Category Archives: Alergi Makanan

Update Immunopathophysiology of Food Allergy

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Dr Widodo Judarwanto
Allergy Clinic Online. Jakarta Indonesia

Immunopathophyisiology of food allergy is a disease with much left to determine. The mechanisms of tolerance, both in terms of what prevents most people from developing responses as well as why some individuals outgrow or never develop food allergies despite sensitization, remain unclear. Similarly, the environmental and genetic influences over sensitization are just becoming understood. Importantly, studies from animal models are showing that the mechanisms of anaphylactic reactions may well be heterogeneous in terms of routes of exposure, cell types involved, and the mediators responsible for symptoms. A better understanding of this heterogeneity will be crucial in developing future therapies.

Food allergies represent an increasingly prevalent human health problem, and therapeutic options remain limited, with avoidance being mainstay, despite its adverse effects on quality of life. A better understanding of the key immunological mechanisms involved in such responses likely will be vital for development of new therapies. The current understanding of how the immune system is thought to contribute to prevention or development of food allergies. Drawing from animal studies, as well as clinical data when available, the importance of oral tolerance in sustaining immunological nonresponsiveness to food Ags, our current understanding of why oral tolerance may fail and sensitization may occur, and the knowledge of pathways that may lead to anaphylaxis and food allergy-associated responses are addressed.

Food allergies are adverse immune reactions to food proteins that affect up to 6% of children and 3-4% of adults. A wide range of symptoms can occur depending on whether IgE or non-IgE mediated mechanism are involved. Many factors influence the development of oral tolerance, including route of exposure, genetics, age of the host, and allergen factors. Advances have been made in the understanding of how these factors interact in the pathophysiology of food allergy. Currently, the mainstay of treatment for food allergies is avoidance and ready access to emergency medications. However, with the improved understanding of tolerance and advances in characterization of food allergens, several therapeutic strategies have been developed and are currently being investigated as potential treatments and/or cures for food allergy.

Many food proteins can act as antigens in humans. Cow’s milk proteins are most frequently implicated as a cause of food intolerance during infancy. Soybean protein ranks second as an antigen in the first months of life, particularly in infants with primary cow’s milk intolerance who are placed on a soy formula. From school age on, egg protein intolerance becomes more prevalent.

Food protein intolerance can be immunoglobulin E (IgE)-mediated or non-IgE-mediated. Local production and systemic distribution of specific reaginic IgE plays a significant role in IgE-mediated reactions to food proteins. Several clinical reactions to food proteins have been reported in children and adults. Only a few of these have a clear allergic IgE-mediated pathogenesis. For this reason, the term “food protein intolerance” is usually preferred to “food protein allergy,” in order to include all offending specific reactions to food proteins, no matter the pathogenesis. In children, GI symptoms are generally most common, with a frequency ranging from 50-80%, followed by cutaneous symptoms (20-40%), and respiratory symptoms (4-25%).

Update Immunopathophysiology

The major food allergens are water-soluble glycoproteins (molecular weight [MW], 10,000-60,000) that are resistant to heat, acid, and enzymes.

Studies have demonstrated that food allergens are transported in large quantities across the epithelium by binding to cell surface IgE/CD23, which opens a gate for intact dietary allergens to transcytose across the epithelial cells that protect the antigenic protein from lysosomal degradation in enterocytes.

Some antigens can move through intercellular gaps ; however, the penetration of antigens through the mucosal barrier is not usually associated with clinical symptoms. Under normal circumstances, food antigen exposure via the GI tract results in a local immunoglobulin A (IgA) response and in an activation of suppressor CD8+ lymphocytes that reside in the gut-associated lymphoid tissue (oral tolerance).

In some children who are genetically susceptible, or for other as-of-yet-unknown reasons, oral tolerance does not develop, and different immunologic and inflammatory mechanisms can be elicited. Whether nonimmunologic mechanisms can have a role in the development of specific intolerances to food proteins is still disputed.

Some evidence suggests that reduced microbial exposure during infancy and early childhood result in a slower postnatal maturation of the immune system through a reduction of the number of T regulatory (Treg) cells and a possible delay in the progression to an optimal balance between TH1 and TH2immunity, which is crucial to the clinical expression of allergy and asthma (hygiene hypothesis). Genetic variations in receptors for bacterial products are likely to be related to allergic sensitizations. On the other hand, intestinal infections may increase paracellular permeability, allowing the absorption of food proteins without epithelial processing. As a consequence, infectious exposures can be an important contributory factor in the pathogenesis of food protein allergies.

Many immunologic reactions to food allergens are IgE-mediated and usually target several different epitopes. Certain epitopes are homologous in different foods. Non-IgE mediated food allergies involve T-cell mediated immunity to certain food proteins. and large amounts of inflammatory cytokines such as TNF-α are produced by T cells in an antigen-specific manner. TNF-α increases intestinal permeability, which facilitates the uptake of undigested food antigens.

In both IgE-mediated and non-IgE-mediated food allergies, Th2 cytokines (such as IL-4, IL-5 and IL-13) are produced by T cells in response to specific food antigens. However, the precise mechanisms and pathogenesis of GI allergy remain unclear.

Eosinophilic gastrointestinal diseases (EGIDs) have been classified as a combined IgE-mediated and cell-mediated disease because many patients have detectable food-specific IgE antibodies. However, the roles of IgE antibodies in the pathogenesis of EGID remain unclear.

Morphologic studies have demonstrated the role of GI T lymphocytes (ie, intraepithelial lymphocytes) in the pathogenesis of GI food allergy. The pathogenic role of the eosinophils in food-induced eosinophilic GI diseases has not been defined. Vast evidence describes the occurrence of immunoglobulin G (IgG) food protein antibodies. However, their actual role in the pathogenesis of clinically relevant symptoms is, at best, doubtful.

Recent advances in understanding the mechanisms behind food allergy have been fueled by the desire to develop improved therapies. In considering such mechanisms, thrre are three processes that may be important: oral tolerance, sensitization to food allergens, and anaphylactic reactivity to these food allergens. An emerging concept of “non-responsive tolerance”, where anaphylactic reactivity does not occur or is lost despite evidence for IgE-associated sensitization will be highlighted.

1. Oral Tolerance

Oral tolerance to egg proteins was first described over 100 years ago. This natural phenomenon, where ingested food proteins do not elicit a specific immune response, is also observed in humans, but the necessary mechanisms still remain unclear. Despite gastrointestinal enzymes degrading food and the physical barrier of the intestinal mucosa, immune surveillance of food antigens and establishment of tolerance mechanisms are clearly occurring. Several reviews have addressed possible routes of antigen sampling and presentation , including sampling by dendritic cells (DCs) across the epithelial layer; presentation by M cells or goblet cells to DCs; or soluble antigen directly traversing the epithelium through paracellular or transcellular routes. Key cells seem important for oral tolerance and the maintenance of regulatory (FoxP3+) T cell (Treg) populations. CD11c-CD11b+F4/80+macrophages exhibit an anti-inflammatory gene signature and produce IL-10 . Additionally, two distinct subsets of tolerance-associated CD11c+ cells reside in the intestinal lamina propria, expressing either CX3CR1 or CD103. CX3CR1 KO mice show diminished IL-10 production and Treg populations as well as a lack of oral tolerance in a food allergy model. In contrast, CX3CR1+CD103-cells have been implicated in intestinal inflammation. Most evidence supports the role of CX3CR1-CD103+ DCs in tolerance. These cells exhibit lymph-node homing where they activate naïve T cells and promote a FoxP3+ Treg phenotype, a process requiring both transforming growth factor-beta (TGF-β) and retinoic acid. Retinoic acid imprints the gut-homing receptors CCR9 and α4β7 onto both Tregs and IgA-secreting B cells, an event that also seems to contribute to oral tolerance. CD103+ DCs also utilize indoleamine 2,3-dioxygenase (IDO) for tolerance, and loss of IDO function drives T cells towards a Th1 or Th17 phenotype, limiting Tregs and oral tolerance. Recent findings also show that MUC2, a mucin secreted by intestinal goblet cells, supports the anti-inflammatory potential of these CD103+DC cells . IPEX (immune dysregulation, polyendocrinopathy, enteropathy, X-linked) patients with mutations in the FoxP3 locus (20) develop severe food allergy as well as a plethora of other disorders, including autoimmunity, enteropathy, and atopic dermatitis, indicating the importance of Tregs in tolerance. FoxP3-mutant mice (scurfy) and DEREG mice, in which Tregs can be deleted upon diphtheria toxin treatment, have also been used to demonstrate the importance of Tregs in allergic responses. Expression of CCR9 and α4β7 on Tregs are necessary for tolerance, since these molecules support gut homing. While previous reviews have summarized the effects of antigen concentration in oral tolerance (i.e., low doses drive Tregs, while high doses yield anergy and deletion of T cells), most evidence points towards Treg-associated low-dose tolerance as being critical in food allergy. We previously showed that loss of oral tolerance to peanut was associated with diminished Treg responses but also that high-dose antigen feeding could overcome allergic responses.

2. Sensitization

In food allergy, the immune response is clearly biased towards a Type 2 cytokine–associated phenotype. Why specific food antigens trigger this response remains unclear, although some food antigens possess the potential to stimulate innate immune responses. For example, the peanut allergen Ara h1 binds to CD209 on DCs, while milk sphingomyelin activates Type 2 cytokine responses from iNKT cells. Changes in microbial flora have been associated with allergic sensitization, with several lines of evidence supporting protection by specific bacteria and their products, likely through sustaining intestinal Treg populations (Reviewed by Berin and Sampson ). Mice with decreased commensal bacteria colonies, which includes either germ-free or antibiotic-treated mice, exhibit increased food-allergen sensitivity, high serum IgE, and increased circulating basophils. Interestingly, mice with enhanced signaling through IL-4Rα who display profound allergic sensitization and anaphylaxis to food antigens also exhibit an altered microbiota that can be normalized by Treg transfer. Consequently, the interaction of host immunity and commensal microbiota seems bidirectional, with host immune responses not just responding to bacterial presence but also shaping the bacterial flora towards that associated with pathology.

The critical mechanisms responsible for allergic sensitization are beginning to be elucidated. Generally in allergy, epithelial production of TSLP, IL-25, and IL-33 has become a key area of interest. However, a recent study of these cytokines using a cholera-toxin–driven oral peanut model showed that only IL-33 was required for sensitization. IL-33 can increase mucosal permeability and promote Th2 skewing by DCs. Interestingly, while constitutive IL-33 expression occurs in epithelial cells, increasing evidence supports the potential for inducible expression by several immune cells, including DCs, that is sufficient for subsequent Th2 immunity, as has been shown in helminth infection and for IgG immune complexes. However, the key producer of IL-33 in food allergy remains to be determined.

At the level of antigen presentation, several mechanisms that may participate in tipping the balance from tolerance to sensitization have been described. Binding of OX40 ligand to OX40, TIM4 to TIM1, and jagged to notch on DCs and naïve T cells, respectively, can regulate T cell differentiation from Treg towards Th2, as previously reviewed. Environmental interactions may drive this differentiation; for example, Staphylococcal enterotoxin B (SEB) can break tolerance and promote food allergy, and has been shown mechanistically to induce TIM4 expression on DCs that is necessary for Th2 skewine. Th2-associated responses can also occur if Tregs are deleted, or become dysfunctional, as induced by SEB. In contrast, some innate signals may also protect against sensitization, since TLR9-/-mice have impaired IgE and IgA responses, resulting in reduced anaphylaxis to peanut.

Intestinal penetrance by allergens may also enhance allergic sensitization. On intestinal epithelial cells, IL-4 can induce upregulation of the low-affinity IgE receptor, CD23, which binds antigen-specific IgE and facilitates antigen uptake. This potential mechanism may explain why large or low-solubility antigens traverse the epithelium and elicit systemic responses. Similarly, alterations in tight-junction integrity may allow antigen penetrance. For example, deficiency in the desmosomal intercellular adhesion molecule desmoglein-1 has been shown to elicit profound allergic responses (46), while its expression is reduced in tissues of patients with Eosinophilic Esophagitis. Recent interest has also focused on the skin as a potential route for sensitization, since food allergy often associates with eczema in patients. Barrier integrity may also be important here, since filaggrin-deficient mice, which exhibit weak epithelial barrier function, become sensitized to proteins on the skin, and epicutaneous sensitization is sufficient to promote anaphylaxis upon oral challenge. While very few studies have defined specific genes associated with food allergy, it is interesting to note that mutations in desmoglein-1 and filaggrin as well as in TSLP have been shown to be associated with food allergy or Eosinophilic Esophagitis in human cohorts, since these molecules all regulate skin homeostasis. However, it is unclear if these associations relate to food allergy or eczema, since these diseases are often coincident in children, and the number of genes associated with food allergy alone remains relatively limited.

