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First case of homozygous C1 inhibitor deficiency
Journal of Allergy and Clinical Immunology, 2006C1 Inhibitor (C1-Inh) deficiency causes angioedema and can be hereditary (HAE), caused by mutations in the C1-Inh gene (C1NH), or acquired (AAE). Patients with HAE show a complement profile different from that of patients with AAE with normal levels of C1 (C1q, C1r, and C1s).We sought to characterize the complement profile of a patient with HAE and a ...
Blanch, Alvaro +5 more
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Lupus Erythematosus Associated with C1 Inhibitor Deficiency
The Journal of Dermatology, 2002AbstractWe report here a patient with skin lesions of lupus erythematosus (LE) associated with a type 1 hereditary C1 inhibitor deficiency. She had not experienced any episodes of angioedema. A histological examination of the affected skin lesions demonstrated liquefaction of the basal cell layer in the perifollicule. Direct immunofluorescence staining
Masayo, Koide +5 more
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Angioedema and C1 inhibitor deficiency.
Annals of allergy, 1992Deficiency of C1 inhibitor resulting in episodes of angioedema causes significant morbidity and mortality in affected patients, yet often goes undiagnosed for years. As biochemical understanding of the disorder has improved, competing theories for the pathophysiologic mechanism of angioedema have emerged.
N A, Orfan, G B, Kolski
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Cardiac Surgery and C1-Inhibitor Deficiency
Journal of Cardiothoracic and Vascular Anesthesia, 2014Chamaraux-Tran, Thiên-Nga +5 more
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The C1 inhibitor deficiency. A review.
European journal of clinical chemistry and clinical biochemistry : journal of the Forum of European Clinical Chemistry Societies, 1993C1 inhibitor (C1I), a member of the serine protease inhibitor superfamily, is the principal regulator of the activation classical pathway of complement by reducing the proteolytic activity of activated C1r and C1s. A deficiency of active C1 inhibitor is the most commonly identified genetic defect of the complement system.
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Inherited C1 inhibitor deficiency.
Complement and inflammation, 1989The paper reports our experience of a 15-year follow-up of 179 patients with hereditary angioedema (HAE). The disease is transmitted as an autosomal dominant trait and two variants have been described: type I characterized by functional and antigenic C1-inhibitor (C1-INH) deficiency and type II with normal or upper normal C1-INH antigenic levels but no
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