Papular Urticaria, Pressure Urticaria and Solar Urticaria
Widodo Judarwanto. Children Allergy Online Clinic, Jakarta Indonesia
Urticaria (hives) is a vascular reaction of the skin marked by the transient appearance of smooth, slightly elevated patches (wheals) that are erythematous and that are often attended by severe pruritus. Individual lesions resolve without scarring in several hours. Most cases of urticaria are self-limited and of short duration; the eruption rarely lasts more than several days, it but may be recurrent over weeks. Chronic urticaria is defined as urticaria with recurrent episodes lasting longer than 6 weeks).
The development of urticaria is often an isolated event without systemic reaction. Rarely, it can be a prelude to the development of an anaphylactic reaction. If any features of anaphylaxis (eg, hypotension, respiratory distress, stridor, gastrointestinal distress, swallowing problems, joint swelling, joint pain) are present, immediate medical intervention should occur.
New-onset episodes of urticaria can be associated with identifiable causes, and the method of exposure (ie, direct contact, oral or intravenous [IV] routes) can be deduced by taking a careful history. Although clinically distinctive, urticaria may be confused with a variety of other dermatologic diseases that can be similar in appearance and are pruritic, including atopic dermatitis (eczema), maculopapular drug eruptions, contact dermatitis, insect bites, erythema multiforme, pityriasis rosea, and others. Usually, however, the experienced clinician is able to distinguish these conditions from urticaria because of the lesions’ hallmark appearance , a lack of epidermal change, the intense pruritus, the presence of an advancing edge and a receding edge, the complete blanching of the lesions with pressure, and are the transient nature of the lesions
Papular urticaria is a common and often annoying disorder manifested by chronic or recurrent papules caused by a hypersensitivity reaction to the bites of mosquitoes, fleas, bedbugs, and other insects. Individual papules may surround a wheal and display a central punctum. Although the overall incidence rate is unknown, papular urticaria tends to be evident during spring and summer months; in some climates, such as that in San Francisco, California, this condition may affect children throughout the year. In addition, despite no known racial or sex predisposition, certain ethnic groups (specifically Asians) may be more predisposed to more intense reactions, and a small Nigerian study reported a slight female predominance for skin diseases such as papular urticaria and atopic dermatitis.
Papular urticaria is a common reaction to insect bites. It is more common in children than in adults. Crops of very itchy red bumps, 0.2 – 2 cm in diameter, appear every few days during the summer or autumn months. Sometimes each spot develops a fluid-filled blister up to one centimetre in diameter. They are most often on the legs and other uncovered areas such as forearms and face but sometimes they are scattered in small groups all over the body. It is difficult not to scratch the spots, which become crusted and may get infected – they are then pussy and sore. Sometimes one new spot provokes all the old ones to come up again and itch intensely. The spots seem to remain for a few days to a few weeks and can leave persistent marks or scars, especially if they have been scratched deeply.
Papular urticaria may clear up on holiday or on moving house. One or several members of the family may be affected. Occasionally the eruption can clear up for years and then recur unexpectedly. It is not associated with any internal complaint and is never a serious disease.
This eruption is primarily self-limited, and children eventually outgrow this disease, probably through desensitization after multiple arthropod exposures. However, adults can be affected, albeit at a much lower rate.
Papular urticaria is generally regarded to be the result of a hypersensitivity or id reaction to bites from insects, such as mosquitoes, gnats, fleas, mites, bedbugs, caterpillars, and moths. Varicella vaccines have also been implicated. However, it is unusual to identify an actual culprit in any given patient.
Papular urticaria is thought to be an allergic reaction to insects in the environment. Often after a few years the person becomes desensitized to these insects and the reaction dies down. A bite isn’t usually noticed and it is thought that the reaction can occur simply from skin contact with parts of the insect such as its faeces and eggs – this accounts for spots in unexpected places. The most common identified causes are insects that live on cats and dogs, such as fleas and mites.
Fleas are easily seen with the naked eye but can be difficult to get rid of. Mites are too small to see but are equally common. The animal gets repeatedly infested and has to be treated with flea powder or a leave-on preparation such as fipronil every few weeks. Unfortunately flea collars are not very effective. Fleas produce many eggs, which become larvae and pupae. The average cat has only twenty fleas, but is surrounded by 20,000!
