, penderita bisa memperbaiki penglihatannya dengan menggunakan kaca mata. Tetapi sejalan dengan memburuknya astigmata, penderita harus menggunakan lensa kontak untuk mengurangi astigmata dan agar penglihatannya lebih baik.  Pada kebanyakan kasus, kornea akan kembali stabil beberapa tahun kemudian tanpa pernah menyebabkan gangguan penglihatan yang berat.  Tetapi pada sekitar 10-20% penderita, pada akhirnya kornea membentuk jaringan parut atau tidak dapat mentolerir lensa kontak.  Jika hal ini terjadi, maka perlu dilakukan pencangkokan kornea.

Daftar pustaka

  • Kornerup T, Lodin A. Ocular changes in 100 cases of Besnier’s prurigo (atopic dermatitis). Acta Ophthalmol (Kbh) 1959; 37:508-21.
  • Davies PD, Lobascher D, Menon JA, Rahi AHS, Ruben M. Immunological studies in keratoconus. Trans Ophthalmol Soc UK 1976;9:173-8.
  • Marechal-Courtois C. Topographic study of the cornea at different stages of  the development of keratoconus. Bull Soc Belge Ophtalmol 1967;147: 495-505.
  • Troutman RC, Meltzer M. Astigmatism and myopia inkeratoconus. Trans Am Ophthalmol Soc 1972; 70: 265-77.
  • Woodward EG. Keratoconus-the disease and its progression. Doctoral thesis. London: City University, 1980: 11.
  • Copeman, P. W. M. (1965). Eczema and Keratoconus. British Medical Journal, 2, 977-979.
  • Brunsting LA, Reed WB, Blair HL(1955) Occurrence of cataract and keratoconus with atopic dermatitis. Arch Dermatol 72:237–241.[Abstract/FREE Full text]
  • Galin MA, Berger R(1958) Atopy and keratoconus. Am J Ophthalmol 45:904–906.[Medline]
  • Spencer WH, Fisher JJ. (1959) The association of keratoconus with atopic dermatitis. Am J Ophthalmol 47:332–334.[Medline]
  • Roth HL, Kierland RR. (1964) The natural history of atopic dermatitis. Arch Dermatol 89:209–214.[Medline]
  • Lowell FC, Carroll JM. (1970) A study of the occurrence of atopic traits in patients with keratoconus. J Allergy Clin Immunol 46:32–39.
  • Copeman PWM (1965) Eczema and keratoconus. BMJ 2:977–979.
  • Davies PD, Lobascher D, Menon JA, et al.(1976) Immunological studies in keratoconus. Trans Ophthalmol Soc UK 96:173–178.[Medline][Web of Science]
  • Rah A, Davies P, Ruben M, et al.(1977) Keratoconus and coexisting atopic disease. Br J Ophthalmol 61:761–764.[Abstract/FREE Full text]
  • Gasset AR, Hinson WA, Frias JL(1978) Keratoconus and atopic disease. Ann Ophthalmol 10:991–994.[Medline][Web of Science]
  • Harrison RJ, Klouda PT, Easty DL, et al.(1089) Association between keratoconus and atopy. Br J Ophthalmol 73:816–822.[Abstract/FREE Full text]
  • Rabinowitz YS, Nesburn AB, McDonnell PJ(1993) Videokeratography of the fellow eye in unilateral keratoconus. Ophthalmology 100:181–186.[Medline][Web of Science]
  • Williams HC, Burney PGJ, Pembroke AC, et al. (1994) The UK working party’s diagnostic criteria for atopic dermatitis. III. Independent hospital validation. Br J Dermatol 131:406–416.[CrossRef][Medline][Web of Science]
  • Karseras AG, Ruben M(1976) Aetiology of keratoconus. Br J Ophthalmol 60:522–524.[Abstract/FREE Full text]
  • Coyle JT (1984) Keratoconus and eye rubbing. Am J Ophthalmol 97:527–528.[CrossRef][Medline][Web of Science]
  • A Rahi, P Davies, M Ruben, D Lobascher. Keratoconus and coexisting atopic disease. J MenonBr J Ophthalmol 1977;61:761-764 doi:10.1136/bjo.61.12.761
  • Davies, P. D., Lobascher, D., Menon, J. A., Rahi, A. H. S.,and Ruben, M. (1976). Immunological studies in keratotoconus. Transactions of the Ophthalmological Societies of the United Kingdom, 96, 173-178.
  • Easty, D., Entwistle, C., Funk, A., and Witcher, J. (1975). Herpes simplex keratitis and keratoconus in atopic patient: A clinical and immunological study. Transactions of the Ophthalmological Societies of the United Kingdom,95,267-276.
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Curriculum Vitae Widodo Judarwanto

