Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of our study was to report the frequency of sensitization to hairdressing allergens in a group of patients with contact dermatitis, in whom previous treatments with hair dyes or permanent wave solutions were suspected to be the cause. 49 of 261 hairdressers' clients (18.7%), who were patch tested with the hairdressers' screening series in the years 1985-1990, showed one (27) or more (22) positive reactions to hairdressing chemicals. This study confirms hair dyeing to be the procedure associated with the highest risk of sensitization among hairdressers' clients. Among hair dye allergens, PPD is the most frequent sensitizer (7.3%). A low rate of sensitization to the PPD derivatives PAP, ONPPD and PTD was detected in these clients, there being no differences in the frequency of sensitization to the 3 substances (4.2%, 4.6% and 4.6%, respectively). Only 0.4% of clients were positive to resorcinol, while pyrogallol showed a 2.3% rate of sensitization. Sensitization to GMTG was found in 3.3% of patients. ATG was an infrequent sensitizer (1.1%). Allergic contact dermatitis due to APS is quite rare (2.7%), in view of the widespread use of this compound. A positive open patch test in 1 hairdressers' client, who complained of generalized urticaria after hair bleaching, confirmed the diagnosis of immediate contact reaction due to APS. Sensitization to hairdressing allergens among consumers (18.7%) is possibly more frequent than sensitization to other cosmetic ingredients. We previously detected a 14.3% rate of sensitization to cosmetic ingredients in patients with suspected allergic contact dermatitis caused by cosmetics. On the other hand, reactions to cosmetic ingredients were also common in our patients. This may indicate that hairdressers' clients make greater use of cosmetics than average.
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PMID:Contact dermatitis in hairdressers' clients. 836 66

The epidermis, as the body's first line of defense against many pathogens, reacts in a variety of ways to the assault of foreign antigens. Allergic contact dermatitis, drug eruption, urticaria, and erythema multiforme are examples. The clinician must usually rely on clinical evidence for diagnosis. The first therapeutic strategy is to identify and avoid the antigen or drug causing the reaction. Beyond this, therapy consists of relief of symptoms in mild to moderate cases. In severe cases, systemic treatment can be helpful, but the therapeutic options and their efficacy are limited.
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PMID:Allergic and reactive dermatoses. How to identify and treat them. 182 18

Because the pathophysiology of many drug eruptions is unknown, the presumption that a drug eruption is due to immune mechanisms is often based on clinical features. The drug exanthem, urticaria, and contact dermatitis are the most common adverse cutaneous reactions to medications. Drug exanthems occur in 2 to 3 per cent of medical inpatients and are most commonly caused by antibiotics and blood products. The incidence of drug exanthems is much higher in certain patient populations (for example, patients with AIDS treated with trimethoprim-sulfamethoxazole). Urticaria is the second most common allergic cutaneous reaction to drugs. Individual urticarial lesions last for less than 24 hours and do not leave hyperpigmentation or scarring. Urticaria not accompanied by systemic symptoms should not be treated with systemic corticosteroids or parenteral epinephrine. Allergic contact dermatitis is commonly caused by neomycin, benzocaine, ethylenediamine, diphenhydramine, and transdermal patches. The clinical spectrum of other, less common drug eruptions is wide. Toxic epidermal necrolysis, erythema multiforme, and fixed drug eruptions share similar pathologic features, are caused by many of the same drugs, and may have a similar pathogenesis. Photoallergic drug reactions require the interaction of drugs, UV irradiation, and the immune system. Drugs implicated in causing photoallergy include thiazide diuretics, sulfonamides, and phenothiazines. Eruptions seen in serum sickness include the drug exanthem, urticaria, vasculitis, urticarial vasculitis, and erythema multiforme. Identifying and discontinuing the responsible drug is usually essential for successful therapy of drug eruptions.
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PMID:Allergic cutaneous reactions to drugs. 252 77

Polyfunctional aziridine (PFA) is increasingly used as a water-based cross-linker in 2-component paints, paint primers, lacquers, topcoats and other protective coatings. The cross-linker (PFA hardener) is made by reacting multifunctional acrylic monomer with a highly reactive aziridine compound. During 1992-1993, we came across 2 patients with allergic patch test reactions provoked by PFA hardener. One of the patients was a parquet layer, and the other a printer. Allergic contact dermatitis (ACD) was diagnosed by positive allergic patch test reactions to PFA hardener in a dilution series in pet.:0.3%-1% gave ++ to allergic reactions in both patients, whereas 0.1% gave a weak (+) or questionable reaction (?+), respectively. The methacrylate patch test series was negative in both patients, although gas chromatography/mass spectrometry analysis showed that PFA hardener contained 0.3% of trimethylolpropane triacrylate (TMPTA), a multifunctional acrylic monomer. One of the patients also had symptoms of contact urticaria, and a prick test with PFA hardener (1% aq.) induced a histamine-sized prick test reaction. The positive reactions with the PFA hardener and the negative reactions with the starting chemicals and additives in PFA, namely acrylates, propyleneimine and dimethylethanolamine, indicate that PFA caused ACD. This is in accordance with our previous observations, but differs from the reports of others, whose patients had been sensitized to acrylates present as remnants in the PFA hardener. As test substance, 0.5% PFA hardener in pet. is recommended for patch testing. Testing should be performed in patients with contact dermatitis if exposure to PFA has occurred. Skin prick tests may be of help to detect contact urticaria.
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PMID:Occupational allergic contact dermatitis and contact urticaria caused by polyfunctional aziridine hardener. 856 84

