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 hypothesis that deficiencies of plasma protease inhibitors might play a role in the pathogenesis of chronic urticaria was evaluated. Plasma levels were measured in patients with urticaria and a matched control group for alpha1-antitrypsin, alpha2-macroglobulin, total trypsin-inhibiting capacity, kallikrein-inhibiting capacity, and the complement factors C1 esterase inhibitor, C3, and C4. A total of 92 patients with chronic urticaria or more than three months' duration was studied. Patients with acquired cold urticaria had significantly decreased levels of alpha1-antitrypsin and total antitrypsin activity. In patients with acquired angioneurotic edema, alpha1-antitrypsin levels and antichymotrypsin activities were lowered, with less significant decreases in anti-trypsin and antikallikrein activities. Levels of C1 esterase inhibitor , C3, and C4 were normal in all groups. There was no correlation between the increased sensitivity to intracutaneously administered kallikrein injection and deficiencies of of protease inhibitors.
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PMID:Protease inhibitors in plasma of patients with chronic urticaria. 6 Sep 15

Proteins of the serpin family (serine protease inhibitor) control key steps in the inflammatory, coagulation and complement systems. C1-inhibitor deficiency predisposes to hereditary angioneurotic oedema, and other serpins control proteolytic enzymes that may cause complement activation or the forming of oedema. We investigated whether deficiency of proteins of the serpin family may predispose to cold urticaria and therefore screened 7 male patients with severe cold urticaria for the presence of deficiency alleles of some of the members of the serpin antiprotease family. There were no findings of C1-inhibitor, alpha 1-antitrypsin, alpha 2-antiplasmin, antithrombin III, tissue plasminogen activator inhibitor or thyroxine binding protein deficiency. The prevalence of heterozygous alpha 1-antichymotrypsin deficiency was significantly higher than expected (prevalence ratio 25.8 (95% confidence interval 6.0-112), p < 0.0001). This finding is in concert with previous studies that have shown lower mean levels of alpha 1-antichymotrypsin among patients with cold urticaria and suggests that heterozygous deficiency of this antiprotease, which controls neutrophil cathepsin G and mast cell chymase may predispose to cold urticaria. The present series is, however, small and the results need confirmation in larger materials.
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PMID:Heterozygous alpha 1-antichymotrypsin deficiency may be associated with cold urticaria. 148 47

In a double-blind placebo-controlled study, danazol, an attenuated androgen, was effective in reducing exercise-induced weals in cholinergic urticaria. Danazol treatment also caused significant elevations of several protease inhibitors, particularly antichymotrypsin which has been reported previously to be low in cholinergic urticaria.
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PMID:Beneficial effects of danazol on symptoms and laboratory changes in cholinergic urticaria. 355 98

Since a protease inhibitor or anaphylatoxin inactivator deficiency might explain why certain individuals are prone to develop chronic urticaria/angioedema or anaphylactoid reactions to radiographic contrast media, serum alpha 1-protease inhibitor, alpha 1-antichymotrypsin, alpha 2-macroglobulin, inter-alpha-inhibitor, antithrombin III, alpha 2-plasmin inhibitor, C1 inhibitor, and serum carboxypeptidase N were assessed by immunologic or functional methods. These values all were within normal limits in both groups of patients except for a low mean alpha 1-protease inhibitor level in chronic idiopathic urticaria/angioedema and cold urticaria patients and marginal decreases of alpha 1-protease and inter-alpha-inhibitor levels in radiographic contrast medium reactors. However, these abnormalities were not thought to be of pathogenetic significance.
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PMID:Plasma protease inhibitor and anaphylatoxin inactivator levels in chronic urticaria/angioedema and in patients experiencing anaphylactoid reactions to radiographic contrast media. 394 18

Plasma levels of six protease inhibitors have been measured in patients with chronic urticaria, chronic urticaria with angio-oedema, cold and cholinergic urticaria. In chronic urticaria C1 esterase inhibitor activity was increased compared with a reference control population but there was no detectable abnormality of any other protease inhibitor. Patients with chronic urticaria/angio-oedema showed a reduction in inter-alpha trypsin inhibitor. They also manifested a rise in C1 esterase inhibitor. In cold urticaria there was a significant lowering of alpha 1 antichymotrypsin. The reduction in alpha 1 antitrypsin in this group probably reflects a genetic difference compared with the control population. Patients with cholinergic urticaria also showed a reduction of alpha 1 antichymotrypsin. The elevated levels of alpha 2 macroglobulin in the three groups are probably due to differences in the mean age of these groups compared with the reference population. Comparison of levels of subgroups of patients with and without active lesions suggest that a consumptive effect may contribute to the reduced values, although it seems unlikely to account for them entirely. The results suggest that involvement of pharmacologically active products of protein digestion may be involved in the pathogenesis of urticaria and should prompt attempts to identify these agents and encourage trial of medications which lead to inhibition of proteolytic activity in urticaria.
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PMID:Protease inhibitor profiles in urticaria and angio-oedema. 696 79