3. Reactivity

The mechanisms of anaphylaxis––the hallmark of food-allergy reactivity––are generally biphasic: an acute reaction occurs immediately after allergen exposure, followed by a late-phase reaction several hours later. Symptoms occurring during the acute reaction are due to release of pre-formed mediators, while the late-phase response involves influx of inflammatory cells. Clinically, heterogeneity in responses is observed, with some patients experiencing either the acute or late-phase reaction, and others experiencing both the acute and late-phase reactions. In addition to clinical heterogeneity, anaphylactic responses can be elicited through multiple mechanisms.

Antibodies in Anaphylaxis

First shown in 1997 by Miyajima and colleagues, both IgE and IgG can play a role in anaphylaxis in the mouse. IgE functions via its high-affinity receptor, FcεRI, which is highly expressed on mast cells and basophils. FcεRI-/-mice do not respond in a passive IgE-mediated systemic anaphylaxis model (56) and have reduced responses in models of allergic diarrhea and food allergy. IgG has several receptors: the high-affinity FcγRI and FcγRIV, and the low-affinity FcγRIIB and FcγRIII. These receptors are all expressed on several cell types involved in anaphylaxis, including mast cells, basophils, neutrophils, and macrophages. Using a model of systemic anaphylaxis, Strait et al. showed that inhibition of FcγRII/III abolished temperature drops associated with shock in IgG-, but not IgE-, mediated anaphylaxis. Similarly, Jönsson et al. used knockout mice to show that FcγRIV is necessary for systemic anaphylaxis. While these pathways have been differentially defined using these passive models, both antibodies appear to participate in active food allergy: Arias et al. showed that IgE-/- and IgG1-/- mice were only partially protected from peanut-induced anaphylaxis, but blockade of IgG1in IgE-/- mice completely abolished the response; similarly, FcRγ-/- mice, which lack the common chain for both the IgE and IgG receptors, were protected. Importantly, recent studies using humanized mice have supported the potential anaphylactic functions of IgG via human receptors.

Mediators of Anaphylaxis

Histamine, platelet-activating factor (PAF), and 5-hydroxytryptamine (5-HT, serotonin) are all sufficient to induce early-phase anaphylaxis. Several groups have also looked at the necessity for each of these mediators in anaphylaxis, and there appears to be heterogeneity here also. Histamine, produced from both mast cells and basophils, is a well-established mediator necessary for anaphylaxis. In IgE-mediated systemic anaphylaxis, histamine synthesis as well as histamine H1 and H2 receptors are necessary for responses, and blockade of these receptors is therapeutically beneficial in patients with acute allergic reactions. Additionally, PAF and 5-HT have been shown to contribute to anaphylaxis. Several inflammatory cells make PAF, including macrophages/monocytes, mast cells, basophils, neutrophils, and platelets. While associated with platelet activation, PAF also influences vascular permeability, leukocyte recruitment, and leukocyte activation. Studies using models of allergic diarrhea, food allergy, or systemic anaphylaxis models have shown that responses may be due to either PAF and histamine, or PAF and 5-HT.

While other mast cell– and basophil-derived mediators have been implicated in food allergy, their role is less defined. These include other pre-formed mediators (e.g., tryptase, chymase, and heparin), lipid mediators (e.g., PGD2, LTC4, LTD4, and LTE4), and several cytokines. IgE activation of mast cells has the potential to generate several cytokines that have been shown to direct late-phase inflammation, including release of preformed TNF and synthesis of IL-33. TNF has been shown to be necessary for late-phase recruitment of neutrophils as well as for a late-phase increase of PAF in the serum. The IL-33 receptor, ST2, is necessary for IgE-triggered tissue inflammation. IL-33 does not directly cause mast cell degranulation, but promotes expression of several cytokines and chemokines, including IL-6 and IL-13, from mast cells, as well as eosinophils. Similarly, IL-9 can both stimulate and be produced by mast cells. IL-9 has been shown to be critical for the initiation and severity of food-associated anaphylaxis by promoting intestinal mastocytosis.

Pathways of Anaphylaxis and Food Allergy

Largely from murine studies of passive sensitization models, mast cells, basophils, macrophages, and neutrophils have been shown to contribute to anaphylactic shock responses. Four distinct pathways of response seem to be possible—a “classic” pathway involving IgE, FcεRI, mast cells, and histamine; an “alternative” pathway mediated by IgG1, FcγRIII, macrophages, and PAF; an IgG-basophil-PAF pathway; and an IgG-neutrophil-PAF pathway via FcγRIV activation.

In active sensitization models, IgE, FcεRI, and mast cells are responsible for inducing allergic diarrhea. While both allergen-specific IgE and IgG antibodies are increased by sensitization, only FcεRI, and not FcγRII/III, is required. Interestingly, the diarrhea response seems to be mediated by a combination of PAF and 5-HT. In contrast, the mast cell responses that are key in anaphylactic food allergy models (with contributions from macrophages and basophils) occur via IgE- and IgG-dependent mechanisms requiring both histamine and PAF. Recently, the necessity for basophils in peanut anaphylaxis was also defined. Interestingly, the pathways to systemic anaphylaxis models may relate to the antigen dose required to trigger each mechanism, since small doses activate the classical pathway and large doses activate the alternative pathway.

4. Non-responsive Tolerance

Clinical studies have shown that the incidence of food allergen–specific IgE is ten times greater than the incidence of food allergy, suggesting an additional level of tolerance regulation above that of simply preventing immunological priming towards Th2 and IgE. Furthermore, in patients with Stat3 mutations leading to hyper-IgE syndrome, anaphylactic reactivity to food allergens is actually diminished. Recent work has shown that Tregs can suppress IgE-primed mast cell degranulation to antigen exposure via OX40/OX40 ligand interactions. In food allergy, we demonstrated that Treg transfer could suppress anaphylaxis and restore intestinal Th17 homeostasis by enhancing mast cell–derived IL-6. Interestingly, this cytokine-mediated process was OX40-independent and instead mediated via TGF-β. Additionally, Tregs can downregulate FcεRI on mast cells in vitro. This emerging form of active tolerance occurring despite the presence of an antigen-specific IgE–primed immune system seems distinct from antigen desensitization, which is associated with internalization of FcεRI and IgE and altered Syk activation

IgE and cell-mediated process, prick skin testing and serum specific IgE levels may not identify all the allergic triggers. Atopy patch testing has been investigated as an additional diagnostic tool to identify foods that cause delayed symptoms.

Mechanism of Food Allergy

Normally, there is a delicate balance of the gastrointestinal mucosal immune system distinguishing between potentially harmful pathogens, beneficial commensal bacteria, and harmless food allergens which do not induce active immune responses. The mechanisms by which ingested proteins are able to interact with unique populations of antigen presenting cells leading to suppression of cellular and humoral immune responses has been termed oral tolerance. This has been demonstrated in a murine model in which subcutaneous antigen exposure resulted in cell-mediated and humoral responses to the antigen in vitro, but mice that were first orally exposed to the antigen then immunized subcutaneously had decreased immune responses in vitro.27 Transfer of T cells from the orally fed mice to naïve mice resulted in decreased immune responses as well. Different mechanisms of tolerance can occur depending on the dose of allergen exposure. Studies suggest that “high dose” tolerance is due to deletion of effector T cells, whereas “low dose” tolerance involves activation of regulatory T cells. Loss of oral tolerance can occur or may be bypassed by antigen presentation via alternative routes, such as through cutaneous exposures or via the respiratory tract. Using a murine model, epicutaneous or epidermal exposure to peanut was demonstrated to induce Th2 immune responses and promoted allergic sensitization. In addition, higher rates of peanut allergy have been found in children with atopic dermatitis who used topical creams containing peanut oil (OR 6.8). Respiratory exposures are seen in pollen-food syndrome (PFS), an IgE-mediated allergy that is due to cross-reacting proteins in pollens (the initial sensitizing allergen) and foods, which results in oropharyngeal symptoms to raw fruits and vegetables.

Breakdown of oral tolerance can also occur as a result of defective regulatory T cells. The disorder of immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is due to a mutation in the FOXP3 gene, a transcription factor on CD4+CD25+ regulatory T cells that has been implicated in blocking Th1 and Th2 responses. Atopic dermatitis and food allergies are known manifestations of this disorder.32 The importance of T regulatory cells in tolerance was also demonstrated in a study of non-IgE milk allergy. The development of tolerance to milk was associated with higher numbers of circulating CD4+CD25+ regulatory T cells.

Host factors

Several host factors can influence the development of food allergies. Different mouse strains are not equally susceptible to food allergies, suggesting that genetic predisposition is important. Furthermore, the age of exposure to food allergens can determine whether tolerance or allergy develops. In a murine model, sensitization occurred when mice were orally fed ovalbumin in the first week of life, however, tolerance was induced when the mice were orally exposed to ovalbumin at 2-3 weeks of age. In humans, epidemiologic studies show a higher rate of food allergies in young children as compared to adults,1suggesting that gut maturity may be a factor in the development of food allergies. On the other hand, population studies suggest that early introduction may be beneficial in some cases. In Israel, where infants are fed peanut proteins starting at an early age, there is a lower incidence of peanut allergy as compared to the UK where peanut is not introduced to children until a much later age. The Learning Early About Peanut Allergies (LEAP) study is currently exploring the role of timing of peanut allergen exposure in the development of peanut allergy.

Several studies suggest that disruption of normal gut barrier functions, such as gastric pH and commensal bacteria, can increase the risk of food allergies. Gastric digestion normally serves to breakdown food proteins, and in many cases destroys immunogenic epitopes in the process. The role of gastric acidity was investigated by Untersmayr et al. using a murine model. Mice fed caviar extract in combination with antacids had elevated specific IgE and demonstrated immediate skin reactivity to the protein after immunization. However, mice which were not fed antacids did not demonstrate these immunologic responses, suggesting that use of antacid medications increased the risk of food allergen sensitization.38 In a human study of 152 patients on antacid treatment for dyspepsia, increased food allergen sensitization was seen in 25% after 3 months. Gastric enzymes can affect allergenicity of food proteins. Specifically, the allergenicity of ovomucoid has been demonstrated to be reduced after gastric digestion. Additionally, commensal bacterial serve an important role. Mice raised in a germ-free environment do not develop normal tolerance,41 and mice treated with antibiotics or those lacking in toll like receptor 4 (TLR4) are more easily sensitized to peanut than wild-type control mice.

Additional host factors can modulate the clinical response of food allergy. For example, asthma has been shown to be a risk factor for more severe anaphylaxis. In a study of fatal food allergic reactions, the majority of victims had underlying asthma.11 Host factors such as exercise, use of medication (alcohol, aspirin, beta-blockers, angiotensin converting enzyme inhibitors, monoamine oxidase inhibitors, tricyclic antidepressants), and concurrent infection may increase the severity of anaphylactic reactions or diminish the efficacy of epinephrine. Recently, low serum platelet-activating factor acetylhydrolase (PAF-AH) activity has been found to be a risk factor for more severe food-induced anaphylaxis.

Food allergen factors

Food allergies can produce an array of clinical symptoms. The presence of specific IgE to sequential or conformational epitopes can distinguish between different phenotypes of milk and egg allergy. Several studies show that binding of conformational epitopes is associated with transient allergy to milk and egg whereas binding of sequential epitopes in these proteins is a marker for persistent allergy. Recent studies demonstrate that the majority of milk and egg allergic individuals can tolerate extensively heated or baked forms of these foods, indicating that these individuals identify conformational epitopes that are disrupted by heating. Furthermore, studies show that different patterns of epitope recognition or epitope diversity may correlate with clinical manifestations of allergic reactions to peanut and milk.

Although heating appears to render many proteins less allergenic, heating does not have the same effect on all food proteins. Roasting peanuts involves very high temperatures, and this causes a Maillard reaction leading to increased stability and allergenicity of peanut allergens. This finding may explain the differences in prevalence of peanut allergy in the U.S. where peanuts are primarily consumed in the roasted form and China where boiled or fried peanuts predominate. Additional properties of peanut make it a highly allergenic protein. Glycosylated Ara h 1, a major peanut allergen, has been shown to act as a Th2 adjuvant by activating dendritic cells to drive Th2 cell maturation.In contrast, deglycoslyated Ara h 1 did not activate dendritic cells. Recently, peanut proteins were shown to have the ability to induce production of complement (C3a) leading to increased platelet-activating factor and histamine production by macrophages, basophils, and mast cells.

References

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Update References and Bibliography Of Food Allergy

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Food allergies are immunologically mediated adverse reactions to foods. Any food protein can trigger an allergic response, and allergic reactions to a large number of foods have been documented; however, only a small group of foods account for most of these reactions. Eggs, milk, peanuts, soy, fish, shellfish, tree nuts, and wheat are the foods most often implicated.

The only proven medication therapy against a food allergy is strict elimination of the offending food allergen from the diet and avoidance of any contact with the food by ingestion, skin contact, inhalation, or injection.