The skin represents a unique immunologic organ poised to protect the host from invading organisms and environmental antigens. The skin is also an important target for a variety of allergic and autoimmune responses. Mast cells are key to the pathogenesis of urticaria, angioedema, and mastocytosis. Atopic dermatitis is the consequence of an immunoregulatory abnormality resulting in a skin-directed T helper type 2 response. Allergic contact dermatitis is an example of classic delayed type hypersensitivity. Circulating autoantibodies against the epidermis are a key mechanism by which bullous skin diseases occur.
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PMID:Allergic and immunologic skin disorders. 939 53

The selection of dental materials for specific treatment purposes is primarily based on their physical properties. The composition of materials available indicates that there is the potential for adverse biological effects. The amounts of substances released are usually too low to cause any overt systemic toxic effects. However, many of the chemicals used in dentistry are irritating and may cause local damage. Also, in reactions mediated via the amplifying mechanisms of the immune system, small amounts may lead to clinical manifestations of allergic contact dermatitis and urticaria. A special problem in the diagnosis of adverse events occurs when intraoral exposure leads to generalized urticarial reactions. Due to a low level of suspicion, extraoral reactions are rarely associated with dental treatment modalities. Occupational dermatoses represent a serious problem, especially the development of an allergy to constituents of the resin-based filling materials and adhesives. The monomers of resin-based materials are volatile and penetrate latex and vinyl gloves easily. Allergic contact dermatitis related to resin-based materials may be occupationally disabling.
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PMID:Skin and mucosal reactions associated with dental materials. 958 4

Allergic contact dermatitis (ACD) in children is underrecognized. It is often confused with antibody-mediated allergies such as urticaria or allergic rhinitis, but the mechanism in ACD involves T lymphocytes and not antibody. Surprisingly, sensitization to common allergens is likely to occur in infancy. All contact allergens are weak allergens requiring repeated exposure over long periods of time. Detection of specific allergens is by epicutaneous (patch) testing and will provide the basis for allergen avoidance therapeutic strategies.
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PMID:Allergic contact dermatitis. 1094 64

Allergic contact dermatitis caused by acyclovir is rare. We report the 5th case of systemic acyclovir reaction subsequent to acyclovir contact dermatitis, with investigations made to determine an alternative antiviral treatment. A 23-year-old woman, after dermatitis while using Zovirax cream, went on to develop urticaria after oral acyclovir. Patch tests were performed with the components of Zovirax cream (acyclovir, propylene glycol and sodium lauryl sulfate) and with other antiviral drugs. Patch tests were positive to Zovirax cream, acyclovir, valacyclovir and propylene glycol. Patch and prick tests with famciclovir were negative, but its oral administration caused an itchy erythematous dermatitis on the trunk and extremities. Our patient developed a systemic acyclovir reaction subsequent to acyclovir allergic contact dermatitis, with cross-reactions to valacyclovir and famciclovir. Their common chemical structure is the 2-aminopurine nucleus. It is probably this part of the molecule that provokes both contact allergy and systemic reactions. The only antiviral drugs not having this core are foscarnet and cidofovir, and these could therefore be alternatives.
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PMID:Systemic acyclovir reaction subsequent to acyclovir contact allergy: which systemic antiviral drug should then be used? 1467 12

There is little literature regarding conventional patch tests and photopatch tests to oxybenzone resulting in both immediate- and delayed-type hypersensitivity reactions. A patient was patch-tested and photopatch-tested to various sunscreen chemicals. Both immediate- and delayed-type hypersensitivity reactions were observed with oxybenzone. The positive patch tests were also photoaccentuated. Oxybenzone, a common sunscreen allergen, can result in both contact urticaria and delayed-type hypersensitivity on both conventional patch testing and photopatch testing. Allergic contact dermatitis to sunscreen chemicals has traditionally included contact urticaria, allergic contact dermatitis, and photoallergic contact dermatitis. Due to the recognition of p-aminobenzoic acid (PABA) and its esters as sensitizers, the presence of benzophenones in "PABA-free" sunscreens has become more prevalent, especially in sunscreens with a sun protection factor (SPF) greater than 8. In our patient, immediate- and delayed-type hypersensitivity reactions were seen to oxybenzone (2-hydroxy-4-methoxybenzophenone, 2-benzoyl-5-methoxyphenol, benzophenone-3, Eusolex 4360, Escalol 567, EUSORB 228, Spectra-Sorb UV-9, Uvinul M-40) upon conventional patch testing and photopatch testing.
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PMID:Contact urticaria, allergic contact dermatitis, and photoallergic contact dermatitis from oxybenzone. 1474 20

Allergic contact dermatitis from poison ivy, oak, or sumac is common among people who work or exercise outdoors. The plants, classified in the genus Rhus or Toxicodendron, contain allergens that can cause reactions ranging from mild pruritus to severe urticaria or generalized maculopapular eruptions. Initial management includes cleansing, cold compresses, and, possibly, oral antihistamines for symptomatic relief. Topical corticosteroids are given for localized nonfacial eruptions; systemic corticosteroids are used for severe eruptions. Prevention involves avoiding contact with the plants and washing exposed skin within 2 hours.
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PMID:Poison ivy, oak, and sumac dermatitis identification, treatment, and prevention. 2008 17


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