We are guilty of many errors and many faults. But our worst crime is abandoning the children, neglecting the fountain of life.
,
Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider

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Allergic Conjunctivitis, Rhinitis and Asthma: One Disease?

Allergic Conjunctivitis, Rhinitis and Asthma: One Disease?

C.A. Riedi, G.G.L.C. Westphal, N.A. Rosario, H.L.B.S. Santos, K. Takizawa, R.V.S. Souza, C.D. Aguilera
 
RATIONALE: asthma and rhinitis are common co-morbidities suggesting the concept of one disease. Allergic conjunctivitis may be part of this entity, but the association between them has not been specifically evaluated as co-morbidity. The objective of this study was to evaluate the relationship between allergic diseases (rhinitis and conjunctivitis) in asthmatic children.

METHODS: Clinical data were obtained from a standardized allergy work-up form that includes specific questions on common allergic diseases. Medical records of 1549 asthmatic children were evaluated. Asthma was diagnosed according to the Global Initiative for Asthma. The diagnosis of rhinitis and conjunctivitis were based on the presence of symptoms. Symptoms related to rhinitis and conjunctivitis were (runny, blocked nose, pruritus and sneeze) and (itching, tearing, burning, redness), respectively.

RESULTS: Of 1549 asthmatic children 628 (41%) have at least one symptom of allergic conjunctivitis and 1257 (81%) have diagnosis of rhinitis. Of these, 829 (66%) have at least one symptom of ocular allergy.

CONCLUSIONS: as many as two thirds of asthmatics patients have symptoms of allergic rhinoconjunctivitis. This suggests there is a close relationship between allergic diseases and a reason to include conjunctivitis in the concept of “one airway disease”.

Source : Federal University of Paraná, Curitiba, Brazil

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Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Upadate Reference: Conjunctivitis, Allergy and Future Management

Allergic conjunctivitis is in actuality a group of diseases affecting the ocular surface and is usually associated with type 1 hypersensitivity reactions.

Acute allergy conjunctivitis disorders :
1. Seasonal allergic conjunctivitis
2. Perennial allergic conjunctivitis, exist,

Chronic conjunctivitis disorders :
1. vernal keratoconjunctivitis
2. Atopic keratoconjunctivitis
3. Giant papillary conjunctivitis.

The ocular surface inflammation (usually mast cell driven) results in itching, tearing, lid and conjunctival edema–redness, and photophobia during the acute phase and can lead to a classic late-phase response (with associated eosinophilia and neutrophilia) in a subset of individuals. As is the case in other allergic diseases, a chronic disease can also develop, accompanied by remodeling of the ocular surface tissues. In severe cases the patient experiences extreme discomfort and sustains damage to the ocular surface. For such cases, there is no highly effective and safe treatment regimen. Topical administration of corticosteroids is used in severe cases but is associated with an increased risk for the development of cataracts and glaucoma.

Thus there is a worldwide search for new biotargets for the treatment of these diseases. Here we provide a brief update of the clinical symptoms associated with these diseases, the rationale for disease classification, recent advances in our understanding of the pathogenesis of the diseases, and an update on both preclinical and clinical advances toward refined therapies for these diseases.

Upadate Reference: Conjunctivitis, Allergy and Future Management

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Miyazaki D, Nakamura T, Toda M, Ohbayashi M, Sherry B, Richardson RM, et al. Requirement of MIP1α as an obligate costimulatory signal for mast cell degranulation in the conjunctiva. J Clin Invest. In press.

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Toda, M, Nakamura T, Richardson RM, Ono SJ. Signaling-cross talk between Fc(epsilon)RI and CC chemokine receptor1 in mast cells. Immunology 2004, Medimond International Proceedings; 2004. p. 517-20.

