Immunological parameters and α₁‐antitrypsinin chronic urticaria

Abstract

Serum immunoglobulins, complement and a,-antitrypsin were assayed in forty-eight patients with chronic urticaria. Thirteen cases had chronic cold urticaria and thirtytwo had chronic idiopathic urticaria. Elevated mean serum IgM was found in chronic cold urticaria. Seven patients had partial immunoglobulin deficiencies. IgE was elevated in sixteen cases of chronic idiopathic and in two with chronic cold urticaria. Eight patients had depressed serum total haemoiytic complement activity. Low C3 and normal C4 serum protein concentrations in four cases suggested alternative complement pathway activation. Twenty of forty-six patients were atopic, although specific allergies responsible for the urticaria were not identified in any of them, a^antitrypsin levels were normal in all patients. The data suggest that the aetiology and pathogenesis of chronic urticarias in this study are heterogeneous. No evidence of abnormality of the protease inhibitor system in either chronic idiopathic or chronic cold urticaria was found.

Acute-phase response and its biomarkers in acute and chronic urticaria

“…However in our study we did not find any statistically differences in the serum concentration of AT between patients with different types of urticaria and the control group. Similarly, Chodirker et al did not find any significant decrease in the AT level within the group of patients suffering from spontaneous or cold-induced urticaria vs the control group [ 34 ].…”

Chronic urticaria and angioedema

“…Although IgE-mediated mechanisms of mediator release from mast cells have classically been recognized as being involved in the pathophysiology of urticaria, a number of recent studies has suggested that other mechanisms may be of primary importance. (Berrens, Jankowski & Jankowski-Berntsen, 1976;Sissons et al, 1974;Balbow & Ward, 1975;Chodirker, Bauman & Komar, 1979;Mathison et al, 1977;Soter, 1977;McDuffie e? a/., 1973;McLean e?…”

“…Activation of complement, with subsequent anaphylatoxin formation may lead to mediator release. Hypocomplementaemia has been noted in a sub-population of urticaria patients, and activation by both or either classical or alternative pathways documented (Sissons et al, 1974;Balbow & Ward, 1975;Chodirker et al, 1979;Mathison et al, 1977;Soter, 1977;McDuffie, 1973;McLean et al, 1980;Zeiss et al, 1980;Phanupak et al, 1980). Those patients with classical-pathway-activation often have a vasculitis-like clinical presentation, differing clinically from the idiopathic variety of chronic urticaria.…”

Specific desensitization in ‘aspirin‐sensitive’ urticaria; plasma prostaglandin levels and clinical manifestations

“…The pathological physiology of urticaria and angioedema is not fully understood. Urticaria and angioedema are cutaneous forms of anaphylaxis, but although the lesions resemble the weal and flare reactions induced by histamine and may be accompanied by immunological abnormalities (Ballow, Ward & Gershwin, 1975;Chodirker, Bauman & Komar, 1979;Oehling et al, 1982) there does not always appear to be an immunological cause. The release of vasodilators and permeability-enhancing factors may be involved (Warin & Champion, 1974) and exacerbations can be provoked by almost any agent which dilates the superficial blood vessels in the skin, such as heat, exertion, emotion, and drugs (e.g.…”