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)

It appears that when hives are fleeting, as is seen in physically induced hives, they are caused by a rapid burst of local mast cell degranulation. There is no tissue infiltration with cells, no late-phase component to the reaction, and therapy is dependent on antihistaminics or mast cell stabilizing agents. The nonsustained mediator release may be a result of the absence of a defined antigen, a very brief encounter with the initiating physical stimulus, and rapid removal of vasoactive substances and chemotactic factors so that the hive disappears quickly and a chemotactic factor gradient is not sustained so as to attract cells. Chronic urticaria differs in that the hive forms slowly, disappears over many hours, and is due to a perivascular accumulation of mononuclear cells and mast cells. These mononuclear cells appear to be critical for development of the lesion. Indirect evidence in support of this is the efficacy of corticosteroids in abrogating this type of hive and new concepts regarding mast cell proliferation and stimulation that are mononuclear cell-dependent.
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PMID:Urticaria: the relationship of duration of lesion to pathogenesis. 2838 90

Several studies have suggested that complement activation processes are frequently involved in the pathogenesis of urticaria. We report clinical evolution and studies of complement-mediated functions in a 47-year-old previously described patient presenting with chronic urticaria, in whom we found persistent low complement hemolytic activity (65-75% of normal values), depressed levels of third complement component (C3, between 55% and 65%) and of factor B (between 60% and 75%), together with C1, C4, C2, C5, C5b neoantigen and fluid phase terminal complement (SC5b-9) complex within the normal range, pointing to activation of the alternative pathway. A circulating low affinity C3 nephritic factor (C3NeF), known to enhance cleavage of human serum C3, was detected. The urticarial lesions, which were initially pruritic and persisted for less than 24 hours, became subsequently fixed and burning, and were accompanied by fever and arthralgia. Skin biopsy specimens showed moderate leukocytoclastic vasculitis. Response to varied treatment regimens, including antihistamines and colchicine, was poor. Therapy with oral corticosteroids produced some improvement. The association of chronic urticaria with C3NeF without clinical and biological signs of membranoproliferative glomerulonephritis and partial lipodystrophy has not to our knowledge been reported before. This observation raises the question of a possible role of C3NeF in the pathogenesis of urticaria.
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PMID:[Chronic urticaria and acquired complement deficiency due to a nephritic factor (C3NeF)]. 221 45

Two patients with chronic idiopathic urticaria in whom remissions were achieved with dye- and preservative-elimination diet had exacerbations of their urticaria when they were challenged under double-blind, placebo-controlled conditions with butylated hydroxyanisole and butylated hydroxytoluene. After elimination of butylated hydroxyanisole and butylated hydroxytoluene from their diets, there was marked abatement of the frequency, severity, and duration of their urticaria. These antioxidants appear capable of aggravating symptoms in certain patients with chronic urticaria.
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PMID:Chronic urticaria exacerbated by the antioxidant food preservatives, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT). 222 16

Twelve cases of chronic urticaria with histopathologic features of lecocitoclastic allergic angitis are studied. The type of cutaneous lesion, personal and familiar atopic history and the presence of autoimmune disease are described. Light microscopy, direct immunofluorescence, anti DNA, antinuclear, antithyroid, Ro, La, Rnp and Sm antibodies, total complement levels, C3 and C4, rheumatoid factor, latex, ASTO, cryoglobulines and complete workup were investigated, taking into account natural progression and response to therapy. Two different groups are defined: 1) normocomplementemic (5 patients) and 2) hypocomplementemic (7 patients). They were all women except one. The cutaneous lesions were indistinguishable in the two groups. Only in the second group there was an associated disease (systemic lupus erythematosus, Sjogren syndrome disease, lupus-Sjogren overlap, autoimmune thyroid disease). Urticaria had been present from the onset of the disease in 4 patients, and occurred later during its course in 8 others. Five patients had thyroid disease (Hashimoto thyroiditis or Graves disease), two of them being mother and daughter. Another patient had a family history of Grave's disease and urticaria. Anti DNA antibodies were found in 7 cases, and anti Ro + La + in 3 cases. Response to treatment was variable with spontaneous cycles of worsening and remissions. One of the patients found a relationship with certain foods. Histopathologic results are related in both clinical normocomplementemic and hypocomplementemic groups. No significant differences were found between the two groups, but Ro+ and La+ patients exhibit more intense cariorexis and neutrophilic infiltrates.
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PMID:[Vasculitic urticaria: study of 12 cases]. 226 94