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Schreiber SL, Crabtree GR. The mechanism of action of cyclosporin A and FK506. Immunol Today. 1992;13:136–142

Pleyer U, Lutz S, Jusko WJ, Ngyen K, Narawane M, Ruckert D, et al.  Ocular absorption of topically applied FK506 from liposomal and oil formulations in the rabbit eye. Invest Ophthalmol Vis Sci. 1993;34:2737–2742

Takano T, Kobayashi C, Alba RM, Kanai A. The immunosuppressive effects of 0.025% cyclosporine eye drops in alpha cyclodextrin on rabbit corneal allografts. Acta Societatis Ophthalmologica Japonicae. 1992;96:834–840

Nussenblatt RB, Caspi RR, Mahdi R, Chan CC, Roberge F, Lider O, et al.  Inhibition of S-antigen induced experimental autoimmune uveoretinitis by oral induction with S-antigen. J Immunol. 1990;144:1689–1695

Vrabec TR, Gregerson DS, Dua HS, Donosal LA. Inhibition of experimental autoimmune uveitis by oral administration of S-antigen and synthetic peptides. Autoimmunity. 1992;12:175–184

Dick AD, Cheng YF, McKinnon A, Liversidge J, Forrester JV. Nasal administration of retinal antigens suppresses the inflammatory response in experimental allergic uveoretinitis: a preliminary report of intranasal induction of tolerance with retinal antigens. Br J Ophthalmol. 1993;77:171–175

Dua HS, Donoso LA, Laibson PR. Conjunctival instillation of retinal antigens induced tolerance. Ocul Immunol Inflamm. 1994;2:29–36

Koizumi T, Abe T, Sakuragi S. Suppression of experimental allergic conjunctivitis in guinea pigs by oral administration of antigen. Ocul Immunol Inflamm. 1995;3:113–119

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Provided by

CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation

htpp://www.allergyclinic.wordpress.com/

  • CLINIC FOR CHILDREN JL Taman bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021) 70081995 – 5703646
  • CHILDREN GROW UP CLINIC , MENTENG SQUARE Jl Matraman 30 Jakarta Pusat

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Respiratory, allergy and eye problems in bagasse-exposed sugar cane workers in Costa Rica

Occup Environ Med 2011

Respiratory, allergy and eye problems in bagasse-exposed sugar cane workers in Costa Rica

Mireia Gascon, Hans Kromhout, Dick Heederik, Wijnand Eduard, Berna van Wendel de Joode

Abstract

Aims To evaluate bagasse (sugar cane fibres) and microbiological exposure among sugar cane refinery workers in Costa Rica and its relationships with respiratory, allergy and eye problems.

Methods Ventilatory lung function and total serum IgE were measured in 104 sugar cane workers in five departments at one refinery before the harvesting season, and repeated for 77 of the workers at the end of the season. Information on the prevalence of respiratory and other symptoms was collected with a standardised questionnaire. During the harvesting season, inhalable dust, endotoxin and mould levels were measured among 74 randomly selected sugar cane workers across departments.

Results During the harvesting season, dust levels were relatively high in some departments, while endotoxin and mould levels were around background levels. Workers’ ventilatory lung function differed between departments before, but not during the harvesting season or between seasons. During the harvesting season, the prevalence of wheeze and eye problems almost doubled in workers exposed to bagasse and other types of dust, whereas shortness of breath and rhinitis increased only in bagasse-exposed workers. Reporting wheeze and shortness of breath was positively associated with the number of years working at the refinery, suggesting a long-term health effect.

Conclusion In this refinery, the differences in workers’ ventilatory lung function before the harvesting season are unlikely to be explained by bagasse exposure. However, the increase in reported symptoms (wheeze, shortness of breath, eye problems and rhinitis) over the season is likely due to irritation by dust, in particular bagasse, rather than microbiological agents.