Not everyone with papular urticaria has pets, and it can be nearly impossible to work out what a patient is reacting to. There have been reports of allergy to bird mites, carpet beetles, caterpillars and insects that live in masonry disturbed by renovation. A similar disorder, called ‘chronic papular urticaria’ or ‘prurigo simplex’ in adults is not due to insects; the cause is unknown. It may be a variant of atopic dermatitis.
The histopathologic pattern in papular urticaria consists of mild subepidermal edema, extravasation of erythrocytes, interstitial eosinophils, and exocytosis of lymphocytes. These findings suggest a pathophysiologic process that is immunologically based. Morphologic and immunohistochemical evidence suggest that a type I hypersensitivity reaction plays a central role in the pathogenesis of papular urticaria. The reaction is thought to be caused by a hematogenously disseminated antigen deposited by an arthropod bite in a patient who is sensitive. This theory is supported by the fact that these lesions can and often do occur in areas away from the bites. The putative antigen is unknown.
The presence of immunoglobulin and complement deposits in the skin of some patients with papular urticaria suggests that the lesions may be due to a cutaneous vasculitis. The deposits were most frequently seen in lesions within 24 hours of their development. The presence of granular deposits of Clq, C3, and immunoglobulin M (IgM) in superficial dermal blood vessel walls suggests that immune complexes (IgM aggregates) may be primarily involved in the pathogenesis, with complement activation initiated by Clq through the classic pathway. A T helper 2 (Th2) shift may be present, similar to what is observed in atopy.
In a study of the specific pattern of flea antigen recognition by IgG subclass and IgE during the progression of papular urticaria caused by flea bite, variations in the antibody responses of both subclasses to flea antigens were identified. Among these 25 patients, those with 2-5 years of papular urticaria had more IgE bands than patients with shorter or longer durations of symptoms. Thus, the predominant specific antibody isotypes appear to vary according to the time elapsed from the onset of fleabite-induced papular urticaria
Children, adult males, nonlocal inhabitants, and those belonging to urban or periurban areas may be more vulnerable to papular urticaria. Patients usually report chronic or recurrent episodes of a papular eruption that tends to occur in groups or clusters associated with intense pruritus. The most common first appearance is of papules and urticarial plaques in clusters over exposed and covered parts of the body.
The eruption is characterized by crops of symmetrically distributed pruritic papules and papulovesicles. The lesions can also appear in an area localized to the site of insect bites, but they occur on any body part. The lesions tend to be grouped on exposed areas (see the image below), particularly the extensor surfaces of the extremities. Scratching may produce erosions and ulcerations. Secondary impetigo or pyoderma is common.
Pressure urticaria also known as delayed pressure urticaria is a physical urticaria caused by pressure applied to the skin, and is characterized by the development of swelling and pain that usually occurs 3 to 12 hours after local pressure has been applied. Delayed pressure urticaria is a type of chronic hives called physical urticaria because the hives are caused by a certain stimulus on the body. In this case, the stimulus is pressure that’s applied to the skin. Delayed pressure urticaria is common. One investigator found that 37% of people with chronic hives had this type of urticaria. Delayed pressure urticaria is diagnosed based on the appearance of the rash in areas where pressure has been applied to the skin. No lab tests help diagnose this physical urticaria.
Patients with urticaria for more than 6 weeks are given the diagnosis of chronic urticaria. This distinction is important because an inciting event or etiology is not identified for the majority of patients with chronic urticaria, giving rise to the often-used term, chronic idiopathic urticaria (CIU). A proportion of patients with chronic urticaria have physical urticaria, which is urticaria incited by a physical stimulus such as cold, vibration, or pressure. Also see Urticaria, Cholinergic; Urticaria, Contact Syndrome; Urticaria, Dermographism; and Urticaria, Solar.
Pressure urticaria is an uncommon form of physical urticaria. Pressure urticaria may occur immediately (within minutes) after a pressure stimulus, however, more commonly, pressure urticaria develops after a delay of 4-6 hours after a pressure stimulus; hence, the designation delayed pressure urticaria (DPU) is used. The wheals may last for 8-72 hours. The hands, feet, trunk, buttocks, legs, and face are the most common areas affected. Lesions can be induced by a variety of stimuli, including standing, walking, wearing of tight clothes, or sitting on a hard surface.