In 2010, Guidelines for the Diagnosis and Management of Food Allergy in the United States were published. These provide evidenced-based, expert panel recommendations for the diagnosis and management of food allergies. The guidelines do not cover issues for schools, which are of interest to pediatricians, but a 2010 Clinical Report reviews this topic area.

Injectable epinephrine is the drug of choice for the initial management of a food-induced anaphylactic reaction. Ensure that the patient has self-injectable epinephrine readily available at all times. Advanced medical therapy of food allergen–induced anaphylaxis may include antihistamines, bronchodilators, histamine 2 (H2) blockers, corticosteroids, and administration of intravenous fluids, glucagon, and oxygen. In severe anaphylaxis, ventilatory and circulatory support may be neede

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Odze RD, Wershil BK, Leichtner AM, Antonioli DA. Allergic colitis in infants. J Pediatr. 1995 Feb. 126(2):163-70. [Medline].

James JM. Respiratory manifestations of food allergy. Pediatrics. 2003 Jun. 111(6 Pt 3):1625-30. [Medline].

James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. 1996 Feb. 153(2):597-603. [Medline].

Weber RW. Food additives and allergy. Ann Allergy. 1993 Mar. 70(3):183-90. [Medline].

Chehade M, Mayer L. Oral tolerance and its relation to food hypersensitivities. J Allergy Clin Immunol. 2005 Jan. 115(1):3-12; quiz 13. [Medline].

Vickery BP, Scurlock AM, Jones SM, Burks AW. Mechanisms of immune tolerance relevant to food allergy. J Allergy Clin Immunol. 2011 Mar. 127(3):576-84.[Medline].

Lack G. Update on risk factors for food allergy. J Allergy Clin Immunol. 2012 May. 129 (5):1187-97. [Medline].

Berin MC. Immunopathophysiology of food protein-induced enterocolitis syndrome. J Allergy Clin Immunol. 2015 May. 135 (5):1108-13. [Medline].

Abernathy-Carver KJ, Sampson HA, Picker LJ, Leung DY. Milk-induced eczema is associated with the expansion of T cells expressing cutaneous lymphocyte antigen.J Clin Invest. 1995 Feb. 95(2):913-8.[Medline]. [Full Text].

Commins SP, James HR, Stevens W, Pochan SL, Land MH, King C, et al. Delayed clinical and ex vivo response to mammalian meat in patients with IgE to galactose-alpha-1,3-galactose. J Allergy Clin Immunol. 2014 Jul. 134 (1):108-15. [Medline].

Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. 2001 Jan. 107(1):191-3. [Medline].

Sloan AE, Powers ME. A perspective on popular perceptions of adverse reactions to foods. J Allergy Clin Immunol. 1986 Jul. 78(1 Pt 2):127-33. [Medline].

Altman DR, Chiaramonte LT. Public perception of food allergy. J Allergy Clin Immunol. 1996 Jun. 97(6):1247-51.[Medline].

Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: a meta-analysis.J Allergy Clin Immunol. 2007 Sep. 120(3):638-46. [Medline].

Zuidmeer L, Goldhahn K, Rona RJ, Gislason D, Madsen C, Summers C, et al. The prevalence of plant food allergies: a systematic review. J Allergy Clin Immunol. 2008 May. 121(5):1210-1218.e4. [Medline].

Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study. J Allergy Clin Immunol. 2003 Dec. 112(6):1203-7.[Medline].

Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol. 2010 Feb. 125(2 Suppl 2):S116-25.

Sicherer SH. Epidemiology of food allergy.J Allergy Clin Immunol. 2011 Mar. 127(3):594-602. [Medline].

Grundy J, Matthews S, Bateman B, Dean T, Arshad SH. Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts. J Allergy Clin Immunol. 2002 Nov. 110(5):784-9. [Medline].

Kagan RS, Joseph L, Dufresne C, Gray-Donald K, Turnbull E, Pierre YS, et al. Prevalence of peanut allergy in primary-school children in Montreal, Canada. J Allergy Clin Immunol. 2003 Dec. 112(6):1223-8. [Medline].

Hourihane JO, Aiken R, Briggs R, Gudgeon LA, Grimshaw KE, DunnGalvin A, et al. The impact of government advice to pregnant mothers regarding peanut avoidance on the prevalence of peanut allergy in United Kingdom children at school entry. J Allergy Clin Immunol. 2007 May. 119(5):1197-202.[Medline].

Kristen D. Jackson, M.P.H.; LaJeana D. Howie, M.P.H., C.H.E.S.; Lara J. Akinbami, M.D. Trends in Allergic Conditions Among Children: United States, 1997-2011. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Available athttp://www.cdc.gov/nchs/data/databriefs/db121.pdf. 2013 May;

Wood RA. The natural history of food allergy. Pediatrics. 2003 Jun. 111(6 Pt 3):1631-7. [Medline].

Skripak JM, Matsui EC, Mudd K, Wood RA. The natural history of IgE-mediated cow’s milk allergy. J Allergy Clin Immunol. 2007 Nov. 120(5):1172-7. [Medline].

Savage JH, Matsui EC, Skripak JM, Wood RA. The natural history of egg allergy. J Allergy Clin Immunol. 2007 Dec. 120(6):1413-7. [Medline].

Savage JH, Kaeding AJ, Matsui EC, Wood RA. The natural history of soy allergy. J Allergy Clin Immunol. 2010 Mar. 125(3):683-6. [Medline].

Mehr S, Kakakios A, Frith K, Kemp AS. Food protein-induced enterocolitis syndrome: 16-year experience. Pediatrics. 2009 Mar. 123(3):e459-64. [Medline].

Assa’ad AH, Putnam PE, Collins MH, Akers RM, Jameson SC, Kirby CL, et al. Pediatric patients with eosinophilic esophagitis: an 8-year follow-up. J Allergy Clin Immunol. 2007 Mar. 119(3):731-8. [Medline].

Horan RF, Sheffer AL. Food-dependent exercise-induced anaphylaxis. Immunol Allergy Clin North Am. 1991. 757.

Nowak-Wegrzyn A, Assa’ad AH, Bahna SL, Bock SA, Sicherer SH, Teuber SS, et al. Work Group report: oral food challenge testing. J Allergy Clin Immunol. 2009 Jun. 123 (6 Suppl):S365-83. [Medline].

Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol. 2001 May. 107(5):891-6. [Medline].

Maloney JM, Rudengren M, Ahlstedt S, Bock SA, Sampson HA. The use of serum-specific IgE measurements for the diagnosis of peanut, tree nut, and seed allergy. J Allergy Clin Immunol. 2008 Jul. 122(1):145-51. [Medline].

Sampson HA, Ho DG. Relationship between food-specific IgE concentrations and the risk of positive food challenges in children and adolescents. J Allergy Clin Immunol. 1997 Oct. 100(4):444-51. [Medline].

Wang J, Godbold JH, Sampson HA. Correlation of serum allergy (IgE) tests performed by different assay systems. J Allergy Clin Immunol. 2008 May. 121(5):1219-24. [Medline].

Sicherer SH, Wood RA. Advances in diagnosing peanut allergy. J Allergy Clin Immunol Pract. 2013 Jan. 1 (1):1-13; quiz 14. [Medline].

Klemans RJ, van Os-Medendorp H, Blankestijn M, Bruijnzeel-Koomen CA, Knol EF, Knulst AC. Diagnostic accuracy of specific IgE to components in diagnosing peanut allergy: a systematic review. Clin Exp Allergy. 2015 Apr. 45 (4):720-30.[Medline].

Lin J, Bruni FM, Fu Z, Maloney J, Bardina L, Boner AL, et al. A bioinformatics approach to identify patients with symptomatic peanut allergy using peptide microarray immunoassay. J Allergy Clin Immunol. 2012 May. 129 (5):1321-1328.e5. [Medline].

Eigenmann PA, Sampson HA. Interpreting skin prick tests in the evaluation of food allergy in children. Pediatr Allergy Immunol. 1998 Nov. 9(4):186-91. [Medline].

Bock SA, Lee WY, Remigio L, et al. Appraisal of skin tests with food extracts for diagnosis of food hypersensitivity. Clin Allergy. 1978 Nov. 8(6):559-64. [Medline].

Knight AK, Shreffler WG, Sampson HA, Sicherer SH, Noone S, Mofidi S, et al. Skin prick test to egg white provides additional diagnostic utility to serum egg white-specific IgE antibody concentration in children. J Allergy Clin Immunol. 2006 Apr. 117(4):842-7. [Medline].

Roberts G, Lack G. Diagnosing peanut allergy with skin prick and specific IgE testing. J Allergy Clin Immunol. 2005 Jun. 115(6):1291-6. [Medline].

Nowak-Wegrzyn A, Assa’ad AH, Bahna SL, Bock SA, Sicherer SH, Teuber SS. Work Group report: oral food challenge testing. J Allergy Clin Immunol. 2009 Jun. 123(6 Suppl):S365-83. [Medline].

Bock SA, Sampson HA, Atkins FM, et al. Double-blind, placebo-controlled food challenge (DBPCFC) as an office procedure: a manual. J Allergy Clin Immunol. 1988 Dec. 82(6):986-97.[Medline].

Spergel JM, Brown-Whitehorn T, Beausoleil JL, Shuker M, Liacouras CA. Predictive values for skin prick test and atopy patch test for eosinophilic esophagitis. J Allergy Clin Immunol. 2007 Feb. 119(2):509-11.[Medline].

Fogg MI, Brown-Whitehorn TA, Pawlowski NA, Spergel JM. Atopy patch test for the diagnosis of food protein-induced enterocolitis syndrome. Pediatr Allergy Immunol. 2006 Aug. 17(5):351-5. [Medline].

Mehl A, Rolinck-Werninghaus C, Staden U, Verstege A, Wahn U, Beyer K, et al. The atopy patch test in the diagnostic workup of suspected food-related symptoms in children. J Allergy Clin Immunol. 2006 Oct. 118(4):923-9. [Medline].

Boyce JA, Assa’ad A, Burks AW, Jones SM, Sampson HA, Wood RA, et al. Guidelines for the Diagnosis and Management of Food Allergy in the United States: Summary of the NIAID-Sponsored Expert Panel Report. J Allergy Clin Immunol. 2010 Dec. 126(6):1105-18. [Medline].

Sicherer SH, Mahr T. Management of Food Allergy in the School Setting. Pediatrics. 2010 Dec. 126(6):1232-1239. [Medline].

Sicherer SH, Sampson HA. Food Allergy: Recent Advances in Pathophysiology and Treatment. Annu Rev Med. 2008 Aug 19.[Medline].

Nowak-Wegrzyn A, Sampson HA. Future therapies for food allergies. J Allergy Clin Immunol. 2011 Mar. 127(3):558-73.[Medline].

Lieberman P, Nicklas RA, Oppenheimer J, Kemp SF, Lang DM, et al. The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol. 2010 Sep. 126 (3):477-80.e1-42.[Medline].

Lever R, MacDonald C, Waugh P, Aitchison T. Randomised controlled trial of advice on an egg exclusion diet in young children with atopic eczema and sensitivity to eggs.Pediatr Allergy Immunol. 1998 Feb. 9(1):13-9. [Medline].

Bock SA. Respiratory reactions induced by food challenges in children with pulmonary disease. Pediatr Allergy Immunol. 1992. 3:82.

Roberts G, Patel N, Levi-Schaffer F, et al. Food allergy as a risk factor for life-threatening asthma in childhood: a case-controlled study. J Allergy Clin Immunol. 2003 Jul. 112(1):168-74.

Bock SA, Atkins FM. Patterns of food hypersensitivity during sixteen years of double-blind, placebo-controlled food challenges. J Pediatr. 1990 Oct. 117(4):561-7. [Medline].

Bock SA. Prospective appraisal of complaints of adverse reactions to foods in children during the first 3 years of life.Pediatrics. 1987 May. 79(5):683-8.[Medline].

Gupta RS, Springston EE, Warrier MR, et al. The prevalence, severity, and distribution of childhood food allergy in the United States.Pediatrics. 2011 Jul. 128(1):e9-e17.[Medline].

Pastorello EA, Stocchi L, Pravettoni V, et al. Role of the elimination diet in adults with food allergy. J Allergy Clin Immunol. 1989 Oct. 84(4 Pt 1):475-83. [Medline].

Lemon-Mule H, Sampson HA, Sicherer SH, Shreffler WG, Noone S, Nowak-Wegrzyn A. Immunologic changes in children with egg allergy ingesting extensively heated egg. J Allergy Clin Immunol. 2008 Nov. 122(5):977-983.e1. [Medline].

Greer FR, Sicherer SH, Burks AW. Effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, timing of introduction of complementary foods, and hydrolyzed formulas. Pediatrics. 2008 Jan. 121(1):183-91. [Medline].

Allen KJ, Koplin JJ, Ponsonby AL, Gurrin LC, Wake M, Vuillermin P, et al. Vitamin D insufficiency is associated with challenge-proven food allergy in infants. J Allergy Clin Immunol. 2013 Apr. 131(4):1109-1116.e6.[Medline].