Source : Central American Institute for Studies on Toxic Substances (IRET), Universidad Nacional de Costa Rica (UNA), Heredia, Costa Rica

Provided by

CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation

htpp://www.allergyclinic.wordpress.com/

  • CLINIC FOR CHILDREN JL Taman bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021) 70081995 – 5703646
  • CHILDREN GROW UP CLINIC , MENTENG SQUARE Jl Matraman 30 Jakarta Pusat

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Salivary cortisol levels and allergy in children: The ALADDIN birth cohort

Fredrik Stenius, MD, PhD, Magnus Borres, MD, PhD, Matteo Bottai, PhD, Gunnar Lilja, MD, PhD, Frank Lindblad, MD, PhD, Göran Pershagen, MD, PhD, Annika Scheynius, MD, PhD, Jackie Swartz, MD, Töres Theorell, MD, PhD, Johan Alm, MD, PhD

Abstract

Background
Pre- and postnatal stress have been related to allergy in children, but evidence from prospective studies is limited. Several environmental factors can influence the salivary cortisol level, which is used as a measure of activity of the hypothalamic-pituitary-adrenal axis.

Objective
The aim of this study was to assess the association between salivary cortisol levels at 6 months of age and allergic manifestations during the first 2 years of life.

Methods
Salivary samples for the analysis of cortisol level were collected at 6 months of age on 3 occasions during 1 day from 203 children. Blood samples were collected at 6, 12, and 24 months of age for analyses of specific IgE. Information on allergy-related symptoms was obtained by repeated examinations of the children. Generalized estimating equation statistics were used to calculate the overall risk for outcome measures.

Results
The adjusted odds ratio for the relationship between morning cortisol level and IgE sensitization was 1.60 (95% CI, 1.22-2.10, P = .001) and for eczema it was 1.28 (95% CI, 1.03-1.59, P = .026). The odds ratio for afternoon cortisol level in relation to sensitization and eczema was 1.56 (95% CI, 1.26-1.94, P < .001) and 1.33 (95% CI, 1.12-1.58, P = .001), respectively, and for evening cortisol level it was 1.49 (95% CI, 1.22-1.83, P < .001) and 1.37 (95% CI, 1.18-1.59, P < .001). Salivary cortisol level in the evening was associated with food allergy.

Conclusion
The association between salivary cortisol levels in infancy and allergic sensitization and allergic symptoms suggests a role of an altered hypothalamic-pituitary-adrenal axis in the etiological process of allergies.

Key words: Allergy, sensitization, salivary cortisol, children, stress

Provided by

CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation

htpp://www.allergyclinic.wordpress.com/

  • CLINIC FOR CHILDREN JL Taman bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021) 70081995 – 5703646
  • CHILDREN GROW UP CLINIC , MENTENG SQUARE Jl Matraman 30 Jakarta Pusat

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Tear IgE concentrations in allergic conjunctivitis

Eye (1998) 12, 296–298; doi: 10.1038/eye.1998.68

Tear IgE concentrations in allergic conjunctivitis

Keiko Nomura1 and Etsuko Takamura1

Abstract

Purpose Tear IgE has been considered to play an important role in allergic conjunctivitis and the measurement of tear IgE concentrations can help to diagnose this condition. Locally produced IgE levels have been shown to be the largest contributor to the severity of allergic conjunctivitis.

Methods One hundred and thirteen allergic conjunctivitis patients (70 seasonal allergic conjunctivitis (SAC), 21 perennial allergic conjunctivitis (PAC), 22 vernal keratoconjunctivitis (VKC)), 14 bacterial conjunctivitis (BC) patients, 13 epidemic keratoconjunctivitis (EKC) patients and 18 normal controls were recruited. Tear samples were collected using the microcapillary method and tear IgE levels were measured using an immunoenzyme assay.

Results Tear IgE concentrations showed significant increases in the VKC (322.2 ± 45.7 ng/ml), SAC (194.7 ± 21.7 ng/ml) and PAC (134.8 ± 23.1 ng/ml) groups when compared with controls (52.1 ± 9.7 ng/ml, p > 0.01). No significant difference was found between EKC (97.2 ± 11.7 ng/ml) and BC (92.6 ± 13.8 ng/ml) groups and controls (p = 0.1).

Conclusions Tear IgE concentrations showed a significant increase in allergic conjunctivitis patients when compared with controls. Our results suggest that measuring tear IgE concentrations can help to diagnose allergic conjunctivitis.