The pathogenesis of delayed pressure urticaria is unknown. No allergen can usually be identified. Mast cells and histamine release are believed to play roles because the injection of compound 48/80, which causes depletion of mast cell mediators, prevents the induction of lesions in the injected area. Histamine levels are increased in lesional skin, and intracellular histamine levels are decreased in peripheral white blood cells. Despite these findings and the finding of increased stimulated histamine release, histamine is not likely to be the sole mediator in pressure urticaria, given the relative unresponsiveness of the condition to antihistamine treatment.
Other possible mediators include eosinophils, given the elevated numbers of eosinophils, eosinophil cationic protein (ECP), and eosinophil cationic factor (ECF) found in biopsy specimens from some patients with delayed pressure urticaria, particularly bullous delayed pressure urticaria. Elevated concentrations of interleukins 5 and 6 and leukotrienes have also been found in lesional skin of pressure urticaria patients. Abnormalities in platelets and fibrin/fibrinolysis are also being investigated.
Delayed pressure urticaria is considered a rare entity. Some investigators suggest that delayed pressure urticaria is more prevalent but is not consistently recognized. One study of 2310 patients with urticaria, seen over 32 years, found the prevalence of delayed pressure urticaria to be 2%. Depending on the severity of the disease and the associated symptoms, delayed pressure urticaria can be disabling, especially in patients who perform manual labor. Delayed pressure urticaria is a chronic disease, with a mean duration of 9 years (range, 1-40 y). The morbidity of delayed pressure urticaria varies, depending on the severity and the response to treatment.
Quality-of-life (QOL) tools have demonstrated an impairment in QOL scores similar to patients with cardiac disease or chronic dermatoses such as psoriasis and atopic eczema. QOL scores were lowest for energy, social isolation, emotional reaction, and sleep disturbance. The dimension of daily living activities was more profoundly impaired in patients with chronic idiopathic urticaria than in those with atopic eczema or psoriasis. Delayed pressure urticaria is slightly more common in men than in women. The peak age of onset of delayed pressure urticaria is in the 20s and 30s (range, 5-63 y)
Areas of the body that often develop delayed pressure urticaria include:
- Under the waistband of tight clothes
- Under the elastic part of socks
- Buttocks after sitting for a long time on a hard surface
- Feet in tight shoes
- Soles of feet after walking or climbing a ladder
- Palms after manual labor
The hives of delayed pressure urticaria are deeper and more painful than hives caused by other stimuli and they start 2 to 6 hours after pressure is applied to the body. The hives last from 8 to 72 hours and many people get a low-grade fever, fatigue, chills, muscle aches, and headaches with the hives. The disease is chronic, lasting on average for 9 years.
Solar urticaria (SU) is an abnormal reaction to sunlight or artificial light. When exposed to light, the skin cells of someone with solar urticaria release potent chemicals (including histamine), causing their blood vessels to open and fluid to collect within the skin. Their skin feels itchy and has red patches, which may be swollen. These may look like weals or a nettle rash, and can take up to an hour to appear after exposure to light, then coming on quickly and settling within a similar period. There is no permanent change to the skin.
Solar urticaria is a rare photodermatosis characterized by pruritus, stinging, erythema, and wheal formation after a brief period of exposure to natural sunlight or an artificial light source emitting the appropriate wavelength. Initially described by Merklen in 1904, solar urticaria is localized to exposed areas of the skin, although it can occur through thin clothing. Solar urticaria disappears within several minutes to a few hours, without pigmentary change if further sun exposure is avoided. Solar urticaria can be quite disabling and difficult to manage. Solar urticaria often has a sudden, dramatic onset, and little information is available regarding its duration and eventual outcome.
Solar urticaria is possibly caused by an antigen-antibody reaction. Solar irradiation may induce an antigen in the serum or plasma of affected individuals. Intradermal injection of serum from a solar urticaria patient passively, but not consistently, transfers the condition to a healthy individual.
The following types of solar urticaria have been proposed:
- Type I: This type is an immunoglobulin E (IgE)–mediated hypersensitivity to specific photoallergens generated only in solar urticaria patients.
- Type II: This type is an IgE-mediated hypersensitivity to nonspecific photoallergens found in both solar urticaria patients and healthy individuals.
