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At least 1,315 records · Page 73Linked to original sources
PubMed1988

[Familial studies of patients with hereditary angioedema].

25 families with 607 members were studied. 165 persons of them suffer from hereditary angioneurotic edema and 28 persons had died from this disease. The clinical forms of the disease are discussed. A classification of angioneurotic edema caused by C-inactivator deficiency is presented. The importance of the examination of C1 inactivator (quantitatively and qualitatively) and of C4 complement fraction in patients with hereditary angioneurotic edema is pointed out.

Adolescent↗
PubMed1987

[Hereditary angioedema: changes in serum levels of C4 in response to danazol].

12 patients (7 males and 5 females) suffering from the common form of HAE were included in the study protocol. All patients were older than 18 years. They were evaluated Cl INH, C4, Clq, Cls, C3, C5, C8, Bf, CH 50% and CIC. For the purpose of the study they were only considered Cl INH, C4, CH 50%, CIs and CIC levels. The rest of the complement components were among normal values. Data were recorded at day 0 and after 10 days on treatment with 400 mg/day of Danazol. Results were as follows: 50% of the patients had CIC when CH 50% values were below 120 U/ml., after treatment CIC disappeared and CH 50, Cls, C4 and Cl INH increased significatively. C4 seemed to increase more and quicker than Cl INH in terms of absolute values. We postulate that in the group of patients with CIC, the primary cause of the disease may be an alteration in C4 synthesis and that Cl INH may be lowered because of its consumption. We postulate that Danazol could act in these cases stimulating C4 synthesis independently or in accordance with Cl INH.

Adult↗
PubMed1977

Alternative complement pathway in bovine serum: lysis of human erythrocytes.

The hemolysis of unsensitized human erythrocytes by fresh bovine serums was investigated. Lysis occurred in ethylene glycol bis-amino tetraacetate buffers and with serums depleted of Clq. Serums extensively absorbed with packed human erythrocytes at 0 C effectively lysed human erythrocytes, but optimal lytic capacity required target cells "sensitized" with a heat-stable serum factor. Lysis did not occur with serums absorbed with zymosan at 17 C or heat inactivated at 50 C. These results indicate that human erythrocytes can activate the alternative pathway of complement in bovine serums. Lysis can proceed in the apparent absence of antibodies, although their presence may enhance the reaction.

ABO Blood-Group System↗
PubMed1985

[Nonspecific immunity factors and elimination of circulating immune complexes in patients with myocardial infarct in the 1st phase of rehabilitation].

A considerable increment of humoral immunity parameters was demonstrated during the 3d-5th week after the onset of myocardial infarction (MI). The levels of IgG and IgE were increased, and those of circulating immune complexes (CIC), decreased significantly in patients with their first diagnosed infarction, as compared to those with repeated MI. Patients with repeated MI showed significantly reduced blood C3c, C4 and the phagocyte index in the presence of high blood levels of CIC and C-reactive protein, as compared to patients with primary infarction. The results are indicative of a considerable activation of the complement and the phagocytic system and CIC elimination in patients with their first MI diagnosis, and the absence of such a stimulation in repeated MI cases.

Adult↗
PubMed1979

[Significance of the complement system in acute pancreatitis in rats].

The influence of complement system in acute pancreatitis in the rat was examined. Two different experimental procedures were used to induce pancreatitis: distal choledochal ligature and the Pfeffer model as modified by NEVALAINEN. In both procedures an acute pancreatitis developed and complement depression was noted. These results showed that consumption of complement will occur even in pancreatitis induced by other than immunologic models. In a second series the same experimental procedures were used in rats that had been decomplemented by application of cobra venom factor. It was possible to produce an acute pancreatitis of moderate severity.

Acute Disease↗
PubMed1982

Complement: activation, consequences, and control.

The activation of complement provides the humoral (fluid-phase) effector mechanism most responsible for immune-mediated injury. The classical pathway is activated by an antigen-antibody reaction. The binding of C1q initiates the sequential activation of the eleven proteins. The classical pathway has a calcium-dependent step (C1q, C1r, C1s) and a magnesium-dependent reaction (the enzymatic action of C1s on C4 and C2). The alternative pathway appears to be spontaneously activated, but the perpetuation of that activation is dependent upon the availability of an activating (or protective) surface which interferes with the inactivation of C3b by control proteins. The alternative pathway has a magnesium-dependent step, the binding of B to C3b to form the C3 convertase. Once initiated, the alternative pathway activation results in the sequential activation of nine proteins, six of which are common to both pathways. The activation of complement results in a variety of biologic consequences which can result in injury to the host. The potential destructiveness of the effects of complement activation is modulated by a series of control proteins.

Carrier Proteins↗