Keywords: Allergic conjunctivitis; Tear IgE; Serum IgE; Eosinophils

Source : Department of Ophthalmology, Tokyo Women’s Medical College, Tokyo, Japan

Provided by

CHILDREN ALLERGY CLINIC ONLINE

Yudhasmara Foundation

htpp://www.allergyclinic.wordpress.com/

  • CLINIC FOR CHILDREN JL Taman bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021) 70081995 – 5703646
  • CHILDREN GROW UP CLINIC , MENTENG SQUARE Jl Matraman 30 Jakarta Pusat

Clinical and Editor in Chief :

Dr Widodo Judarwanto, pediatrician email : judarwanto@gmail.com, Curiculum Vitae

Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider.

Copyright © 2012, Children Allergy Clinic Online Information Education Network. All rights reserved

Can conjunctival provocation test facilitate the diagnosis of food allergy in children?

Can conjunctival provocation test facilitate the diagnosis of food allergy in children?

Krane Kvenshagen B, et al.

Allergol Immunopathol (Madr). 2010 Nov-Dec;38(6):321-6. Epub 2010 Jun 4.

Abstract

BACKGROUND: Food allergy is common in children, occurring in 5-7.5%. The diagnosis may, however, be difficult. Elevated IgE or positive skin prick test to a food allergen is often considered proof of allergy, but may represent sensitisation without clinical manifestations. For a precise diagnosis oral challenge is necessary, but this is often not performed because of risk of serious allergic reactions. The aim of this study was to evaluate whether conjunctival provocation test would facilitate the diagnosis of IgE-mediated food allergy.

METHODS:

One hundred and forty-nine children with 174 possible diagnoses of food allergy were included. General examination, skin prick test and specific IgE were performed, as well as conjunctival provocation test of the suspected food allergen. Open food challenges and double-blind placebo controlled tests were performed in order to diagnose possible food allergy.

RESULTS:

Forty-six children with strongly positive conjunctival reactions (rubor, itching, oedema) to fifty food allergens were all proven to have allergy to the food in question. The children with negative conjunctival provocation tests showed no allergic reactions when challenged.

CONCLUSIONS:

We find that a strongly positive conjunctival reaction to a food allergen correlates well with true allergy. An oral challenge should be carefully performed. With a negative conjunctival test an oral challenge may safely be performed.

Source : Oestfold Hospital Trust, Department of Pediatrics, Fredrikstad, Norway.

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 www.allergycliniconline.com

ALLERGY ONLINE CLINIC FOR CHILDREN, TEEN AND ADULT Yudhasmara Foundation www.allergyclinic.me   GROW UP CLINIC I JL Taman Bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021)  5703646 – 44466102 GROW UP CLINIC II  MENTENG SQUARE Jl Matraman 30 Jakarta Pusat 10430 phone 44466103 – 97730777 http://growupclinic.com  http://www.facebook.com/GrowUpClinic Creating-hashtag-on-twitter@growupclinic Working together support to health of all by clinical practice, research and educations. Advancing of the future pediatric and future parenting to optimalized physical, mental and social health and well being for fetal, newborn, infant, children, adolescents and young adult

“GRoW UP CLINIC” Jakarta Focus and Interest on: ***Allergy Clinic Online *** Picky Eaters and Growup Clinic For Children, Teen and Adult (Klinik Khusus Gangguan Sulit Makan dan Gangguan Kenaikkan Berat Badan)*** Children Foot Clinic *** Physical Medicine and Rehabilitation Clinic *** Oral Motor Disorders and Speech Clinic *** Children Sleep Clinic *** Pain Management Clinic Jakarta *** Autism Clinic *** Children Behaviour Clinic *** Motoric & Sensory Processing Disorders Clinic *** NICU – Premature Follow up Clinic *** Lactation and Breastfeeding Clinic *** Swimming Spa Baby & Medicine Massage Therapy For Baby, Children and Teen ***
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Curriculum Vitae Widodo Judarwanto

We are guilty of many errors and many faults. But our worst crime is abandoning the children, neglecting the fountain of life.
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Information on this web site is provided for informational purposes only and is not a substitute for professional medical advice. You should not use the information on this web site for diagnosing or treating a medical or health condition. You should carefully read all product packaging. If you have or suspect you have a medical problem, promptly contact your professional healthcare provider

Copyright © 2013, Allergy Clinic Online Information Education Network. All rights reserved