Passive transfer test findings are positive in patients with type II solar urticaria, but they may be positive or negative in those with type I.
The wide action spectrum (290-800 nm) implicated for this condition may be related to the specific photoallergen and its molecular weight. Diversity in the reported action spectra may be due to differences in photoallergens. In addition, spectra believed to be responsible for either inhibition or augmentation of the reaction have been detected. Complex interactions occur between the various wavelengths and the photoallergen.
The result of these interactions is mast cell degranulation with subsequent histamine release. Mediators other than histamines may also be involved. Inhibition of solar urticaria with light suppresses the wheal-flare response following intradermal injection of photoactivated autologous serum but does not suppress the wheal and flare associated with compound 48/80.
Solar urticaria comprises only 4% of US patients with photosensitive disorders. Solar urticaria comprises 5.3% of the cases of photosensitive dermatoses worldwide. The mortality rate for solar urticaria has not been determined. In some cases, skin eruption is accompanied by symptoms such as headache, nausea, vomiting, bronchospasm, and syncope.
Solar urticaria occurs in all races. A slight female predilection is noted for solar urticaria. Solar urticaria has a wide range of onset (10-70 y). The mean age of onset for solar urticaria is 35 years, but it has been reported to occur in infanc
Management and Prevention
- The treatment of papular urticaria should be conservative and is symptomatic in most cases. Mild topical steroids and systemic antihistamines for relief of the itching that often accompanies this condition may be used. On occasion, papular urticaria may be severe enough to warrant the use of short-term systemic corticosteroids. If secondary impetigo occurs, topical or systemic antibiotics may be needed. Note that the use of insect repellents while the patient is outside and the use of flea and tick control on indoor pets are necessary when these individuals are being treated for papular urticaria.
- Rigorous use of an effective insecticide may prevent insect bites and, accordingly, papular urticaria. Insecticides containing diethyltoluamide (DEET) are among the most beneficial. For safety purposes, topical insecticides used on infants and children should be in accordance with their age. An oral desensitization vaccine has been attempted, but the vaccine was deemed ineffective and the study sample size was too small for statistical significance
- Topical steroid cream should be applied as soon as the itchy spots appear.
- Antihistamine tablets at night may be useful for severe itching.
- Apply antiseptic cream if the spots get infected.
- Clear the house, and if possible work place or school, of insects.
- Use a kennel and carpet spray containing a pyrethroid, followed by vacuuming. Apply a long lasting insect growth regulator in November each year.
- Keep pets outside.
- Wear fully covering clothing.
- Apply insect repellents to exposed skin to prevent insect bites outdoors.
- Patients should attempt to limit pressure stimuli. A simple intervention is to broaden the handles on heavy items or straps on clothing to disperse the pressure over a larger area. However, avoidance is not easy and may not be helpful in patients with moderate-to-severe disease.
- Antihistamines can reduce the severity of symptoms and are helpful in controlling associated chronic idiopathic urticaria (CIU).
- Systemic corticosteroids and/or nonsteroidal anti-inflammatory drugs (NSAIDs) produce variable responses. Patients with improvement with systemic steroids often relapse upon discontinuation. The adverse effects of steroids must also be considered and managed. Patients may already be taking H2 blockers in an attempt to manage their urticaria; however, these are also used to treat gastritis from systemic steroids. Long-term steroid use also affects the bones, and patients are often advised to take calcium with vitamin D daily, with additional consideration of adding a bisphosphonate such as alendronate.
- Other possible therapies include colchicine, dapsone, sulfasalazine, and montelukast. Case reports have demonstrated successful treatment with chloroquine. Cyclosporine, intravenous immunoglobulin, and omalizumab have each been used in a small number of patients with severe and refractory disease. Consult a dermatologist or allergist for evaluation for other causes of urticaria. Restrictions in activity depend on the severity of the disease.
- The results of treatment of delayed pressure urticaria (DPU) are relatively disappointing. Antihistamines are helpful but may not completely control symptoms of delayed pressure urticaria. Some authors have used up to 4 times the recommended dose of nonsedating antihistamines to achieve control.
- Combination therapy may decrease disease activity. Reported successful adjunctive agents include leukotriene antagonists (eg, montelukast, zafirlukast) and H2-receptor antagonists (eg, famotidine, ranitidine).