James JM, Burks AW, Roberson PK, Sampson HA. Safe administration of the measles vaccine to children allergic to eggs. N Engl J Med. 1995 May 11. 332(19):1262-6. [Medline].

Centers for Disease Control and Prevention. Prevention and control of influenza with vaccines: recommendations of the Advisory Committee on Immunization Practices (ACIP), 2011.MMWR Morb Mortal Wkly Rep. 2011 Aug 26. 60(33):1128-32. [Medline].

National Institute of Allergy and Infectious Diseases. Updated recommendations on influenza vaccine and people with egg allergy. Available athttp://www.niaid.nih.gov/topics/vaccines/research/Pages/eggAllergy.aspx. Accessed: September 20, 2011.

Varshney P, Jones SM, Scurlock AM, et al. A randomized controlled study of peanut oral immunotherapy: Clinical desensitization and modulation of the allergic response. J Allergy Clin Immunol. 2011 Mar. 127(3):654-60. [Medline].

Kim EH, Bird JA, Kulis M, Laubach S, Pons L, Shreffler W. Sublingual immunotherapy for peanut allergy: Clinical and immunologic evidence of desensitization. J Allergy Clin Immunol. 2011 Mar. 127(3):640-646.e1. [Medline].

Thyagarajan A, Varshney P, Jones SM, et al. Peanut oral immunotherapy is not ready for clinical use. J Allergy Clin Immunol. 2010 Jul. 126(1):31-2. [Medline]. [Full Text].

Fisher HR, du Toit G, Lack G. Specific oral tolerance induction in food allergic children: is oral desensitisation more effective than allergen avoidance?: a meta-analysis of published RCTs. Arch Dis Child. 2011 Mar. 96(3):259-64. [Medline].

Joint Task Force on Practice Parameters; American Academy of Allergy, Asthma and Immunology; American College of Allergy, Asthma and Immunology; Joint Council of Allergy, Asthma and Immunology. The diagnosis and management of anaphylaxis: an updated practice parameter. J Allergy Clin Immunol. 2005 Mar. 115(3 Suppl 2):S483-523. [Medline].

Begin P, Dominguez T, Wilson SP, et al. Phase 1 results of safety and tolerability in a rush oral immunotherapy protocol to multiple foods using Omalizumab. Allergy Asthma Clin Immunol. 2014 Feb 20. 10(1):7.[Medline]. [Full Text].

Begin P, Winterroth LC, Dominguez T, et al. Safety and feasibility of oral immunotherapy to multiple allergens for food allergy. Allergy Asthma Clin Immunol. 2014 Jan 15. 10(1):1. [Medline]. [Full Text].

Food-allergic kids need current Epi script.Medscape Medical News. November 18, 2013. [Full Text].

Hackethal V. Omalizumab Aids Desensitization to Several Food Allergies.Medscape Medical News. Feb 28 2014. [Full Text].

Johnson K. Antibiotic exposure in infancy linked to food allergies. Medscape Medical News. February 28, 2013. Available athttp://www.medscape.com/viewarticle/780023. Accessed: March 4, 2013.

References

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Sicherer SH. Clinical implications of cross-reactive food allergens. J Allergy Clin Immunol. 2001 Dec. 108(6):881-90.[Medline].

Fleischer DM, Burks AW, Vickery BP, Scurlock AM, Wood RA, Jones SM, et al. Sublingual immunotherapy for peanut allergy: a randomized, double-blind, placebo-controlled multicenter trial. J Allergy Clin Immunol. 2013 Jan. 131(1):119-27.e1-7. [Medline]. [Full Text].

Jones SM, Burks AW, Dupont C. State of the art on food allergen immunotherapy: oral, sublingual, and epicutaneous. J Allergy Clin Immunol. 2014 Feb. 133 (2):318-23.[Medline]. [Full Text].

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Bock SA, Munoz-Furlong A, Sampson HA. Further fatalities caused by anaphylactic reactions to food, 2001-2006. J Allergy Clin Immunol. 2007 Apr. 119(4):1016-8.[Medline].

Sicherer SH, Sampson HA. Food hypersensitivity and atopic dermatitis: pathophysiology, epidemiology, diagnosis, and management. J Allergy Clin Immunol. 1999 Sep. 104(3 Pt 2):S114-22. [Medline].

Burks AW, James JM, Hiegel A, et al. Atopic dermatitis and food hypersensitivity reactions. J Pediatr. 1998 Jan. 132(1):132-6. [Medline].

Eigenmann PA, Sicherer SH, Borkowski TA, Cohen BA, Sampson HA. Prevalence of IgE-mediated food allergy among children with atopic dermatitis. Pediatrics. 1998 Mar. 101(3):E8. [Medline].

Sampson HA, McCaskill CC. Food hypersensitivity and atopic dermatitis: evaluation of 113 patients. J Pediatr. 1985 Nov. 107(5):669-75. [Medline].

Sampson HA, Scanlon SM. Natural history of food hypersensitivity in children with atopic dermatitis. J Pediatr. 1989 Jul. 115(1):23-7. [Medline].

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Flohr C, Perkin M, Logan K, Marrs T, Radulovic S, Campbell LE, et al. Atopic Dermatitis and Disease Severity are the Main Risk Factors for Food Sensitization in Exclusively Breastfed Infants. J Invest Dermatol. 2013 Jul 18. [Medline].

Webber CM, England RW. Oral allergy syndrome: a clinical, diagnostic, and therapeutic challenge. Ann Allergy Asthma Immunol. 2010 Feb. 104 (2):101-8; quiz 109-10, 117. [Medline].

Furuta GT, Liacouras CA, Collins MH, Gupta SK, Justinich C, Putnam PE, et al. Eosinophilic esophagitis in children and adults: a systematic review and consensus recommendations for diagnosis and treatment. Gastroenterology. 2007 Oct. 133(4):1342-63. [Medline].

Liacouras CA, Furuta GT, Hirano I, et al. Eosinophilic esophagitis: Updated consensus recommendations for children and adults. J Allergy Clin Immunol. 2011 Jul. 128(1):3-20.e6. [Medline].

Powell GK. Food protein-induced enterocolitis of infancy: differential diagnosis and management. Compr Ther. 1986 Feb. 12(2):28-37. [Medline].

Järvinen KM, Nowak-Węgrzyn A. Food protein-induced enterocolitis syndrome (FPIES): current management strategies and review of the literature. J Allergy Clin Immunol Pract. 2013 Jul-Aug. 1 (4):317-22.[Medline].

Odze RD, Wershil BK, Leichtner AM, Antonioli DA. Allergic colitis in infants. J Pediatr. 1995 Feb. 126(2):163-70. [Medline].

James JM. Respiratory manifestations of food allergy. Pediatrics. 2003 Jun. 111(6 Pt 3):1625-30. [Medline].

James JM, Eigenmann PA, Eggleston PA, Sampson HA. Airway reactivity changes in asthmatic patients undergoing blinded food challenges. Am J Respir Crit Care Med. 1996 Feb. 153(2):597-603. [Medline].

Weber RW. Food additives and allergy. Ann Allergy. 1993 Mar. 70(3):183-90. [Medline].

Chehade M, Mayer L. Oral tolerance and its relation to food hypersensitivities. J Allergy Clin Immunol. 2005 Jan. 115(1):3-12; quiz 13. [Medline].

Vickery BP, Scurlock AM, Jones SM, Burks AW. Mechanisms of immune tolerance relevant to food allergy. J Allergy Clin Immunol. 2011 Mar. 127(3):576-84.[Medline].

Lack G. Update on risk factors for food allergy. J Allergy Clin Immunol. 2012 May. 129 (5):1187-97. [Medline].

Berin MC. Immunopathophysiology of food protein-induced enterocolitis syndrome. J Allergy Clin Immunol. 2015 May. 135 (5):1108-13. [Medline].

Abernathy-Carver KJ, Sampson HA, Picker LJ, Leung DY. Milk-induced eczema is associated with the expansion of T cells expressing cutaneous lymphocyte antigen.J Clin Invest. 1995 Feb. 95(2):913-8.[Medline]. [Full Text].

Commins SP, James HR, Stevens W, Pochan SL, Land MH, King C, et al. Delayed clinical and ex vivo response to mammalian meat in patients with IgE to galactose-alpha-1,3-galactose. J Allergy Clin Immunol. 2014 Jul. 134 (1):108-15. [Medline].

Bock SA, Munoz-Furlong A, Sampson HA. Fatalities due to anaphylactic reactions to foods. J Allergy Clin Immunol. 2001 Jan. 107(1):191-3. [Medline].

Sloan AE, Powers ME. A perspective on popular perceptions of adverse reactions to foods. J Allergy Clin Immunol. 1986 Jul. 78(1 Pt 2):127-33. [Medline].

Altman DR, Chiaramonte LT. Public perception of food allergy. J Allergy Clin Immunol. 1996 Jun. 97(6):1247-51.[Medline].

Rona RJ, Keil T, Summers C, Gislason D, Zuidmeer L, Sodergren E, et al. The prevalence of food allergy: a meta-analysis.J Allergy Clin Immunol. 2007 Sep. 120(3):638-46. [Medline].

Zuidmeer L, Goldhahn K, Rona RJ, Gislason D, Madsen C, Summers C, et al. The prevalence of plant food allergies: a systematic review. J Allergy Clin Immunol. 2008 May. 121(5):1210-1218.e4. [Medline].

Sicherer SH, Munoz-Furlong A, Sampson HA. Prevalence of peanut and tree nut allergy in the United States determined by means of a random digit dial telephone survey: a 5-year follow-up study. J Allergy Clin Immunol. 2003 Dec. 112(6):1203-7.[Medline].

Sicherer SH, Sampson HA. Food allergy. J Allergy Clin Immunol. 2010 Feb. 125(2 Suppl 2):S116-25.

Sicherer SH. Epidemiology of food allergy.J Allergy Clin Immunol. 2011 Mar. 127(3):594-602. [Medline].

Grundy J, Matthews S, Bateman B, Dean T, Arshad SH. Rising prevalence of allergy to peanut in children: Data from 2 sequential cohorts. J Allergy Clin Immunol. 2002 Nov. 110(5):784-9. [Medline].

Kagan RS, Joseph L, Dufresne C, Gray-Donald K, Turnbull E, Pierre YS, et al. Prevalence of peanut allergy in primary-school children in Montreal, Canada. J Allergy Clin Immunol. 2003 Dec. 112(6):1223-8. [Medline].

Hourihane JO, Aiken R, Briggs R, Gudgeon LA, Grimshaw KE, DunnGalvin A, et al. The impact of government advice to pregnant mothers regarding peanut avoidance on the prevalence of peanut allergy in United Kingdom children at school entry. J Allergy Clin Immunol. 2007 May. 119(5):1197-202.[Medline].

Kristen D. Jackson, M.P.H.; LaJeana D. Howie, M.P.H., C.H.E.S.; Lara J. Akinbami, M.D. Trends in Allergic Conditions Among Children: United States, 1997-2011. U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES. Available athttp://www.cdc.gov/nchs/data/databriefs/db121.pdf. 2013 May;

Wood RA. The natural history of food allergy. Pediatrics. 2003 Jun. 111(6 Pt 3):1631-7. [Medline].

Skripak JM, Matsui EC, Mudd K, Wood RA. The natural history of IgE-mediated cow’s milk allergy. J Allergy Clin Immunol. 2007 Nov. 120(5):1172-7. [Medline].

Savage JH, Matsui EC, Skripak JM, Wood RA. The natural history of egg allergy. J Allergy Clin Immunol. 2007 Dec. 120(6):1413-7. [Medline].

Savage JH, Kaeding AJ, Matsui EC, Wood RA. The natural history of soy allergy. J Allergy Clin Immunol. 2010 Mar. 125(3):683-6. [Medline].

Mehr S, Kakakios A, Frith K, Kemp AS. Food protein-induced enterocolitis syndrome: 16-year experience. Pediatrics. 2009 Mar. 123(3):e459-64. [Medline].

Assa’ad AH, Putnam PE, Collins MH, Akers RM, Jameson SC, Kirby CL, et al. Pediatric patients with eosinophilic esophagitis: an 8-year follow-up. J Allergy Clin Immunol. 2007 Mar. 119(3):731-8. [Medline].

Horan RF, Sheffer AL. Food-dependent exercise-induced anaphylaxis. Immunol Allergy Clin North Am. 1991. 757.

Nowak-Wegrzyn A, Assa’ad AH, Bahna SL, Bock SA, Sicherer SH, Teuber SS, et al. Work Group report: oral food challenge testing. J Allergy Clin Immunol. 2009 Jun. 123 (6 Suppl):S365-83. [Medline].

Sampson HA. Utility of food-specific IgE concentrations in predicting symptomatic food allergy. J Allergy Clin Immunol. 2001 May. 107(5):891-6. [Medline].

