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)

A woman with cutaneous vasculitis had a severe bullous eruption that was suggestive of erythema multiforme. The patient also had a history of recurrent urticaria that continued intermittently for over a year of follow-up examination. Skin biopsy specimens of both urticarial and erythema and multiforme lesions showed leukocytoclastic vasculitis. An illness resembling systemic lupus erythematosus (SLE) is suggested by transient, low-titer, positive antinuclear antibody tests, persistent deposits of immunoglobulin and complement in normal skin, arthralgias, circulating immune complexes, and chronic hypocomplementemia. This case is similar to cases previously reported as "hypocomplementemic vasculitis," an "unusual SLE-related syndrome," and "urticaria with vasculitis."
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PMID:Urticarial vasculitis: report of a case and review of the literature. 15 33

Erythema multiforme developed in an 80-year-old man following the use of scopolamine hydrobromide ophthalmic drops. The erythema multiforme cleared when the medication was discontinued and recurred on challenge. Later, he was given tropicamide, an anticholinergic ophthalmic preparation that, like scopolamine, has a tropic acid residue. Within 15 minutes an immediate hypersensitivity reaction with generalized urticaria developed in the patient.
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PMID:Erythema multiforme and urticaria. Eruptions induced by chemically related ophthalmic anticholinergic agents. 15 20

Seven patients had autoimmune progesterone dermatitis. The morphological findings illustrate the polymorphous nature of the disease in which urticaria, erythema multiforme, and dyshidrosiform lesions were seen. Recurrence of the eruption five to ten days prior to the menses with spontaneous resolution following the menses was present in all cases. Intradermal skin testing to progesterone was done to confirm the diagnosis. Six of the seven patients has a history of use of artificial progestational hormones prior to the beginning of their eruption. It is postulated that the artificial progesterones may have been the trigger for the development of their autosensitivity. Treatment with conjugated estrogens resulted in remission of the disease in five of the seven cases reported.
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PMID:Autoimmune progesterone dermatitis. 19 55

One hundred forty-two allergic children aged three to 18 years were studied for evaluation of the usefulness of skin testing with influenza vaccine as a means of identifying those children who could be immunized safely despite their allergies to chickens, eggs, or feathers. One hundred twenty-eight children were fully immunized with bivalent influenza A/New Jersey/76-A/Victoria/75 vaccine. Twelve children had positive skin tests and were not immunized, and two developed positive skin tests after their first injection. One child had urticaria 8 hr later, one had a nonspecific reaction, and one had a self-limited erythema multiforme reaction eight days after the second injection. All others tolerated the procedure well. History of sensitivity to eggs was not as reliable an indication of vaccine sensitivity as skin testing with vaccine. A negative result of an intradermal skin test with a 1:100 dilution of the vaccine in saline appeared to be a reliable indicator of allergic subjects who could be immunized against influenza without fear of life-threatening acute allergic reactions.
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PMID:Safety of influenza vaccination in allergic children. 56 76

Among drug exanthemata (AE) are included allergic reactions of the cutaneous system which are of a cutaneous vascular type after hematogenous supply of the allergen, which run an immunological course according to the early, Arthus or late type. They are manifested morphologically as urticaria (monosymptomatic or a partial symptom of an anaphylactic or serum sickness syndrome), as macular or maculopapular exanthema (9 days AE) predominantly after ampicillin, as a fixed AE, as Lyell's disease (fatal in about 30% of cases), as erythema multiforme-like AE, as purpura (allergic vasculitis, "carbromal purpura"), as rare lichenoides or nodose AE and as erythematodes-like drug reactions.
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PMID:[Drug-induced allergic skin reactions of a cutaneous vascular type (author's transl)]. 80 98

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

Cutaneous adverse drug reactions are a frequent occurrence and have been reported in more than 2% of hospitalised patients. Among the most commonly involved drugs are sulphonamides, penicillins, anticonvulsants and non-steroidal anti-inflammatory drugs. Two groups of mechanisms are involved in the pathogenesis of drug reactions: immunological, with all 4 types of hypersensitivity reactions described; and non-immunological, accounting for at least 75% of all drug reactions. Besides minor skin reactions like urticaria, maculopapular rash, fixed eruptions or erythema nodosum, which are generally self-limited, severe life-threatening manifestations also occur. Erythema multiforme is secondary to drugs in half the cases; the minor form is characterised by typical target and iris lesions and is usually benign. However, a much more severe condition, erythema multiforme major or Stevens-Johnson syndrome, is associated with mucosal, ocular and visceral involvement, and carries a mortality of 5 to 15% if untreated. Toxic epidermal necrolysis, which could represent an even more dramatic form of the same disease, is characterised by severe widespread erythema, blisters and loss of skin in sheets, with denudation of more than 10% of the body surface area. This entity is frequently due to drugs. Mortality is 25 to 70%, and 90% of the survivors will have sequelae. Exfoliative dermatitis is an erythematous scaling disease often produced by drugs and carrying significant mortality. Photodermatitis may at times present with severe eczematous features. For clinical and epidemiological reasons it is important to try to identify the culprit drug following an approach based on previous experience with the drug, timing of events, patient reaction to dechallenge, patient reaction to rechallenge (if feasible), alternative aetiological candidates, and drug concentration or evidence of overdose. Management of severe skin reactions to drugs should require admission to a burn unit, where patients should be placed in warmed air-fluidised beds, receive excellent nursing care, analgesics and tranquillisers. Peeling necrotic epidermis should be removed and denuded dermis covered with biological grafts or synthetic dressings. Fluid balance must be adequately maintained; nutritional support and careful monitoring of early signs of skin infections is mandatory to ensure immediate antimicrobial treatment. Ocular care must be excellent to avoid serious sight-threatening sequelae. Steroids are presently not recommended. With these therapeutic modalities, morbidity and mortality can be markedly decreased.
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PMID:Clinical features and management of severe dermatological reactions to drugs. 213 20

Carbamazepine is an important drug used in the management of seizures, trigeminal neuralgia, and chronic pain syndromes. It has been associated with a variety of adverse skin reactions including urticaria, lichenoid eruptions, erythroderma, erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis. A 39-year-old white male had been started on carbamazepine for intractable pain which resulted from a right foot crush injury. Approximately 3 months after the start of therapy, the patient had developed a generalized skin eruption following an entire day of sun exposure. Skin biopsies revealed an atypical lymphoid infiltrate in the dermis with collections of the atypical lymphocytes within spongiotic vesicles in the epidermis, suggestive of mycosis fungoides. The patient was treated with systemic prednisone. Subsequent biopsies failed to reveal atypical lymphocytes. Previous reports have described spongiotic eruptions with foci of atypical lymphocytes in contact dermatitis and in patients treated with phenytoin. To the best of our knowledge, this is the first reported case of a carbamazepine-induced eruption simulating mycosis fungoides histologically.
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PMID:Carbamazepine-induced eruption histologically mimicking mycosis fungoides. 214 Jan 16

The histopathology of systemic allergic contact dermatitis is usually characterized by spongiosis. A number of other much less common to rare histological findings have also been reported, including erythema multiforme-like eruption, vasculitis, urticaria, and miscellaneous groups.
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PMID:Histopathology of exogenous and systemic contact eczema. 220 24

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


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