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Results for “Factor XII Deficiency”

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PubMed1978

Hageman trait.

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Adult↗
PubMed1982

Factor XII and other hemostatic protein abnormalities in nephrotic syndrome patients.

Factor XII clotting activities and antigen levels were assayed in 14 plasma samples from 10 patients with nephrotic syndrome; the group was heterogeneous clinically and histologically. Factor XII was low at initial sampling in 7 of the 10 patients; in 7 of the 14 samples, factor XII antigen was in excess over clotting activity. Inhibition of factor XII could not be demonstrated; excess plasma antigen and urinary antigen (when present) had normal patterns on crossed-immunoelectrophoresis, indicating no major changes in charge or size. In 3 patients tested more than once, plasma levels of factor XII were increased up to 6fold in steroid-induced remission. Of other hemostatic factors assessed for comparison, factor VIII was elevated in 11 of the 14 samples; eight of these had elevated factor VII levels as well. Eight samples from six patients showed low antithrombin III levels; one of these patients had recurrent thromboses. Antithrombin III levels correlated with the serum albumin concentration. Only two of the eight urines tested had detectable factor XII antigen; a third had factor IX and prothrombin and no factor XII. Plasminogen and antithrombin III were readily demonstrated in all urine samples with higher concentrations in those patients with less selective proteinuria. Urinary and plasma levels were not correlated, suggesting that increased consumption or turnover was not simply related to increased filtration.

Adolescent↗
PubMed1980

The "contact system" in health and disease.

In the last 10 years, our understanding of the contact system, particularly its biochemistry, has greatly increased. The components of this system and their interactions have been elucidated from in vitro experiments. Although the activation of the contact system have been implicated in various types of human disease, in only a few instances is its role clearly defined. The physiologic role of the contact system is totally unknown at present. Obviously, more studies are needed to bridge a big gap between in vitro observations and in vivo phenomena.

Blood Coagulation↗
PubMed1981

Tobacco, cocoa, coffee, and ragweed: cross-reacting allergens that activate factor-XII-dependent pathways.

A glycoprotein antigen has been isolated from cured tobacco leaves (TGP-L) Nicotiana tabacum) and from cigarette smoke condensate (TGP-CSC) to which approximately one-third of human volunteers, smokers and non-smokers, exhibit immediate cutaneous hypersensitivity. TGP-L and TGP-CSC contain polyphenol haptens that activate the factor XII (Hageman factor) dependent pathways of coagulation, fibrinolysis, and kinin generation in normal human plasma. The purpose of this communication is to describe the isolation antigens from cocoa powder (Theobroma cacao), ground coffee (Coffea arabica), and ragweed (Ambrosia eliator) pollen that are immunologically cross-reactive with TGP-L and TGP-CSC, contain similar polyphenol haptens, and are capable of activating factor-XII-dependent pathways in normal human plasma.

Allergens↗
PubMed1981

Role of splenic red pulp in endotoxin-induced disseminated intravascular coagulation.

As an extension of our studies on vascular responses to endotoxemia, we evaluated sequential ultrastructural lesions of splenic red pulp and correlated these lesions with coagulation changes observed in rhesus monkeys following infusion with endotoxin either as a single bolus (10 mg. per kg.) or at a continuous rate of 10 mg. per kg. per hour for periods up to 16 hours. Controls included monkeys infused with Ringer's lactate solution. Progressive reactions of the splenic cords included increased phagocytic activity of macrophages in association with aggregation and degranulation of platelets and prominent fibrinous deposits characteristically abutting basement membranes of endothelial and reticular cells. The sinuses demonstrated endothelial damage, platelet-fibrin microthrombi obstructing interendothelial slits, and severe engorgement with entrapment of erythrocytes by tactoids of fibrin. The thrombotic lesions of the red pulp developed earlier than similar lesions in hepatic sinusoids, and they were accompanied by progressive thrombocytopenia and disseminated intravascular coagulation. The findings suggest that the unique microcirculation of the spleen is an early target and trigger of endotoxin-induced microthrombosis. It is proposed that phagocytosis of endotoxin by splenic phagocytic cells and associated inflammatory events result in disruption of reticular cells and endothelium leading to massive microthrombosis with breakdown of the splenic filter. In addition, rapid activation of coagulation mechanisms in the red pulp as well as liver sinusoids may promote the development of thrombocytopenia and disseminated intravascular coagulation in endotoxic shock.

Animals↗