Maloney JM, Rudengren M, Ahlstedt S, Bock SA, Sampson HA. The use of serum-specific IgE measurements for the diagnosis of peanut, tree nut, and seed allergy. J Allergy Clin Immunol. 2008 Jul. 122(1):145-51. [Medline].

Sampson HA, Ho DG. Relationship between food-specific IgE concentrations and the risk of positive food challenges in children and adolescents. J Allergy Clin Immunol. 1997 Oct. 100(4):444-51. [Medline].

Wang J, Godbold JH, Sampson HA. Correlation of serum allergy (IgE) tests performed by different assay systems. J Allergy Clin Immunol. 2008 May. 121(5):1219-24. [Medline].

Sicherer SH, Wood RA. Advances in diagnosing peanut allergy. J Allergy Clin Immunol Pract. 2013 Jan. 1 (1):1-13; quiz 14. [Medline].

Klemans RJ, van Os-Medendorp H, Blankestijn M, Bruijnzeel-Koomen CA, Knol EF, Knulst AC. Diagnostic accuracy of specific IgE to components in diagnosing peanut allergy: a systematic review. Clin Exp Allergy. 2015 Apr. 45 (4):720-30.[Medline].

Lin J, Bruni FM, Fu Z, Maloney J, Bardina L, Boner AL, et al. A bioinformatics approach to identify patients with symptomatic peanut allergy using peptide microarray immunoassay. J Allergy Clin Immunol. 2012 May. 129 (5):1321-1328.e5. [Medline].

Eigenmann PA, Sampson HA. Interpreting skin prick tests in the evaluation of food allergy in children. Pediatr Allergy Immunol. 1998 Nov. 9(4):186-91. [Medline].

Bock SA, Lee WY, Remigio L, et al. Appraisal of skin tests with food extracts for diagnosis of food hypersensitivity. Clin Allergy. 1978 Nov. 8(6):559-64. [Medline].

Knight AK, Shreffler WG, Sampson HA, Sicherer SH, Noone S, Mofidi S, et al. Skin prick test to egg white provides additional diagnostic utility to serum egg white-specific IgE antibody concentration in children. J Allergy Clin Immunol. 2006 Apr. 117(4):842-7. [Medline].

Roberts G, Lack G. Diagnosing peanut allergy with skin prick and specific IgE testing. J Allergy Clin Immunol. 2005 Jun. 115(6):1291-6. [Medline].

Nowak-Wegrzyn A, Assa’ad AH, Bahna SL, Bock SA, Sicherer SH, Teuber SS. Work Group report: oral food challenge testing. J Allergy Clin Immunol. 2009 Jun. 123(6 Suppl):S365-83. [Medline].

Bock SA, Sampson HA, Atkins FM, et al. Double-blind, placebo-controlled food challenge (DBPCFC) as an office procedure: a manual. J Allergy Clin Immunol. 1988 Dec. 82(6):986-97.[Medline].

Spergel JM, Brown-Whitehorn T, Beausoleil JL, Shuker M, Liacouras CA. Predictive values for skin prick test and atopy patch test for eosinophilic esophagitis. J Allergy Clin Immunol. 2007 Feb. 119(2):509-11.[Medline].

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Update on Current Care Guideline: Food allergy (children).

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Duodecim. 2015;131(7):694-5.Featured image

Update on Current Care Guideline: Food allergy (children).

Mäkelä M, Jartti T, Kolho KL, Poikonen S, Remes S, Schwab U, Sipilä R, Tulonen-Tapio J, Voutilainen H.

Abstract

This guideline, targeted to healthcare workers dealing with food-allergic children, provides a review on the clinical aspects of pediatric food allergy. The main updates include: elimination diets are not recommended for breast-feeding mothers; probiotics are not recommended for allergy prevention or treatment; food challenges are the basis of the diagnosis, but it can be improved by IgE component diagnostics. The treatment for severe symptoms is specific food avoidance, mildly symptomatic children should continue with versatile diet. Specific oral tolerance induction is a safe and effective treatment in most of the pediatric patients.

Current Allergy Immunology by Widodo Judarwanto

www.allergycliniconline.com

Supported by: ALLERGY ONLINE CLINIC FOR CHILDREN, TEEN AND ADULT Yudhasmara Foundation www.allergycliniconline.com GROW UP CLINIC I Address: JL Taman Bendungan Asahan 5 Jakarta Pusat, Jakarta Indonesia 10210 Phone : (021) 5703646 – 085101466102 – 085100466103 GROW UP CLINIC II MENTENG SQUARE Address: Jl Matraman 30 Jakarta Pusat 10430 phone 29614252 – 081315922012 – 081315922013 www.growup-clinic.com Facebook: FB-Growup Clinic Page Facebook : Allergy Clinic Online. Professional Healthcare Provider “GRoW UP CLINIC” Dr Narulita Dewi SpKFR, Physical Medicine & Rehabilitation curriculum vitae HP 085777227790 PIN BB 235CF967 Clinical – Editor in Chief : Dr Widodo Judarwanto, Pediatrician Editor: Audi Yudhasmara email : judarwanto@gmail.com Mobile Phone O8567805533 PIN BBM 76211048 Komunikasi dan Konsultasi online : twitter @widojudarwanto facebook dr Widodo Judarwanto, pediatrician Komunikasi dan Konsultasi Online Alergi Anak : Allergy Clinic Online Komunikasi dan Konsultasi Online Sulit makan dan Gangguan Berat Badan : Picky Eaters Clinic Komunikasi Profesional Pediatric: Indonesia Pediatrician Online

“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 ***

Curriculum Vitae Widodo Judarwanto

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Alergi Hidung, Tenggorok dan Telinga Pada Penderita Dewasa dan Alergi Makanan

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Alergi Hidung, Tenggorok dan Telinga Pada Penderita Dewasa dan Alergi Makanan

Benarkah Aku Alergi Dingin dan Debu. Benarkah Aku Tidak Alergi Makanan ?

Gejala Alergi pada Hidung, Tenggorok dan Telinga Pada Penderita Dewasa

 

Telinga Hidung Tenggorokan

Hidung : Hidung buntu, bersin, hidung gatal, pilek, post nasal drip, epitaksis, tidur mendengkur, mendengus

Tenggorok : tenggorokan nyeri/kering/gatal, palatum gatal, suara parau/serak, batuk pendek (berdehem)

Telinga : telinga terasa penuh/ bergemuruh / berdenging, telinga bagian dalam gatal, nyeri telinga dengan gendang telinga kemerahan atau normal, gangguan pendengaran hilang timbul, terdengar suara lebih keras, akumulasi cairan di telinga tengah, pusing, gangguan keseimbangan. Pembesaran kelenjar di sekitar leher dan kepala belakang bawah

Banyak kasus penderita alergi pada orang dewasa sering frustasi karena hilang timbulnya keluhan dan tanpa diketahui secara pasti penyebabnya. Selama ini sebagian besar penderita atau bahkan Dokter masih menganggap bahwa penyebab utama debu dan dingin. Tetapi anehnya keluhan alergi hanya timbul pagi dan malam hari, justru lebih berat saat siang hari. Justru saat pagi debu sedikit dan siang hari debu lebih banyak. Selama ini alergi dianggap karena dingin atau hujan. Tetapi juga aneh, saat siang hari di kantor ata saat tidur siang AC nya sangat dingin keluhan alergi tiba-tiba hilang dan napas menjadi lega. Sehingga berbagai dokter telah dikunjungi namun seringkali semakin bingung karena pendapat berbagai dokter tersebut tidak ada yang sama. Seorang dokter mengatakan makanan tidak berkaitan dengan berbagai gejala yang ada. Tetapi kelompok dokter lain mengatakan bahwa makanan berperanan dengan gangguan yang ada. Perbedaan pendapat ini wajar terjadi, selama ini hipotesa yang masihbanyak dianut bahwa alergi makanan tidak berpengaruh dewasa.

Hal ini wajar tejadi karena sumber kontroversi tersebut sampai saat ini adalah penentuan diagnosis alergi makanan dan banyak faktor yang berpengaruh. Untuk memastikan makanan sebagai penyebab alergi adalah dengan diagnosis klinis bukan dengan pemeriksaan laboratorium atau tes alergi. Bukan hanya perbedaan pendapat antara klinisi, hasil penelitian tentang alergi makanan berkaitan dengan manifestasi berbagai organpun seringkali tidak sama karena sebagian peneliti mengandalkan diagnosis bukan dengan diagnosis klinis tetapi dengan pemeriksaan laboratorium atau tes alergi. Bila kesalahan dasar dalam memastikan penyebab alergi makanan ini terjadi maka perbedaan pendapat dan kontroversi tersebut akan terjadi semakin besar dalam penanganan berbagai kasus alergi.Featured image

Memang sampai saat ini bahkan di negara sudah majupun banyak gangguan alergi tidak disadari bahkan oleh sebagian dokter. Sejauh ini banyak orang tidak mengetahui bahwa berbagai keluhan yang dia alami atau yang dialami anaknya itu adalah gejala alergi. Resource (Marketing Research) Limited melakukan penelitian di Inggris bagian selatan, tahun 2000 dilaporkan lebih dari 50% orang dewasa menderita alergi makanan. Sekitar 70% penderita alergi baru mengetahui kalau ia mengalami alergi setelah lebih dari 7 tahun. Sekitar 50% orang dewasa mengetahui penyebab gejala alergi setelah 5 tahun, bahkan terdapat 22% baru mengetahui setelah lebih 15 tahun mengalami gangguan alergi tersebut. Sebanyak 80% penderita alergi mengalami gejala seumur hidupnya. Hal ini menunjukkan bahwa di negara maju seperti Inggrispun para dokter terlambat mendiagnosis alergi apalagi di Indonesia. Ternyata para dokter di Inggrispun menganggap bahwa selama ini berbagai gangguan yang ada tidak berkaitan dengan alergi.

Berbagai gangguan alergi atau hipersensitifitas makanan tersebut adalah gangguan fungsional sehingga dianggap normal dan dikatakan dengan pertambahan usia akan membaik. Mungkin saja saja sebagian pendapat tersebut benar. Memang penderita alergi makanan terutama yang mengganggu saluran cerna dan ssusunan saraf pusat mengalami gangguan fungsional. Gangguan alergi makanan khususnya gangguan pada saran cerna dan susunan saraf pusat adalah gangguan fungsi bukan gangguan organnya. Hal inilah yang melatarbelakngi mengapa semua gangguan yang berkaitan dengan alergi makanan dan hipersensitifitas makanan sering dianggap normal. Karena, memang manifestasi yang ada tidak didapatkan kelainan organ dengan pemeriksaan USG, foto kontras dan CT scan. Karena pemeriksaan tersebut tidak didapatkan kelainan maka dianggap penderita tidak punya kelainan, tetapi anehnya keluhan penderita hilang timbul. Bahkan beberapa dokter menganggap bahwa gangguan tersebut dipengaruhi karena stres. Saat dilakukan eliminasi provokasi makanan ternyata gangguan yang dianggap normal itu bisa membaik. Memang gangguan fungsional pada umumnya adalah masalah imaturitas atau ketidakmatangan sistem tubuh, karena dengan pertambahan usia setelah usia 2 hingga 7 tahun akan membaik. Meski ada yang masih mengalami hingga usia 12 tahun dan sebagian masih mengalami hingga dewasa meski dengan tingkat gangguan yang berkurang. Tetapi bukan berarti harus menunggu sampai usia tertentu membaik karena bila dilakukan elminasi provokasi makanan untuk mencari penyebab makanan penyebabnya gangguan tersebut akan membaik.

