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 therapeutic results of hypnosis with relaxation therapy were evaluated in 15 patients with chronic urticaria of 7.8 years' average duration. Compared with baseline and control session values, the hypnosis session provided relief of pruritus as measured by three self-report parameters. There was no change in the number of hives. All subjects were given a standard test for hypnotizability. Assuming that the results were not biased by their preceding relaxation sessions, we determined that six subjects were hypnotizable and nine were nonhypnotizable. Subjects in both groups improved symptomatically, but hypnotizable subjects had fewer hives and became more symptomatic during the control (testing and history taking) session. Hypnotizable subjects also more frequently related stress as a causative factor. At a follow-up examination five to 14 months after the completion of the experimental sessions, six patients were free of hives and an additional seven reported improvement.
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PMID:Effects of relaxation therapy and hypnotizability in chronic urticaria. 330 May 66

In a recent study, all patients with delayed pressure urticaria (DPU) developed late cutaneous reaction (LCR) after intradermal injection of compound 48/80 and after skin testing with certain food antigens. In the present study, we analyzed the histologic changes in the pressure lesions and compared them with those found in normal skin injected with diluent and in LCR to 48/80. The study included five patients with DPU associated with chronic urticaria (CU) and four patients with CU but without DPU. Six to eight hours after pressure challenge and intradermal skin testing with 48/80 and diluent, skin biopsy specimens were obtained from the pressure lesions, the LCRs, and normal skin (diluent injection). Specimens were assessed by Giemsa staining of 1-micron sections and immunofluorescence of frozen sections. Total cells were counted in each specimen. Interstitial deposits of fibrin were observed by immunofluorescence in LCR and pressure lesions. The total numbers of infiltrating cells in the dermis among LCR sites and pressure lesions were not significantly different, while both LCR sites and pressure lesions contained significantly more infiltrating cells than did normal skin injected with saline diluent. The differential counts in LCR and DPU were mostly mononuclear cells. Infiltrates in the DPU and LCR were mostly perivascular. No histopathologic changes were seen at skin sites challenged with pressure in the control patients with CU without clinical manifestations of DPU. We conclude that lesions seen in DPU are morphologically similar to classic LCR.
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PMID:Delayed pressure urticaria histologically resembles cutaneous late-phase reactions. 334 4

In this study, four patients presented with chronic urticaria that required glucocorticosteroid therapy for control. In the first patient, the urticaria began during pregnancy and persisted after delivery with symptoms flaring premenstrually thereafter. Danazol was selected in an attempt to suppress progesterone levels, theoretically by inhibiting ovulation. The patient's urticaria markedly improved, however, within 24 hours. Several months later, she was switched to stanozolol with further improvement. Three other individuals were treated with stanozolol with dramatic improvement. In all, three patients have experienced the induction of five remissions (there were two recurrences), and one patient remains much improved. All subjects have stopped both stanozolol and glucocorticosteroids. Stanozolol appears to act synergistically with glucocorticosteroids, and together, they may be capable of inducing remission in some patients.
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PMID:The treatment of glucocorticosteroid-dependent chronic urticaria with stanozolol. 340 67

We have used a panel of monoclonal antibodies and enzyme histochemistry in order to characterize further the perivascular mononuclear cell infiltrate found in chronic idiopathic urticaria. Biotinylated anti-mouse immunoglobulin was exposed to avidin-biotin-peroxidase-labeled complex followed by peroxidase development in order to detect binding of monoclonal antibodies. The mean percent staining obtained for 12 patients with chronic urticaria was 47% T-lymphocytes, 22% monocytes (14% by alpha-naphthyl acid esterase), and 11% mast cells. B-lymphocytes were not detectable, and approximately 20% of cells could not be identified. Although patients varied greatly in the ratio of Leu 3a positive helper-inducer T cells to T8 positive cytotoxic-suppressor cells, the average of all patients was not significantly different from the T4/T8 ratio in plasma. Our results suggest that the infiltrate resembles that observed in cellular immune reactions (although no antigen has been identified) and that interaction of T-lymphocytes and/or monocytes with mast cells to cause mediator release appears likely.
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PMID:Studies of the cellular infiltrate of chronic idiopathic urticaria: prominence of T-lymphocytes, monocytes, and mast cells. 349 Nov

In some cases of chronic urticaria it is suspected that food additives such as tartrazine and sodium benzoate or salicylates may play a role in the pathogenesis of the condition. Since, at times, chronic urticaria may appear histologically similar to a mild cell-mediated immune response, the release of the T cell-derived lymphokine leucocyte inhibitory factor (LIF), in response to incubation with these additives and with acetylsalicylic acid (ASA), was measured in vitro using cells from normal controls, from patients with chronic urticaria with or without clinically associated additive sensitivity and from patients with asthma with or without associated ASA sensitivity. It was found that significant production of LIF occurred in response to tartrazine and sodium benzoate in those individuals with chronic additive induced urticaria. In addition, tartrazine caused LIF release from mononuclear cells of ASA-sensitive asthmatics. These results may indicate a possible role for additive-induced cell-mediated immune responses in the pathogenesis of some cases of chronic urticaria and suggest a potential diagnostic test for this condition.
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PMID:Cell-mediated immune responses to artificial food additives in chronic urticaria. 353 8