Thirty seven patients with chronic urticaria were prospectively studied from August 1984 to July 1986. These patients were submitted to regular and immunological laboratory tests. Biopsies were taken from recent urticarial lesions for histologic analysis and also to direct immunofluorescence and immunohistochemistry studies. Vasculitis was found in 27% of the patients. Most of them showed only urticarial lesions except two (20%), that presented residual macula; angioedema occurred in 20% of the urticarial vasculitis (UV) patients; most cases had no systemic manifestations. Serum immunoglobulins and circulant immunocomplexes were increased in both groups. Complement reduction was considered an evidence of vascular aggression, being found in 55% of the UV patients. Direct immunofluorescence studies showed only 10% of positive IgM fluorescence in the vessel walls in the UV group. Immunohistochemical evaluation in the same group revealed mainly slight deposition of immunoglobulins IgG, IgM and IgA in the plasma cells of 80% of the samples and in only 10% there was immunoglobulin deposition in the vessel walls. The authors concluded that conventional histopathology is the best diagnosis method for urticarial vasculitis, direct immunofluorescence and immunoperoxidase being ancillary tools. Therefore, a special group of patients was detected, clinically and therapeutically resembling common urticaria patients, but presenting vasculitis in the histologic exam. This fact leads to the hypothesis that there is a range between common urticaria and urticarial vasculitis with systemic involvement.
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PMID:Urticarial vasculitis. 226 52

Thirty-four dermatology out-patients with chronic idiopathic urticaria and 34 with idiopathic generalized pruritus were investigated using standardized self-assessment psychological questionnaires to determine the incidence of significant symptoms of depression and anxiety. These patients were compared with age- and sex-matched but otherwise unselected general dermatology out-patients. Using the Beck depression inventory, significantly more patients with generalized pruritus (32.4%) had depressive symptomatology (score greater than 14) than controls (13.2%, P less than 0.05). Although more patients with chronic urticaria had depressive symptomatology (14.7%) than controls (4.4%), the difference was not statistically significant. Using the Speilberger state-trait anxiety inventory there were no significant differences between the patients with pruritus or urticaria and their controls with respect to state or trait anxiety scores above the upper 90% probability limit for the general population. Thus, significant depression may be expected in a substantial proportion of patients with idiopathic generalized pruritus but in a relatively small proportion of those with chronic urticaria.
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PMID:Anxiety and depression in patients with chronic urticaria and generalized pruritus. 226 93

In 79 males aged 19-21 years with acute and chronic urticaria living under similar conditions the levels were determined of total IgE (FIST test) and specific IgE (FAST test) against the most frequent inhaled and food allergens. Statistically significant rise of the mean value of total IgE was noted in both groups of patients. In acute urticaria increased concentration of specific IgE against inhaled allergens was significantly more common.
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PMID:[IgE levels and hypersensitivity to certain inhaled and food allergens in acute and chronic urticaria]. 228 42

We have studied 239 patients, 53 males and 186 females, mean age 31.9, affected by urticaria-angioedema syndrome. Fifty-three patients didn't complete the study. One-hundred-three of the other 186 patients went on elimination diet: 111 patients suffered from chronic urticaria-angioedema syndrome and 21 subjects suffered from acute syndrome. Eighty-one out of the 132 patients obtained good results from dietetic management (p less than 0.001). Double blind challenge test was positive in 42 subjects: 29 patients suffered from Food Allergy and 13 patients from Food Intolerance. Thus, the prevalence of Food Allergy in patients who completed dietetic management was 21.9% (29 patients out of 132). If we evaluate all the 186 patients affected by urticaria-angioedema syndrome, the prevalence of Food Allergy is 15.5%.
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PMID:[Prevalence of food allergy in patients with urticaria-angioedema syndrome]. 228 13

Biopsy specimens from lesional and uninvolved skin of nine patients with delayed pressure urticaria, three patients with acute urticaria, six patients with chronic recurrent urticaria, and four patients with urticaria pigmentosa were analyzed by routine histology and by immunochemistry for their reactivity with monoclonal antibodies to three different subsets of macrophages. Skin from 12 healthy volunteers served as control. Uninvolved skin of patients did not differ from that of healthy volunteers. An antibody against activated macrophages (27E10) was reactive to a marked extent with macrophages in wheals of pressure urticaria, more variably in acute and chronic urticaria, and practically not at all in urticaria pigmentosa. Antibodies with specificities for macrophages in healing (RM3/1) and normal (25F9) tissue reacted more markedly in all but pressure urticaria lesions, compared with normal skin. These findings indicate an active involvement of inflammatory macrophages in whealing reactions while these cells play apparently no role in cutaneous mast cell proliferation (urticaria pigmentosa).
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PMID:Macrophage subsets in different types of urticaria. 235 29

Fifteen patients with chronic urticaria were treated with ultraviolet light B (UVB) for 1-3 months during the spring 1984 and a follow-up study was performed in November 1984-January 1985. Patients with cold urticaria, cholinergic urticaria and dermographism became clearly better or got rid of their symptoms more often than those with "non-specific" chronic urticaria. The good results achieved during the phototherapy held during the summer but in the autumn urticaria became worse in one third of the cases. The result suggests that UV-therapy might be worth trying in many patients with chronic urticaria.
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PMID:Ultraviolet light therapy in chronic urticaria. 241 76


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