Ilustrasi Kasus Kontroversi Alergi :

  • Berbagai klinisi dan penelitian banyak yang mengungkapkan bahwa alergi berkaitan dengan berbagai gangguan tubuh dan gangguan perilaku. Hal ini terjadi karena klinisi dan dokter tersebut menentukan tanda dan gejala alergi dengan melakukan diagnosis klinis dengan eliminasi provokasi. Sedangkan dokter lain dan peneliti lain mengungkapkan bahwa alergi tidak berkaitan dengan berbagai manifestasi yang ada karena menggunakan dasar laboratorium atau tes alergi. Padahal dalam menentukan diagnosis alergi makanan yang paling penting adalah diagnosis klinis bukan laboratorium atau tes alergi.
  • Seorang dokter pernah diklaim oleh dokter lainnya ketika menulis bahwa tes alergi tertentu tidak direkomendasikan dan tidak akurat sebagai pengobatan atau diagnosis. Bahkan perbedaan pendapat tersebut berpotensi akan memasuki meja hijau, tetapi dengan komunikasi ilmiah yang dilakukan ternyata perbedaan pendapat tersebut dapat diperbaiki.
  • Seorang dokter ahli dipermasalahkan oleh sebagian dokter ahli lainnya mengungkapkan berbagai tanda dan gejala alergi yang ada berkaitan dengan makanan. Padahal ungkapan tersebut disampaikan ditunjang dengan fakta ilmiah dari berbagai penelitian yang ada. Akhirnya perbedaan pendapat ini masuk dalam ranah komite etik profesi. Dalam pertemuan tersebut juga masih terjadi perbedaan pendapat tajam. Seorang nara sumber bidang yang berkopeten mengatakan bahwa bisa saja pengaruh histamin dapat menganggu berbagai organ tubuh lainnya meski insidennya tidak banyak. Tetapi yang pihak lain bependapat bahwa berbagai pakar dari berbagai keahlian tidak setuju dengan berbagai tanda dan gejala tersebut dikaitkan dengan alergi makanan. Tetapi akhirnya salah satu pihak mengalah untuk tidak mempanjang kontroversi ini demi kesejawatan.
  • Seorang penderita kejang yang berlangsung selama sepuluh tahun dengan minum berbagai obat anti kejang tidak membaik. Dalam pemeriksaan laboratorium, CT scan dan EEG dalam batas normal. Berbagai dokter ahli persarafan di Indonesia bahkan di Singapura di bidangnyapun masih terjadi beda pendapat. Sebagian menyarankan minum obat kejang sebagian dokter lainnya obat kejang tidak perlu. Ketika dilakukan evaluasi ternyata penderita mengalami gangguan alergi makanan dan dicurigai bahwa sangat mungkin gangguan kejang karena berkaitan dengan alergi makanan. Saat dilakukan elminasi provokasi makanan terbukti gejala alergi saluran cerna membaik dan keluhan kejang membaik tanpa pengobatan anti kejang. Saat itu penderita melakukan elminansi provokasi makanan dengan ketat selama 2 bulan. Tetapi saat mendengar informasi dari dokter ahli lainnya bahwa makanan tidak berkaitan dengan gejala tersebut penderita melepas lagi program eliminasi provokasi makanan. Ketika melakukan konsultasi ulang ternyata setelah 2 bulan paska menarik diri dari program elimnasi provokasi tersebut gejala kejang tersebut hilang timbul lagi dengan berganti-ganti obat tetapi responnya tidak membaik seperti yang diharapkan.
  • Penatalaksanaan Alergi pada anak khususnya alergi pada saluran napas dan hidung sering sangat sulit dan tidak optimal. Hal ini terjadi karena sampai saat ini banyak klinisi kesulitan dalam mencari penyebab alergi
  • Permasalahan ini terjadi karena banyak klinisi kesulitan dalam mencari penyebab alergi. Jadi fakta yang kita hadapi selama ini adalah hanyalah mengobati akibat penyakitnya tetapi tetapi tidak mencari akar permasalahan kenapa penyebab penyakit itu bisa timbul jangka panjang dan hilang timbul. Berbagai pemeriksaan alergi ternyata akurasi dan spesifitasnya sangat rendah. Hal inilah yang tampaknya menjadi penyebab utama mengapa kasus alergi sulit sekali dalam mengatasinya.
  • Pemeriksaan yang terbukti secara ilmiah untuk mencari penyebab alergi adalah tes kulit dan RAST. Namun pemeriksaan alergi berupa tes kulit, dan RAST sangat terbatas sebagai alat diagnosis untuk alergi makanan. Sehingga sebaiknya tidak boleh menghindari dan membolehkan makanan penyebab alergi berdasarkan karena tes kulit alergi. Karena, tes kulit ini tidak bisa mendeteksi reaksi alergi tipe lambat seperti alergi makanan tertentu.
  • Pemberian obat terus menerus bukanlah jalan terbaik dalam penanganan alergi. Paling ideal dalam mencegah timbulnya alergi adalah menghindari pencetus atau penyebabnya. Hal ini memerlukan pengamatan yang cermat dan kerjasama yang baik antara dokter, pasien dan keluarga. Untuk mendapatkan hasil penanganan alergi yang optimal harus dipahami perbedaan antara penyebab dan pencetus alergi.

Berdasarkan beberapa fakta ilmiah termasuk berbagai penelitian ilmiah belakangan telah terungkap bahwa alergi makanan menimbulkan komplikasi yang cukup mengganggu, karena alergi dapat mengganggu semua organ atau sistem tubuh kita termasuk gangguan fungsi otak. Karena gangguan fungsi otak itulah maka timbul gangguan perkembangan dan perilaku pada anak seperti gangguan konsentrasi, gangguan tidur, gangguan emosi, gangguan konsentrasi hingga memperberat gejala ADHD dan autism. Meskipun sebenarnya alergi bukan penyebab ADHD atau Autism tetapi hanya memperberat gangguan perilaku yang sudah ada tersebut. Meski berbagai peneilitian klinis juga mengungkapkan hal tersebut ternyata terdapat juga sebagian penelitian klinis yang tidak sependapat bahwa berbagai kelainan tersebut tidak berkaitan dengan alergi.image

Dengan semakin berkembangnya ilmu pengetahuan kedokteran dan teknologi kedokteran, namun kejadian alergi justru meningkat pesat, dan semakin banyak yang masih misterius belum terungkap. Banyak klinisi memvonis alergi pada penderita tetapi tidak bisa mengadviskan dengan pasti penghindaran penyebab karena kesulitan terbesar penanganan alergi adalah mencari penyebabnya.

Alergi dan hipersensitifitas makanan pada anak tidak sesederhana seperti yang pernah kita ketahui. Sebelumnya kita sering mendengar dari dokter spesialis penyakit dalam, dokter anak, dokter spesialis yang lain bahwa alergi itu gejala adalah batuk, pilek, sesak dan gatal. Padahal dapat menyerang semua organ tanpa terkecuali mulai dari ujung rambut sampai ujung kaki dengan berbagai bahaya dan komplikasi yang mungkin bisa terjadi. Belakangan terungkap bahwa menimbulkan komplikasi yang cukup berbahaya, karena alergi dan hipersensitivitas makanan dapat mengganggu semua organ atau sistem tubuh kita termasuk gangguan fungsi otak. Karena gangguan fungsi otak itulah maka timbul gangguan perkembangan dan perilaku pada anak seperti gangguan konsentrasi, gangguan emosi, keterlambatan bicara, gangguan konsentrasi hingga memperberat gejala ADHD dan Autism.

Bila melihat demikian luasnya gangguan yang terjadi dan banyaknya organ yang terganggu, tampaknya alergi dan hipersensitivitas makanan adalah suatu “gangguan sistemik”. Dapat dimaklumi bila ada pendapat, bahwa ungkapan itu terlalu berlebihan karena semua keluhan selalu dikaitkan dengan alergi dan hipersensitifitas makanan. Namun pendapat ini akan sirna, bila banyak penderita alergi dan hipersensitivitas makanan mengungkapkan, memang benar bahwa gangguan dan keluhan tersebut memang terjadi pada dirinya. Secara ilmiahpun hal ini didukung oleh penelitian ilmiah dan laporan ilmiah dari berbagai disiplin ilmu yang mengaitkan bahwa berbagai gejala tersebut penyebabnya adalah alergi. Habnya seringkali terjadi kontroversi yang berlebihan antara sesama dokter dan orangtua karena alergi dan hipersensitivitas makanan hanya bisa ditegakkan diagnosisnya dengan diagnosis klinis bukan dengan pemeriksaan laboratorium. Diagnosis klinis adalah mengamati secara cermat tanda dan gejala yang timbul berkaitan dengan pemberian makanan yang diberikan melalui anamnesa (menanyakan secara cermat semua keluhan) dan pemeriksaan fisaik oleh dokter.

Dalam beberapa puluh tahun lamanya mungkin sering dihadapi oleh masyarakat pada umumnya, masih sering terjadi kontroversi tentang penyakit alergi dan hipersensitifitas makanan. Sering terjadi bukan hanya pada orang awam di kalangan dokterpun masih banyak terjadi perbedaan pendapat. Seorang penderita alergi dan hipersensitivitas makanan mendapat advis dari seorang dokter untuk menghindari makanan tertentu untuk mengurangi keluhan penyakitnya. Tetapi dokter lainnya mengatakan tidak perlu menghindari makanan tersebut, karena makanan tidak berhubungan dengan penyakitnya. Sebagian dokter berpendapat, bahwa gejala alergi dan hipersensitivitas makanan jarang ditemukan. Ada pendapat alergi dan hipersensitivitas makanan hanya berkaitan dengan sedikit penyakit dan sangat jarang menyangkut bahan makanan.

Makanan yang diakui sebagai penyebab alergi masih sangat terbatas misalnya gluten susu dan ikan. Sedangkan kubu dokter lain berpendapat alergi dan hipersensitivitas makanan sangat umum dan bersembunyi dibalik berbagai kelainan yang hingga sekarang tak dapat disembuhkan, seperti radang sendi (artritis), eksim (dermatitis atau alergi kulit), migren (sakit kepala sebelah). Mereka ingin mengungkapkan bahwa seluruh permasalahan kesehatan dapat dicetuskan dan disembuhkan dengan penanganan alergi dan hipersensitivitas makanan. Timbul pendapat bahwa penyebab alergi makanan tidak dibatasi, semua jenis makanan atau minuman dapat dianggap sebagai penyebab alergi.

Bahkan bahan bukan makanan dapat menyebabkan alergi seperti semprotan rambut, uap obat nyamuk, uap bensin, plastik dan semua bahan kimia yang potensial mengganggu dalam lingkungan kita. Penyebab alergi lainnya yang sudah lama diyakini dan tidak disangsikan lagi adalah debu, kutu, bulu binatang, serbuk sari atau bulu unggas lainnya.

Suasana perbedaan pendapat tersebut jauh dari suasana kekeluargaan. Ungkapan dari berbagai pihak seperti “tak terbukti”, “berbahaya”, “orientasi obat”, “berpikiran sempit”, “tidak ilmiah” atau “tidak kompeten” secara tak sadar secara langsung diterima oleh pasien. Jika para pakar medis sudah berbeda pendapat secara tajam, maka orang awam menjadi bingung karena pendapat berbagai dokter berlainan. Dalam menghadapi kontroversi ini tidak heran bila masyarakat semakin bingung tak tahu harus minta bantuan kemana. Fakta ilmiah dan data penelitian telah banyak menunjukkan bahwa ternyata makanan tertentu dapat menyebabkan berbagai gangguan yang selama ini tidak diperkirakan banyak orang. Ternyata, makanan yang bergizi setinggi apapun dan selezat apapun ternyata dapat merugikan mengganggu tubuh manusia yang sebaliknya dapat mengakibatkan berbagai gangguan fungsi tubuh.

Berbagai gangguan dan sistem tubuh telah disepakati sebagai akibat pengaruh makanan. Tetapi sebaliknya justru telah menjadi kontroversi baik masyarakat awam maupun sesama dokter bahwa ternyata berbagai makanan sebagai penyebab gangguan tubuh manusia. Hal itu terjadi karena untuk memastikan pengaruh makanan terhadap tubuh bukan berdasarkan tes alergi atau pemeriksaan laboratorium semata tetapi berdasarkan diagnosis klinis yang di bidang medis di sebut chalenge test atau eliminasi provokasi makanan.

Tidak hanya dalam alergi makanan, tampaknya kontroversi itu adalah hal yang biasa seperti hal penyakit lainnya di bidang kedokteran. Biasanya bila untuk memastikan diagnosis suatu penyakit atau kelainan hanya berdasarkan diagnosis klinis seringkali akan menimbulkan banyak kontroversi krena subyektifitasnya sangat tinggi. Contoh tersebut adalah dalam diagnosis Autism, ADHD, dan diagnosis gangguan fungsional lainnya yang dalam pemeriksaan imunopatobiologis normal. Hal ini mengakibatkan bahwa ADHD adalah wrong diagnosis terbesar di Amerika Serikat. Kondisi tersebut juga mengakibatkan mengapa seorang gangguan perilaku yang sama didiagnosis yang berbeda oleh 5 dokter yang berbeda. Beragamnya diagnosis kepada anak yang sama tersebut seperti diagnosis Autis, Autism Ringan, Bukan Autis, PDD NOS atau ADHD. Padahal klinisi yang mendiagnosisnya adalah sudah berkopeten di bidangnya. Tetapi bila dasar diagnosis tersebut parameternya disertai laboratorium dan pemeriksaan penunjang maka perbedaan pendapat tersebut semakin jarang. Misalnya diagnosis Hepatitis B, Hipertensi, Sindrom Nefrotik (klainan ginjal) atau Diabetes Melitus maka dalam mendiagnosisnya relatif tidak menimbulkan perbedaan persepsi.

