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Hereditary angioneurotic edema (HANE): Lack of close linkage between HLA haplotypes and C1 esterase inhibitor deficiency.
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The HLA haplotypes were defined in a series including 11 patients with hereditary angioneurotic edema (HANE), five symptom-free subjects with pathological laboratory findings characteristic of HANE, and their 33 healthy kinsmen. The subjects belonged to two Finnish families representing the more
The Role of C1-Esterase Inhibitors in the Management of Vasogenic Edema in Glioblastoma.
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Glioblastoma (GB) is one of the most common adult primary brain tumors, classified as a grade IV astrocytoma and highly malignant in nature. As the tumor grows and disrupts the blood-brain barrier (BBB), vasogenic edema can result. The edema has the potential to significantly contribute to a
Mechanisms of activation of C'1 esterase in hereditary angioneurotic edema plasma in vitro.
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The generation of C'1 esterase activity in siliconed plasma obtained from individuals with hereditary angioneurotic edema in remission tends to occur spontaneously, but can be hastened during its incubation with preparations of activated Hageman factor. This effect of activated Hageman factor could
Genetically determined heterogeneity of the C1 esterase inhibitor in patients with hereditary angioneurotic edema.
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Normal human serum contains 18 +/-5 mg/100 ml of C1 esterase inhibitor (alpha-2 neuraminoglycoprotein) as estimated by immunochemical means. Of 118 patients with hereditary angioneurotic edema, the sera of 80, from 42 kindred, contained a mean concentration of 3.15 mg/100 ml or 17.5% of normal. The
Effect of C'1 esterase on vascular permeability in man: studies in normal and complement-deficient individuals and in patients with hereditary angioneurotic edema.
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When purified human C'1 esterase is injected intradermally in man, increased vascular permeability results. This effect is not blocked by soybean trypsin inhibitor and is not abolished by pretreatment with the antihistamine, pyribenzamine, or by compound 48/80. Thus, the effect is not due to the
Effect of complement C1-esterase inhibitor on brain edema and inflammation after mild traumatic brain injury in an animal model
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Objective: Traumatic brain injury (TBI) is characterized by damage to the blood-brain barrier, inflammation, and edema formation. In this pilot study, we aimed to investigate the effects of a complement inhibitor, C1-esterase inhibitor
[Study by means of enzymatic and immunochemical determination of Cl esterase inhibitor in 59 patients with hereditary angioneurotic edema].
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Serum C1 esterase inhibitor was determined in 138 members of 18 italian families with hereditary angioedema by immunochemical and enzymatic assays. On the basis of quantitative and functional findings, the type A of hereditary angioedema was diagnosed in 44 subjects, and the type B in 15. Some
[Hereditary angioneurotic edema: a molecular disease caused by a defect in the O-glycosylation of C1 esterase inhibitor (C1-INH)].
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A quantitative and qualitative study of neutral and aminosaccharides in C 1-esterase inhibitor (C 1-INH), protein of the complement system, was performed. We observe a mixed glycosylation of the molecule with an N-glycosylated: O-glycosylated chain ratio of 1: 4. The loss of the inhibitory activity
[Acquired angioneurotic edema caused by acquired deficiency of C1 esterase inhibitor disclosing lymphoproliferative syndrome. Apropos of a case, review of the literature].
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One case of acquired angio-neurotic oedema is described and discussed with the other cases recorded in literature since Caldwell's one in 1972. This entity is characterized by: --the late onset of angio-oedema but its presence only in about half cases, --a complement deficiency resulting from the
Postburn edema and related changes in interleukin-2, leukocytes, platelet activation, endothelin-1, and C1 esterase inhibitor.
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Interleukin-2 (IL-2) promotes multisystem organ edema, lung neutrophil sequestration, and platelet activation through alterations in the microvascular barriers and permeability. IL-2, complement, platelet, and vascular endothelial activation were evaluated in 60 patients. One-factor analysis of
[The behavior of C'1-esterase and its inhibitors in the serum of patients with hereditary genuine Quincke's edema before, during and after an acute attack].
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Activation of C'1 to C'1 esterase on gel filtration on Sephadex G-200. Studies on normal human serum, euglobulin and hereditary angioneurotic edema serum.
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C1 esterase inhibitor concentrate during surgery with cardiopulmonary bypass: is there an indication beyond substitution therapy in patients with hereditary angioneurotic edema?
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C1 esterase inhibitor concentrate during surgery with cardiopulmonary bypass: is there an indication beyond substitution therapy in patients with hereditary angioneurotic edema?
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Observations on the ultrastructure of lesions induced in human and guinea pig skin by C 1 esterase and polypeptide from hereditary angioneurotic edema (HANE) plasma.
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