- Prednisone and NSAIDs produce variable responses. NSAIDs as a treatment may be suboptimal because they, along with aspirin, may worsen urticaria and angioedema. Indomethacin has not demonstrated efficacy for the treatment of delayed pressure urticaria. Similarly, colchicine has been ineffective as a therapy.
- Prednisone has some clinical efficacy, but long-term therapy is problematic because of its many adverse effects. One study of a small group of patients showed efficacy of high-potency topical steroids for reducing edema, erythema, and pruritus associated with delayed pressure urticaria lesions.
- Antihistamines, H1 blockers
These agents may be useful in helping control symptoms of chronic urticaria, which frequently coexists with delayed pressure urticaria. Many H1 antagonists are metabolized through the P450 system. Important exceptions include cetirizine, levocetirizine, and fexofenadine.
- Levocetirizine (Xyzal)
Histamine1-receptor antagonist. Active enantiomer of cetirizine. Peak plasma levels reached within 1 h and half-life approximately 8 h. Available as a 5-mg breakable (scored) tab and 0.5 mg/mL oral sol. Indicated for uncomplicated skin manifestations of chronic idiopathic urticaria
- Fexofenadine (Allegra)
Nonsedating second-generation medication with fewer adverse effects than first-generation medications. Competes with histamine for H1 receptors on GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate. Available in qd and bid preparations.
- Diphenhydramine (Benadryl)
First-generation antihistamine with anticholinergic effects that binds to H1 receptors in the CNS and the body. Competitively blocks histamine from binding to H1 receptors. Has significant antimuscarinic activity and penetrates CNS, which causes pronounced tendency to induce sedation. Approximately half of those treated with conventional doses experience some degree of somnolence. A small percentage of children paradoxically respond to diphenhydramine with agitation.
For symptomatic relief of pruritus caused by release of histamine in inflammatory reactions.
- Loratadine (Claritin)
Selectively inhibits peripheral histamine H1 receptors.
- Desloratadine (Clarinex)
Long-acting tricyclic histamine antagonist selective for H1 receptor. Major metabolite of loratadine, which, after ingestion, is extensively metabolized to active metabolite 3-hydroxydesloratadine.
- Cetirizine (Zyrtec)
Selectively inhibits histamine H1 receptor sites in blood vessels, GI tract, and respiratory tract, which, in turn, inhibits physiologic effects that histamine normally induces at H1 receptor sites. Once-daily dosing is convenient. Bedtime dosing may be useful if sedation is a problem.
- Hydroxyzine (Atarax, Vistaril)
Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.
- Doxepin (Adapin, Sinequan)
A tricyclic antidepressant that has potent H1-blocking activity, making it quite useful for urticaria. However, has very potent sedative and anticholinergic effects. Can be quite effective if used at bedtime because sedative effects can help patients with pruritus sleep.
- Antihistamines, H2 blockers
Can be used as an adjunctive agent to H1 antagonist therapy.
- Famotidine (Pepcid)
H2 antagonist that when combined with an H1 type may be useful in treating allergic reactions that do not respond to H1 antagonists alone.
- Ranitidine (Zantac)
Second-generation agent that is effective in urticaria. Tolerated very well, with a rate of sedation that is not significantly different from placebo.
- Leukotriene receptor antagonists
Small reports have demonstrated the efficacy for delayed pressure urticaria of leukotriene antagonists, alone or in combination. Other forms of chronic urticaria have not demonstrated similar responses to this treatment.
- Montelukast (Singulair)
Leukotriene inhibitors can be a helpful addition to asthma and allergic rhinitis not well controlled with H1-receptor blockers and inhaled corticosteroids.
- Zafirlukast (Accolate)
Inhibits effects by leukotriene receptor, whose activity has been associated with airway edema, smooth muscle contraction, and cellular activity associated with symptoms.
These agents have been used with variable success for their anti-inflammatory properties.
- Prednisone (Deltasone, Sterapred)
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.
- Corticosteroids, topical
Some small studies have shown efficacy in reducing the size, erythema, and pruritus associated with pressure urticaria lesions.
- Clobetasol propionate (Clobex, Olux, Embeline, Temovate)
Class I superpotent topical steroid; suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction. Decreases inflammation by stabilizing lysosomal membranes, inhibiting PMN leukocytes and mast cell degranulation.