Sumber Kontroversi

  • Di bidang ilmu kedokteran telah disepakati secara ilmiah bahwa untuk memastikan penyebab alergi adalah dengan eliminasi provokasi makanan bukan dengan tes alergi. Tes alergi hanya membantu diagnosis bukan memastikan penyebab alergi. Tetapi kesepakatan ilmiah yang seharusnya tidak terbantahkan ini sering diabaikan dan menjadi sumber berbagai kontroversi yang ada
  • Penyebab lain perbedaan pendapat ini adalah sulitnya untuk memastikan penyebab alergi dengan melakukan eliminai provokasi makanan. Gold Standart atau standar baku emas diagnosis alergi makanan adalah DBPCFC (Double Blind Placebo Chalenge Food Control). Tetapi karena relatif rumit timbul beberapa modifikasi Chalenge test atau eliminasi provokasi makanan yang kelihatan mudah tetapi sulit ini seringkali tidak pernah dilakukan oleh klinisi dan sebagian ahli alergi untuk memastikan penyebab alergi makanan.
  • Gangguan alergi makanan khususnya gangguan pada saran cerna dan susunan saraf pusat adalah gangguan fungsi bukan gangguan organnya. Hal inilah yang melatarbelakngi mengapa semua gangguan yang berkaitan dengan alergi makanan dan hipersensitifitas makanan sering dianggap normal. Karena, memang manifestasi yang ada tidak didapatkan kelainan organ dengan pemeriksaan USG, foto kontras dan CT scan. Karena pemeriksaan tersebut tidak didapatkan kelainan maka dianggap penderita tidak punya kelainan, tetapi anehnya keluhan penderita hilang timbul. Saat dilakukan eliminasi provokasi makanan ternyata gangguan yang dianggap normal itu bisa membaik.
  • Penelitian berbagai manifestasi klinis dan pengaruh alergi makanan masih belum banyak terungkap jelas. Sampai saat ini keterkaitan berbagai manifestasi klinis gangguan fungsi tubuh dengan alergi makanan dan hipersensitifitas lainnya masih relatif sulit dibuktikan secara ilmiah. Dalam penelitian ilmiah penelitian klinis adalah mempunyai kualitas penelitian yang tidak lebih baik dibandingkan penelitian yang diukur dengan parameter imunopatobiologis. Padahal diagnosis alergi makanan dan hipersensitifitas lainnya berdasarkan diagnosis klinis bukan dengan pemeriksaan laboratorium imunopatobiologis Hal inilah yang mengakibatkan bahwa keterkaitan manifestasi klinis dengan alergi makanan sulit dibuktikan dengan standard ilmiah yang lebih baik. Pada umumnya dasar diagnosis penelitian alergi makanan dan hipersensitifita lainya yang membuktikan ketidakbermaknaannya hubungan tersebut dibuat bukan berdasarkan eliminasi provokasi tetapi berdasarkan parameter tes alergi dan laboratorium penunjang. Sehingga kesimpulan yang dibuatpun menjadi lemah. Seharusnya penelitian dampak alergi makanan atau manifestasi alergi makanan berdasarkan eliminasi provokasi makanan bukan berdasarkan parameter laboratorium atau pemeriksaan ts alergi. Di masa datang permasalahan alergi makanan dan hipersensitifitas makanan akan lebih terungkap dengan jelas bila penelitian klinis eliminasi provokasi makanan disertai perubahan klinis dan perubahan biomolekular.
  • Sebagian dokter bahkan masih mendewakan tes alergi sebagai cara untuk mencari memastikan penyebab alergi makanan dan hipersensitifitas makanan. Hal ini tampak dengan banyak pendapat dari beberapa dokter bahwa ketika seseorang dipastikan menderita alergi makanan dan hipersensitifitas makanan dengan eliminasi provokasi masih disangsikan ketika belum dilakukan tes alergi. Padahal justru angka kejadian alergi makanan lebih sedikit dibandingkan hipersensittifitas makanan lainnya. Secara umum penderita alergi makanan adalah berkisar 4-9% tetapi diduga angka kejadian hipersensitifita makanan lainnya sepuluh kali lipat dibandingkan penderita alergi makanan. Tes alergi memang diperlukan untuk diagnosis tetapi untuk memastikannya harus dikonfirmasi lagi dengan eliminasi provokasi atau chalenge test.

Sumber Kontroversi lainnya

  • Pada umumnya gangguan reaksi simpang makanan karena alergi atau hipersensitifitas makanan merupakan gangguan fungsional sistem tubuh. Gangguan fusngsional sistem tubuh mempunyai karakteristik oragan tubuh yag terlibat sering dianggap normal dan dalam pemeriksaan penunjangpun tidak ditemukan kelainan. Sehingga saat dilakukan pemeriksaan penunjang apapun seperti USG, CT Scan, MRI, EEG atau pemeriksaan lainnya pada organ tubuh adalah normal. Bila dikatakan normal sering timbul pertanyaan pada penderta. Mengapa dikatakan normal, padahal saya sangat menderita setiap hari dan berlangsung demikian lama. Dalam kedaan seperti ini biasanya setiap dokter yang memeriksa akan memeberikan pendapat yang bebeda tentang penyebabnya, bahkan sebagian dokter mengatalkan jujur tidak tahu penyebabnya. Beberapa dokter yang mencoba berspekulasi memberikan penilaian tentang penyebab kelainan tersebut biasanya jawaban seputar stres, masuk angin, terlalu capek dan masih bayak penyebab lainnya yang secara ilmiah kadang tidak sesuai. Sehingga saat wajar ketika pasien mengeluhkan gangguan yang selama ini diderita kepada tiga atau lima dokter pendapatnya akan berbeda. Hal ini akan membuat penderita semakin frustasi. Bila penyebabnya masih simpang siur maka akan berimbas pada terapinya akan juga tidak akan pernah fokus pada penyebabnya. Hal inilah yang juga mengakibatkan penderita gangguan reaksi simpang makanan karena alergi atau hipersensitifitas makanan menjadi berkepanjangan hilang timbul terus menerus dengan berpindah-pindah dokter.
  • Berdasarkan beberapa fakta ilmiah belakangan terungkap bahwa alergi menimbulkan komplikasi yang cukup menggaggu, karena alergi dapat mengganggu semua organ atau sistem tubuh kita termasuk gangguan fungsi otak. Karena gangguan fungsi otak itulah maka timbul gangguan perkembangan dan perilaku pada anak seperti gangguan konsentrasi, gangguan tidur, gangguan emosi, keterlambatan bicara, gangguan konsentrasi hingga memperberat gejala ADHD dan autism. Meskipun sebenarnya alergi bukan penyebab ADHD atau Autism tetapi hanya memperberat gangguan perilaku yang sdah ada tersebut.
  • Resiko dan tanda alergi dapat diketahui sejak anak dilahirkan bahkan sejak dalam kandunganpun mungkin sudah dapat terdeteksi. Alergi dapat dicegah sejak dini dan diharapkan dapat mengoptimalkan pertumbuhan dan perkembangan Anak secara menyeluruh. Sehingga “overtreatment” dan “overdiagnosis” yang diberikan terhadap penderita alergi dapat dicegah sedini mungkin. Akhirnya komplikasi yang ditimbulkan khususnya dalam ganguan otak dan gangguan perilaku juga dapat dicegah lebih dini.

Berbagai pendapat dalam kontroversi itu adalah Kesulitan memastikan penyebab alergi makanan dan hipersensitifitas makanan yang seharusnya berdasarkan klinis ini mengakibatkan melebarnya perbedaan pandangan di bidang lainnya. Kontroversi tersebut adalah :

  • Pendapat ekstrim sebagian dokter yang mengatakan bahwa belum di tes dan diperiksa laboratorium tetapi sudah dipastikan alergi
  • Beberapa dokter berulang kali mengatakan bahwa penyebab alergi makanan terbesar di Jakarta adalah udang dan ikan laut, karena berdasarkan tes kulit alergi. Padahal tes kulit bukan untuk memastikan penyebab alergi makanan. Seharusnya yang benar adalah “kemungkinan” penyebab alergi adalah udang. Karena, belum tentu berbagai hasil tes kulit yang negatif adalah bukan penderita alergi makanan bahan yang di tes tersebut.
  • Pemeriksaan alergi dengan tes alternatif yang tidak diakui oleh berbagai institusi kesehatan internasional dan tidak terbukti secara ilmiah seperti bioresonansi, IgG4 (yang dikirim ke Amerika) dan berbagai tes unproven lainnya
  • Penanganan langkah awal penderita alergi adalah mendeteksi penyebab dan menghindarinya. Tetapi karena berbagai kesulitan langkah awal ini diabaikan tetapi langsung masuk ke langkah berikutnya dengan pengobatan dan pencegahan alergi dengan obat-obatan.
  • Berbagai hal gejala dan gangguan fungsi tubuh disebabkan alergi dan hipersensitifitas makanan lainnya sering disangkal. Tetapi justru penyangkalan tersebut tanpa data ilmiah untuk membuktikan memang tidak berhubungan. Tetapi justru penelitian awal yang sudah semakin banyak bahkan tetap masih dipandang sebelah mata karena memang didoinasi penelitian klinis.
  • Pemakaian obat-obatan untuk profilaksis alergi makanan baik dengan ketotifen (profilas) atau obat alergi lainnya yang tidak terbukti sebagai pencegahan.
  • Sebenarnya fakta makanan dapat mengakibatkan berbagai manifestasi penyakit sudah diyakini beberapa praktisi kesehatan sejak lama. Hanya karena keterkaitan masalah tersebut belum dapat dibuktikan secara klinis tentang penyebabnya maka juga timbul berbagai perbedaan pandangan.
  • Berbagai pendekatan diet yang dianggap tidak seuai manifestasi imunopatobiologis bidang kedokteran di antaranya adalah :
  1. Diet berdasarkan Golongan darah
  2. Diet rotasi
  3. Diet Asam basa

Angka kejadian alergi dan hipersensitifitas makanan terus meningkat tajam dalam dekade terakhir ini. Terdapat kecenderungan alergi pada anak, merupakan kasus yang mendominasi kunjungan penderita di klinik rawat jalan pelayanan Kesehatan Anak. Perhatian dan penanganan alergi pada anak masih belum optimal, bahkan sering terjadi keterlambatan penanganan. Tampak pada orang tua penderita alergi baru menyadari bahwa anaknya menderita alergi setelah sekian tahun lamanya anaknya menderita sakit yang berulang dan telah berganti-ganti dokter.

Cara menyikapinya

  • Kontroversi yang sangat tajam tersebut bukan hanya membingungkan para dokter tetapi pasienpun akan lebih bingung dalam menerima perbedaan pendapat para dokter tersebut. Untuk menyikapi hal tersebut sebenarnya bukan dengan langsung memvonis dokter satu paling benar atau dokter lain salah. Tetapi dipihak klinisi atau organisasi profesi harus membuat forum disikusi dan kalau perlu membuat workshop atau debat ilmiah untuk menyelesaikan masalah ini. Kala sudah sepakat maka para klinisi tersebut melalui organisasi profesi mengeluarkan rekomendasinya. Kebenaran ilmiah adalah kebenaran fakta ilmiah sesuai Evidance Base Medicine. Bukan berdasarkan opini pakar atau profesor tanpa mempertimbangkan fakta klinis yang ada.
  • Bagi klinisi yang berseberang pendapat memang wajar terjadi tetapi harus berdasarkan fakta ilmiah dari pengalaman klinis berbasis bukti dengan didasari oleh berbagai penelitian. Tetapi sebaiknya bila klinisi tersebut tidak berbekal data ilmiah tetapi langsung membuat kontroversi semakin panas sangat disayangkan karena penyelesaian perbedaan pendapat tersebut harus diselesaikan dengan cara ilmiah bukan dengan debat tidak ilmiah.
  • Sedangkan di pihak pasien atau orangtua pasien dalam menyikapi hal ini harus secara obyektif. Bila orangtua atau pasien ragu dengan berbagai kontroversi tersebut maka sebaiknya ikuti langkah eliminasi provokasi atau chalenge test di bawah pengawasan dokter ahli. Bila berbagai gangguan yang ada membaik maka sebaiknya penderita harus percaya dengan fakta yang ada, bahwa alergi dapat mengganggu berbagai organ tubuh yang ada. Bila fakta tersebut ada, bukan berarti harus menyalahkan pendapat dokter lainnya bahwa dokter yang lain salah. Bahwa memang kebenaran ilmiah tersebut akan terjadi seiring dengan berjalannya waktu yang membutuhkan proses ilmiah alamiah yang panjang.

Benarkah Berbagai Gangguan ini bukan karena alergi atau hipersensitifitas makanan

ORGAN/SISTEM TUBUH

GEJALA DAN TANDA

1

Sistem Pernapasan

Batuk, pilek, bersin, sesak(astma), napas pendek, wheezing, banyak lendir di saluran napas atas (mucus bronchial) , rattling dan vibration dada.