Intolerance to analgesics is common in patients with bronchial asthma, nasal polyps and urticaria. Symptoms of intolerance resemble those of allergy, but the events precipitating them can rarely be traced to reactions between the drug and a specific antibody or sensitised T-lymphocytes. In 8 to 20% of adult asthmatics, aspirin and several other analgesics provoke asthmatic attacks, probably through inhibition of cyclo-oxygenase. This is a distinct and important clinical syndrome with a specific history, course and clinical presentation and a number of unique peculiarities which still require elucidation at the biochemical level. Up to 40% of patients with chronic urticaria develop an obvious increase in weals and swelling after taking aspirin. These reactions occur only when urticaria is active, and though the reason for them is not known, it appears that different mechanisms may be responsible in different patients. Skin reactions other than exacerbation of chronic urticaria are less common, but may create serious clinical problems. The clinical background of a patient often determines the type of adverse response to an analgesic. Thus, in certain individuals, analgesics can produce anaphylactic reactions and/or urticaria, probably through an immunological mechanism, while in some asthmatics they precipitate bronchoconstriction, probably through inhibition of bronchial cyclooxygenase. Study of untoward reactions to analgesics not only leads to safer pharmacotherapy, but it also offers a fascinating model for better understanding of some diseases.
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PMID:Analgesics, allergy and asthma. 355 81

A case of chronic urticaria associated with thyroiditis is described. The diagnosis of autoimmune thyroid disease (Hashimoto's disease) rested on the presence of nodular goiter, thyroid dysfunction and significantly elevated thyroid microsomal antibodies (greater than 6,400). Skin biopsy showed changes suggestive of leucocytoclastic vasculitis. Immunological studies showed few abnormalities (low titers of antinuclear antibodies and rheumatoid factor) but a search for circulating immune complexes was negative, and serum complement levels were within normal range. The patient complained of severe pruritus and polyarthralgia but no systemic involvement occurred. Urticaria vasculitis has never previously been described in association with thyroid autoimmunity. This suggests the possibility of an autoimmune cause of urticaria. The urticaria improved and disappeared after treatment with levothyroxine. The frequent clinical latency of thyroiditis warrants systematic testing for circulating anti-microsome antibodies in women presenting with an apparently idiopathic chronic urticaria.
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PMID:[Systemic urticaria associated with autoimmune thyroiditis]. 358 5

Double-blind, placebo controlled challenge tests with benzoic acid butylhydroxytoluene, butylhydroxyanisole, beta-carotene, beta-8-apo-carotenal, and sodium metabisulfite were made in 44 cases of chronic urticaria, 91 cases of atopic dermatitis, and 123 cases of contact dermatitis, as a comparison group. Positive reactions were seen in four patients, two of whom had urticaria, one atopic dermatitis, and one contact dermatitis. Two of these reactions were caused by the placebo, one in a patient with urticaria and the other in a contact dermatitis patient. For one patient who reacted to the placebo and one who reacted to benzoic acid, the challenges were repeated with positive results in both instances. In nine patients, equivocal test results were produced with all the active substances and the placebo, but in all nine cases, retesting 4 days later produced negative results. This suggests that common food additives are seldom if ever of significance as precipitating factors in chronic urticaria or atopic dermatitis.
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PMID:Peroral challenge tests with food additives in urticaria and atopic dermatitis. 369 62

Urticaria and angioedema are common disorders that affect approximately 1/5 of the population at some stage in their lives. Although the clinical diagnosis of this disorder is made without difficulty, its etiology and pathogenesis remain obscure. Extensive clinical studies and the application of different laboratory techniques seldom manage to detect the etiology of chronic urticaria or determine its supposed pathogenic mechanism. Thus, a large number of causal agents have been held responsible for the symptoms of chronic urticaria and/or chronic urticaria and angioedema and for the variety of immunologic and nonimmunologic factors involved in its pathogenesis. The controversial laboratory findings in this type of patients prompted us to undertake this study on 48 subjects with chronic urticaria and/or angioedema. We studied the levels of serum immunoglobulins (IgG, IgA, IgM and IgE), the haemolytic activity of the complement (CH50), the levels of the complement components (C1 inhibitor, C3 and C4), the possible presence of circulating immune complexes and the percentages of the T lymphoid subpopulations (using OKT3, OKT4 and OKT8 markers) and the B population. The results obtained showed an alteration of the complement (CH50) and of some of its components (C3 and C4) as well as of the cytotoxic/suppressor lymphocyte subpopulation (OKT8).
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PMID:[Immunologic parameters in chronic urticaria]. 379 6

A group of 281 patients with chronic urticaria was classified into various subtypes and compared with 357 healthy controls for PI types of alpha1-antitrypsin. Total alpha 1-antitrypsin was measured by the Mancini technique, and PI types were determined by isoelectric focusing. The MZ phenotype and the Z gene frequency were significantly more frequent in the urticaria group. The Z gene predominated in the groups with cold urticaria and acquired angio-oedema. The total group of chronic urticaria patients showed a significant decrease in total alpha 1-antitrypsin compared with the control group (P less than 0.03). Deficiencies in alpha 1-antitrypsin may predispose to the development of certain types of urticaria and angio-oedema.
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PMID:Alpha 1-antitrypsin deficiency and PI typing in patients with chronic urticaria. 387 51


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