- Nonsteroidal anti-inflammatory drugs
NSAIDs are the most commonly used medications to control mild to moderate pain and to decrease inflammation. Sulfasalazine, steroids, and immunosuppressive agents are sometimes used. These agents have been used with variable success. NSAIDs can also be a nonimmunologic trigger of mast cell degranulation and subsequent urticaria.
- Ibuprofen (Ibuprin, Advil, Motrin)
NSAID with analgesic, anti-inflammatory, and antipyretic properties. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
- Naproxen (Aleve, Naprelan, Anaprox)
Inhibits inflammatory reactions and pain by decreasing activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.
- In rare systemic cases of solar urticaria, supportive medical measures to maintain blood pressure and adequate ventilation may be required if extensive cutaneous surfaces are simultaneously involved. One case report describes 2 cases of idiopathic solar urticaria treated with intravenous immunoglobulin, with durable remissions of 13 months and 4 years, respectively. Treatment was with 2 g/kg over several 5-day courses approximately 1 month apart.
- Another case report also describes successful treatment of solar urticaria with intravenous immunoglobulin and suggests it should be discussed as an option if high-dose antihistamines provide unsatisfactory results
- Treatment of solar urticaria can be frustrating. A combination of different modalities is often necessary, but the success of these methods is highly variable. Taking measures to avoid or minimize sun exposure is the most important step for patients with solar urticaria. Unfortunately, this often requires major adjustments in lifestyle, which might be impractical for some patients.
- Avoid sunlight when possible, particularly between the hours of 11am and 3pm.
- Use ‘protective’ clothing, such as a wide-brimmed hat, long-sleeved cotton top, and trousers.
- Apply high-protection, broad-spectrum sun barriers frequently.
- Antihistamine tablets can help to abolish or partially induce a remission of the condition in 60 per cent of subjects.
- Phototherapy or desensitisation phototherapy can be used to artificially toughen the skin of those affected by the condition. Patients are usually treated three to five times per week, receiving a total of 15 exposures. The result is skin thickening and pigmentation, which can improve a patient’s tolerance to light.
- Occasionally, specialised forms of treatment are needed.
- Plasmapheresis – a technique in which some of the patient’s blood plasma is removed by machine and the red blood cells are then returned to the patient’s circulation. This removes a circulating factor from the blood that may be involved in causing the urticaria, and is demonstrably present in a small proportion of patients. The technique is still being evaluated and is not always effective.
- Medicines that suppress the immune system– such as prednisolone and ciclosporin may be effective but because of their potential side effects, their use is restricted to the most severely affected people
Because solar urticaria involves IgE-mediated mast cell degranulation with consequent histamine release, the first line of treatment consists of long-acting, nonsedating H1-receptor blockers. Often, such agents achieve a protective factor of 10 or more. The extent to which this is useful depends on the severity of the disease itself. For example, someone who gets hives after just a few seconds of sun exposure is unlikely to benefit from antihistamine monotherapy. A patient requiring 10 minutes or more of exposure would show more benefit. Antihistamines seem to block wheal response and minimize pruritus, but they do not entirely eliminate an erythematous reaction. This tendency should be explained to the patient
- Cetirizine (Zyrtec)
Forms complex with histamine for H1-receptor sites in blood vessels, GI tract, and respiratory tract
- Fexofenadine (Allegra)
Competes with histamine for H1 receptors in GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate
- Loratadine (Claritin)
Selectively inhibits peripheral H1 receptors
- Desloratadine (Clarinex)
Long-acting tricyclic histamine antagonist selective for H1 receptor. Relieves nasal congestion and systemic effects of seasonal allergy. A major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine
Used to treat certain photosensitive eruptions, including solar urticaria. Efficacy is unpredictable
- Hydroxychloroquine (Plaquenil)
Inhibits chemotaxis of eosinophils and locomotion of neutrophils. Impairs complement-dependent antigen-antibody reactions.
Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate
- Histamine H2-receptor antagonists
Usually given in addition to H1 blockers.
- Ranitidine (Zantac)
H2 antagonist that, when combined with H1 type, may be useful in treating allergic reactions that do not respond to H1 antagonists alone.
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