2

Sistem Pembuluh Darah dan jantung

Palpitasi (berdebar-debar), flushing (muka ke merahan), nyeri dada, pingsan, tekanan darah rendah, denyut jantung meningkat, skipped beats, hot flashes, pallor; tangan hangat, kedinginan, kesemutan, redness or blueness of hands; pseudo-heart attack pain (nyeri dada mirip sertangan jantung); nyeri dada depan, tangan kiri, bahu, leher, rahang hingga menjalar di pergelangan tangan. Vaskulitis (sering lebam kebiruan seperti bekas terbentur padahal bukan terbentur pada daerah lengan atas dan lengan bawah)

3

Sistem Pencernaan

GERD (Gastrooesephageal Refluks Disease), Maag, Dispepsia, IBS (Irritable Bowel Syndrome) Nyeri perut, sering diare, kembung, muntah, sulit berak (konstipasi), sering buang angin (flatus), mulut berbau, kelaparan, haus, saliva (ludah) berlebihan atau meningkat, canker sores, sariawan, metallic taste in mouth (rasa logam dalam mulut, stinging tongue, nyeri gigi, burping (glegekan/sendawa), retasting foods, ulcer symptoms, nyeri ulu hati, indigestion, mual, muntah, perut terasa penuh, gangguan mengunyah dan menelan, perut keroncongan, Nyeri Perut (spastic colitis, “emotional colitis,” kolik kandung empedu gall bladder colic, cramp), diare (mudah buang air besar cair dan sering), sering buang angin dan besar-besar dan panjang, timbul lendir atau darah dari rektum, anus gatal atau panas.

4

Kulit

Sering gatal, dermatitis, urticaria, bengkak di bibir, lebam biru (seperti bekas terbentur) bekas hitam seperti digigit nyamuk. Kulit kaki dan tangan kering tapi wajah berminyak. Sering berkeringat.

6

Sistem Saluran Kemih dan kelamin

Sering kencing, nyeri kencing; tidak bisa mengontrol kandung kemih, bedwetting; vaginal discharge; genitalia gatal/bengkak/kemerahan/nyeri; nyeri bila berhubungan kelamin

7

Sistem Susunan Saraf Pusat

Sering sakit kepala, migrain, short lost memory (lupa nama orang, barang sesaat), floating (melayang), kepala terasa penuh atau membesar. Perilaku : Therapy terapi: impulsif, sering Marah, buruknya perubahan suasana hati (gangguan mood), kompulsif mengantuk, mengantuk, pusing, bingung, pusing, ketidakseimbangan, jalannya sempoyongan, lambat, lambat, membosankan, kurang konsentrasi, depresi, menangis, tegang, marah, mudah tersinggung, cemas, panik, dirangsang, agresif, overaktif, ketakutan, gelisah, manik, hiperaktif dengan ketidakmampuan belajar, gelisah, kejang, kepala terasa penuh atau membesar, sensasi melayang, gangguan memori jangka pendek (short memory losy), salah membaca atau membaca tanpa pemahaman, variasi ektrim dalam tulisan tangan, halusinasi, delusi, paranoia, Bicara Gagap, claustrophobia, kelumpuhan, negara katatonik, disfungsi persepsi, gejala khas keterbelakangan mental impulsif. Sensitive dan mudah marah, impulsif (bila tertawa atau bicara berlebihan), overaktif, deperesi, terasa kesepian merasa seperti terpisah dari orang lain, kadang lupa nomor, huruf dan nama sesaat, lemas (flu like symtomp)

8

Sistem Hormonal

Kulit berminyak (atas leher), kulit kering (bawah leher), endometriosis, Premenstrual Syndrome (Nyeri dan gangguan lainnya saat haid, kemampuan sex menurun, Chronic Fatique Symptom (sering lemas), Gampang marah, Mood swing, sering terasa kesepian, rambut rontok. Keputihan, jerawat.

9

Jaringan otot dan tulang

Nyeri tulang, nyeri otot, nyeri sendi: Fatigue, kelemahan otot, nyeri, bengkak, kemerahan local pada sendi; stiffness, joint deformity; arthritis soreness, nyeri dada, otot bahu tegang, otot leher tegang, spastic umum, , limping gait, gerak terbatas

10

Gigi dan mulut

Nyeri gigi atau gusi tanpa adanya infeksi pada gigi (biasanya berlangsung dalam 3 atau 7 hari). Gusi sering berdarah. Sering sariawan. Diujung mulut, mulut dan bibir sering kering, sindrom oral dermatitis. Geraham belakang nyeri sering dianggap sebagai Tooth Impacted (tumbuh gigi geraham miring)

11

Mata

nyeri di dalam atau samping mata, mata berair,sekresi air mata berlebihan, warna tampak lebih terang, kemerahan dan edema palpebra, Kadang mata kabur, diplopia, kadang kehilangan kemampuan visus sementara, hordeolum (bintitan).

BERBAGAI GANGGUAN ALERGI PADA DEWASA

  • Mengalami Gizi Ganda : bisa kurus, sulit naik berat badan atau kegemukan. Pada kesulitan kenaikkan erat badan sering disertai kesulitamn makan dan nafsu makan kurang. Sebaliknya pada kegemukan sering mengalami nafsu makan berlebihan
  • Kesulitan Makan dan gangguan Makan : Nafsu makan buruk atau gangguan mengunyah menelan
  • Kepala,telapak kaki atau tangan sering teraba hangat. Berkeringat berlebihan meski dingin (malam atau ac). Keringat berbau.
  • FATIQUE atau KELELAHAN : mudah lelah, sering minta gendong, Pada dewasa sering mengeluh “capek”
  • 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), atau sinusitis hindari operasi amandel yang tidak perlu atau mengalami Infeksi Telinga Waspadai dan hindari efek samping PEMAKAIAN OBAT ANTIBIOTIKA TERLALU SERING.
  • Mudah mengalami INFEKSI SALURAN KENCING. Kulit di sekitar kelamin sering kemerahan
  • Sering mengalami OVERDIAGNOSIS TBC (MINUM OBAT JANGKA PANJANG PADAHAL BELUM TENTU MENDERITA TBC / ”FLEK ”) KARENA GEJALA ALERGI MIRIP PENYAKIT TBC. BATUK LAMA BUKAN GEJALA TBC PADA ANAKBILA DIAGNOSIS TBC MERAGUKAN SEBAIKNYA ”SECOND OPINION” DENGAN DOKTER LAINNYA
  • INFEKSI JAMUR (HIPERSENSITIF CANDIDIASIS) di lidah, mulut, selangkangan, di leher, perut atau dada, KEPUTIHAN

BERBAGAI PERILAKU, GANGGUAN MOTORIK DAN GANGGUAN FUNGSI SUSUNAN SARAF PUSAT LAINNYA

  • SUSUNAN SARAF PUSAT : sakit kepala, MIGRAIN, vertigo
  • GANGGUAN TIDUR : Sulit untuk memulai tidur malam atau tidur larut malam , Tidur bolak-balik. Berbicara,tertawa,berteriak atau berjalan saat tidur, Mendadak terbangun duduk saat tidur kemudian tidur lagi, Mimpi buruk, “beradu gigi” atau gigi gemeretak atau bruxism
  • AGRESIF MENINGKAT: mudah memukul atau menampar orang lain, berlaku kasar terhadap anak , istri atau suami.
  • GANGGUAN KONSENTRASI: mudah lupa (short mempry lost), sering lupa meletakkan kunci, lupa nama teman tetapi memori lama kuat.
  • EMOSI TINGGI : mudah marah, sering berteriak, mengamuk, keras kepala, negatifisme dan mudah menyangkal (deny) sangat tinggi.
  • DEPRESI DAN MUDAH CEMAS : mudah marah, sedih berlebihan, mudah tersinggung, sering kesepian, mudah menangis meski masalahnya ringan
  • GANGGUAN KESEIMBANGAN KOORDINASI DAN MOTORIK :Jalan terburu-buru mudah tersandung kaki meja atau kaki kursi
  • GANGGUAN SENSORIS : perabaan telapak kaki dan tangan sensitif (mudah geli, mudah jijik, tidak suka memegang bulu, boneka dan binatang berbulu). Rasa perabaan sensoris kaki sangat sensitif (bila lantai kotor sedikit atau berpasir sering geli dan harus pakai sandal), sandal atau sepatu seringkali ausnya tidak rata atau tidak seimbang kiri kanan.
  • GANGGUAN ORAL MOTOR : bicara terburu-buru, cadel, gagap. GANGGUAN MENELAN DAN MENGUNYAH tapi sangat ringan dianggap normal, pilih-pilih makanan tidak sukan makanan berserat seperti daging empal, sayur tertentu.
  • IMPULSIF : banyak bicara, tertawa berlebihan, sering memotong pembicaraan orang lain, bila bicara sangat cepat banyak dan sulit berhenti. Mudah menangis dan tertawa berubah bergantian dengan cepat.

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BERBAGAI GANGGUAN YANG BELUM DIKETAHUI SEBABNYA ATAU berbagai GANGGUAN AUTO IMUN LAINNYA SERING DIPERBERAT KARENA MANIFESTASI ALERGI. Menurut berbagai penelitian berbagai gangguan ini dapat diperberat karena alergi dan hipersensitifitas makanan. Tetapi alergi atau hipersensitifitas makanan bukan sebagai penyebabnya.

  • Lupus
  • Fibromialgia
  • Irritabel Bowel Syndrome
  • Rematoid Artritis
  • Henoch Schonlein Syndrome
  • Prurigo Hebra (gangguan kulit)
  • Psoriasis
  • Epilepsi
  • Autism
  • ADHD
  • Gangguan non organik (gangguan fungsional lainnya) seperti migrain, vertigo, kejang tanpa demam dengan pemeriksaan EEG normal, (SKBE : Serangan kejang Bukan Epilepsi), gangguan konsentras, gangguan perilaku dan gangguan perkembangan lainnya
  • Berbagai Gangguan Metabolisme dan gangguan genetik lainnya

Cara Membuktikan Adanya alergi makanan

  • Bila tanda dan gejala timbul lebih dari 3 dan di sertai salah satu gangguan saluran cerna maka sangat mungkin berbagai gangguan tersebut disebabkan karena alergi atau hipersenitifitas makanan.
  • Penanganan berbagai gangguan yang disebabkan alergi dan hipersensitifitas makanan haruslah dilakukan secara benar, paripurna dan berkesinambungan. Pemberian obat terus menerus bukanlah jalan terbaik dalam penanganan gangguan tersebut tetapi yang paling ideal adalah menghindari penyebab yang bisa menimbulkan keluhan alergi tersebut khuusunya makanan tertentu.
  • Penyebab utama adalah reaksi makanan tertentu tetapi dampaknya ringan. Namun saat yang ringan tersebut tidak dicermati akan diperberat oleh pemicu paling sering adalah infeksi virus atau fluyang sering tidak terdeteksi dan diabaikan oleh dokter sekalipun. Bila hal itu penyebabnya maka setelah 5 hari akan membaik. Tetapi akan timbul lagi bila terkena infeksi virus lagi bila di rumah ada yang sakit lagi
  • Bila berbagai gangguan bila disertai manifestasi alergi lainnya sangat mungkin alergi makanan berperanan sebagai penyebabnya.
  • Penanganan terbaik pada penderita alergi makanan dengan gangguan tersebut adalah adalah dengan menghindari makanan penyebabnya. Pemberian obat anti alergi dan obat untuk saluran cerna penghilang rasa sakit dalam jangka panjang adalah bukti kegagalan dalam mengidentifikasi makanan penyebab alergi.
  • Ikuti langkah-langkah dalam Tes Alergi Makanan : Challenge Tes – Eliminasi Provokasi Makanan Terbuka
  • Kemudian lakukanlah eliminasi provokasi makanan seperti yang tersebut di atas selama 3 minggu di bawah pengawasan dokter ahli. Bila berbagai gangguan tersebut membaik maka dapat dipastikan bahwa anda mengalami alergi makanan. Dan berbagai gangguan yang ada selama ini disebabkan karena alergi makanan. Tetapi dalam melakukan eliminasi makanan selama 3 mingu tersebut haris disiplin dan ketat. Gangguan alergi biasanya masih sering timbul dalam pelaksanaan eliminasi makanan tersebut bila penderita tidak disiplin dan mengalami infeksi virus yang sering tidak terdeteksi seperti badan hangat, bersin, hidung buntu dan sebagainya.
  • Pencetus atau hal yang memperberat (bukan penyebab) adalah udara dingin, stres, aktifitas, udara panas. Bila terdapat pencetus tersebut manifestasi alergi tidak akan timbul bula penyebab alergi makanan dihindari
  • Penyebab lain yang memperberat tersebut adalah Saat terkena infeksi seperti demam, batuk, pilek atau muntah dan infeksi lainnya atau Saat terdapat gangguan hormonal : menstruasi, kehamilan dan paska persalinan
  • Bila setelah 3 minggu berbagai keluhan yang ada tersebut membaik maka pendapat yang selama ini menyebutkan bahwa “Aku Tidak Alergi Makanan Adalah Tidak Benar”

BACA ARTIKEL ALERGI DEWASA LAINNYA

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

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ARTIKEL TEREKOMENDASI:Kumpulan Artikel Alergi Pada Bayi, Dr Widodo Judarwanto Pediatrician

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ARTIKEL FAVORIT:100 Artikel Alergi dan Imunologi Paling Favorit

Current Allergy Immunology by Widodo Judarwanto

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