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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The term "the contact urticaria syndrome," proposed in 1975, has been generally accepted and led to proliferation of new examples. This paper summarizes this clinical material and presents a diagnostic and pathogenetic evaluation method. The risks (and minimization, thereof) of systemic skin test-induced reactions are delineated.
J Am Acad Dermatol 1981 Sep
PMID:The contact urticaria syndrome--an updated review. 645 50

Using a methylcellulose clonal culture method, we found eosinophil colony-forming cells in the blood of two patients: a 46-year-old white woman with a long history of urticaria and allergic rhinitis and complete absence of eosinophils secondary to IgG-mediated and complement-mediated destruction of her eosinophils; and a white woman with a history of allergic rhinitis and asthma and a complete absence of eosinophils in her peripheral blood. Addition of the patients' plasma or IgG to cultures of peripheral blood mononuclear cells derived from normal persons or the patients inhibited formation of eosinophil colonies without influencing colony formation in other hemopoietic cell lineages. In contrast, normal plasma or IgG had no effect on the formation of eosinophil colonies. That the IgG-mediated cytotoxic activity of eosinophils prevents the expression of an apparently normal eosinophilopoietic potential suggests an autoimmune basis for the eosinophil aplasia.
Ann Intern Med 1984 Sep
PMID:Circulating eosinophil colony-forming cells in pure eosinophil aplasia. 646 1

The prevalence of occupational asthma was studied in two snow crab-processing industries in operation since 1980. Before the 1982 season, all except 10 of the 313 employees were investigated by a questionnaire, prick skin tests with common allergens, crab n and crab-boiling water extracts, and spirometry. The diagnosis was confirmed in 46 (15.6%) workers (including 33 of 64 subjects with a history highly suggestive of occupational asthma in the previous seasons) by (1) specific inhalation challenges in 33 subjects (one immediate, nine dual, and 23 late asthmatic responses) and/or (2) a combination of monitoring of peak expiratory flow rates (n = 12) and significant changes in bronchial responsiveness to histamine (n = 16) as well as in spirometry (n = 18) after reappearance of symptoms on return to work. Positive skin tests to crab (p less than 0.001) and, to a lesser degree, smoking history (p = 0.03) but not atopy (p greater than 0.05) were related to the presence of occupational asthma. A high prevalence of rhinoconjunctivitis (35 of 46) and urticaria (16 of 46) was also documented in the affected individuals.
J Allergy Clin Immunol 1984 Sep
PMID:Occupational asthma in snow crab-processing workers. 647 Mar 60

Five individuals with idiopathic cold urticaria but not normal volunteers released platelet factor 4 (PF4) detected by radioimmunoassay into the circulation after cold challenge. In three patients, a biphasic rise in PF4 was noted with increases at 1 and 10 to 20 min after immersion, whereas in two others only the later rise was detected. Peak levels of PF4 were detected in all five patients 20 min after cold immersion, whereas peak levels of other mediators such as histamine and eosinophil and neutrophil chemotactic activity occurred earlier at 10, 3 to 10, and 5 to 10 min, respectively. The identification of PF4 in the circulation of patients with cold urticaria after cold challenge provides further evidence for the activation of platelets in mast cell-dependent disorders and suggests new potential mechanisms for the expression of cold urticaria.
J Allergy Clin Immunol 1984 Sep
PMID:Release of platelet factor 4 into the blood after cold challenge of patients with cold urticaria. 647 Mar 62

Recurrent urticaria and recurrent angioedema are frequent adverse reactions in non-atopic patients who do not tolerate aspirin. Of 1,632 infants and children who visited our allergy department for the first time, nine children (0.55%), five males and four females, presented recurrent urticaria or recurrent angioedema after taking aspirin. No evidence of atopy was disclosed either by clinical history (personal and family), skin testing, eosinophil levels or total IgE. Aspirin intolerance was established by oral challenge. Only three of the nine patients reported aspirin intolerance in their histories.
Ann Allergy 1984 Sep
PMID:Aspirin-induced recurrent urticaria and recurrent angioedema in non-atopic children. 647 85

We studied the clinical features of thirty-two patients with delayed pressure urticaria, and special laboratory tests were performed in seven patients. Striking clinical features included a long duration of the disease (mean 6 years) and an elevated erythrocyte sedimentation rate in 71%, dermographism in 63% and a leukocytosis in 33% of the patients. There was prolongation of weals in response to histamine, compound 48/80, concanavalin A and NaCl. In some patients, histamine and chemotactic factor levels were increased in suction blisters over skin test and delayed pressure sites. In extracts from pressure weals, chemotactic activity was found for leukotriene B4, its 20-omega-oxidation products and mono-HETEs. Studies of peripheral blood leukocytes revealed significantly increased intracellular histamine levels and increased release of histamine, and a trend to increased release of chemotactic activity from stimulated cells. The response of leukocytes to mitogens was normal. We conclude that histamine plays a major role in the pathogenesis of PU. Arachidonate-derived chemotactic factors might account for the variably observed leukocytosis and the cellular infiltrate in lesions of pressure urticaria. Additional mediators must be involved in PU in order to explain the unique prolonged wealing response.
Br J Dermatol 1984 Sep
PMID:Clinical, pharmacological and immunological aspects of delayed pressure urticaria. 647 27

