urticaria/protease

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Serum alpha 1-protease inhibitor levels in patients with chronic idiopathic urticaria.

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A comparative study of serum alpha 1-protease inhibitor levels in patients with chronic idiopathic urticaria and control subjects revealed that the values in the patients were significantly lower than those in the controls, especially in patients over 60 years. The results suggests that some

Plasma protease inhibitor and anaphylatoxin inactivator levels in chronic urticaria/angioedema and in patients experiencing anaphylactoid reactions to radiographic contrast media.

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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,

Protease inhibitors in plasma of patients with chronic urticaria.

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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,

NKp46 regulates the production of serine proteases and IL-22 in human mast cells in urticaria pigmentosa.

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NKp46 (natural cytotoxic receptor 1/CD335) is expressed on natural killer cells and Th2-type innate lymphocytes. However, NKp46 expression in human mast cells has not yet been reported. Here, we explored the expression of, and possible role played by, NKp46 in such cells. NKp46 protein was expressed

Protease inhibitor profiles in urticaria and angio-oedema.

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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

Occupational allergic contact urticaria and rhinoconjunctivitis from a detergent protease.

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Refractory chronic urticaria treated effectively with the protease inhibitors, nafamostat mesilate and camostat mesilate.

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Protease inhibitor profiles in urticaria and angio-oedema [proceedings].

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Demonstrating the potential of a novel spider venom-based biopesticide for target-specific control of the small hive beetle, a serious pest of the European honeybee.

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The parasitic small hive beetle (Aethina tumida) feeds on pollen, honey and brood of the European honey bee (Apis mellifera); establishment in North America and Australia has resulted in severe economic damage to the apiculture industry. We report potential for the "in-hive"

Immunological parameters and alpha 1-antitrypsinin chronic urticaria.

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Serum immunoglobulins, complement and alpha 1-antitrypsin were assayed in forty-eight patients with chronic urticaria. Thirteen cases had chronic cold urticaria and thirty-two had chronic idiopathic urticaria. Elevated mean serum IgM was found in chronic cold urticaria. Seven patients had partial

Mast cells and their role in urticaria.

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Mast cells are the primary effector cell type in urticaria and angioedema. Recognition of different types of mast cells has increased the understanding of their cell biology and may help refine the therapy of human allergic diseases. Mast cells containing chymase and tryptase (MCTC) and tryptase

Beneficial effects of danazol on symptoms and laboratory changes in cholinergic urticaria.

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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

Chronic urticaria: a disease at a crossroad between autoimmunity and coagulation.

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Chronic urticaria (CU), defined as recurrence of wheals with or without angioedema for more than 6 weeks, is a quite common disease that may severely worsen the quality of life. Studies carried out during the last 2 decades have demonstrated an autoimmune pathogenesis mediated by functionally active

Heterozygous alpha 1-antichymotrypsin deficiency may be associated with cold urticaria.

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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

Enzyme activation and inhibition induced by cold provocation in a patient with cold urticaria.

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A 33-year-old female patient with acquired cold urticaria, together with her 8-year-old healthy daughter, was subjected to a brief period of cold exposure. The effect of this treatment upon a number of key factors of the plasma coagulation, kallikrein and complement systems was investigated. Cold

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