Randomized double-blind trials using doxepin and several conventional antihistamines were carried out for treatment of patients with idiopathic cold urticaria. In the first double-blind trial, eight of nine patients preferred doxepin (10 mg three times daily) to cinnarizine (10 mg three times daily). In the second double-blind trial, the results of ice cube tests suppressing the effect of cyproheptadine (4 mg three times daily), doxepin (10 mg three times daily), and hydroxyzine (10 mg three times daily) did not statistically differ. However, doxepin was subjectively the most effective and it had fewer side effects than other treatments that were compared. Doxepin effectively suppressed the wheal and itching responses and shortened the duration of the wheal response in the ice cube test in all patients with cold urticaria who were studied.
J Am Acad Dermatol 1984 Sep
PMID:Comparison of cinnarizine, cyproheptadine, doxepin, and hydroxyzine in treatment of idiopathic cold urticaria: usefulness of doxepin. 648 Sep 53

Hormones of the thyroid gland (thyroxine, tri-iodothyronine) control the metabolism of cells and tissue of the body, while parathormone and calcitonine are balancing the intra- and extracellular levels of calcium and phosphorus by governing some metabolic functions of bones, kidney and small intestine. Growth, maturation and metabolic homeostasis of the organism depend, among other intrinsic factors, on a normal production and secretory rate of both thyroidal and parathyroidal hormones. Clinical conditions of hyperthyroidism induce 1. increased metabolic turnover of the body with transcutaneous heat loss, 2. disordered growth of hairs and nails, 3. hyperpigmentation of skin, 4. pruritus with or without urticaria. Pretibial (usually symmetrical) myxedema may be associated with conditions of either hyper- or hypothyroidism (e.g., Hashimoto's thyroiditis); if combined with bilateral exophthalmus and acropachyderma of fingers and toes, it is called Diamond syndrome, or E.M.O. syndrome. In hypothyroidism, the skin feels chilly and dry, looks pale, and may present follicular keratoses with or without secondary eczema. The hair appears dull and sparse due to disordered anagen phase. Skin wounds heal with delay. Diffuse myxedema originates in the papillary and periadnexal connective tissue and eventually extends to the dermis as a whole. Clinical conditions of hyperparathyroidism rarely cause secondary calcification of the skin; they may induce severe pruritus, particularly in secondary hyperparathyroidism due to renal failure. Impetigo herpetiformis or generalized pustular psoriasis, resp., may be set off by excessive surgical removal of the goiter. Congenital maldevelopment of both thymus and parathyroid gland leads to cellular immune deficiency with secondary chronic muco-cutaneous candidosis.
Z Hautkr 1984 Sep 01
PMID:[The thyroid gland, the parathyroid gland and the skin]. 648 58

Six out of eight patients with a history of aspirin-provoked urticaria/angioedema responded with adverse reactions, including urticaria and bronchospasm, to provoking doses of oral aspirin from 30-515 mg. The other two patients did not react to 1.2 g of aspirin on three occasions. Five of the six patients who had reacted became desensitized after their initial aspirin reaction, tolerating 650 mg on the second day. They then took 650 mg day-1 of aspirin for three weeks, during which time the ingestion of foods which had previously caused a variety of moderate or severe reactions caused no symptoms. The resting plasma PGF2 alpha in ten 'aspirin-sensitive' urticaria patients (24.89 +/- 2.79 pg m-1) was significantly higher than the levels in ten normal subjects (6.75 +/- 1.1 pg ml-1) (P less than 0.01). In the patient group the lowest levels of PGF2 alpha were found in the two patients who subsequently did not experience a positive reaction after aspirin provocation. The PGF2 alpha/PGE2 ratio in 'aspirin-sensitive' urticaria patients (1.83 +/- 0.026) was significantly higher than that in normal subjects (0.63 +/- 0.14) (P less than 0.01).
Clin Allergy 1983 Sep
PMID:Specific desensitization in 'aspirin-sensitive' urticaria; plasma prostaglandin levels and clinical manifestations. 657 89

This report describes an extremely rare case of occupational allergy that developed in a frog handler. A 31-year-old female laboratory technician developed itching and urticaria one year after she began handling frogs and extracting their brains in the laboratory. Nine years later she noticed swelling of the right hand, stridor and dyspnea when she mistakenly injected her finger with a needle contaminated with extracts of frog brain. Specific IgE antibody to frog extracts was demonstrated by RAST and by P-K testing. However, no specific IgG antibody was found by agar gel diffusion or in heterologous PCA testing using guinea pigs. We suggest that allergic symptoms in this case were due to the development of Type I allergic reactivity to frog antigens.
Ann Allergy 1983 Sep
PMID:A new occupational allergy due to frogs. 660 74


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