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PubMed1980

Factors affecting plasma beta-thromboglobulin in diabetes mellitus.

Plasma beta-thromboglobulin, hemoglobin A1c and serum creatinine were measured in 56 diabetic patients. Patients with diabetic complications had a significantly higher beta-thromboglobulin level than the controls, but patients without complications did not differ from the controls. beta-Thromboglobulin correlated positively with serum creatinine and the highest values were encountered in patients with abnormal creatinine concentration. There were, however, patients with normal creatinine but high plasma beta-thromboglobulin levels. In these patients the abnormal beta-thromboglobulin level most probably indicates undue stimulation of platelets. There was no correlation between beta-thromboglobulin and hemoglobin A1c.

Adult↗

PubMed1979

Prevention of navel bleeding in piglets by preparturient administration of ascorbic acid.

Navel bleeding of newborn piglets was completely prevented by dosing the pregnant sows with ascorbic acid. The coagulation defect appeared to be caused by immature collagen which did not efficiently induce platelet plug formation. It seems that piglets depend upon their dams for their supply of vitamin C.

Administration, Oral↗

PubMed1979

beta-Thromboglobulin in plasma; false high values caused by platelet enrichment of the top layer of plasma during centrifugation.

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Beta-Globulins↗

PubMed1978

[Tumor hemorrhages].

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Disseminated Intravascular Coagulation↗

PubMed1973

[Purpura].

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Blood Platelet Disorders↗

PubMedDate not supplied

Circulating activated protein C in subjects with heterozygous Gln506-factor V.

Congenital resistance to activated protein C due to a point mutation in the factor V gene (Gln506-FV) is the most common genetic risk factor for familial venous thrombosis. Considering the central role of activated protein C as a physiological anticoagulant, the question of why the thrombotic risk associated with Gln506-FV was not more pronounced was asked. We hypothesized that in Gln506-FV heterozygotes, enhanced thrombin formation might preferentially activate protein C and thereby constitute a compensatory antithrombotic effect. We compared the circulatory level of activated protein C in twelve heterozygous carriers of Gln506-FV mutation with that in eighteen noncarriers in same families, and used prothrombin fragment 1+2 as a measure of thrombin generation. The circulating level of activated protein C was higher but not significantly different in heterozygotes compared with normal relatives. Activated protein C levels correlated strongly and positively with protein C antigen levels in both carriers (Spearman R 0.684, p < 0.05) and controls (Spearman R 0.642, p < 0.01). Correlation between activated protein C and prothrombin fragment 1+2 levels was of borderline significance (Spearman R 0.354, p = 0.055). In the current study, thrombin formation assessed by prothrombin fragment 1+2 levels was not significantly enhanced in subjects with heterozygous Gln506-FV compared with family members without the mutation. In conclusion, enhanced thrombin formation is not present in all healthy Gln506-FV heterozygotes in basal conditions. It seems that enhanced protein C activation by thrombin does not constitute a compensatory anticoagulant feedback loop in heterozygous carriers of Gln506-FV. However, the positive correlation between prothrombin fragment 1+2 and activated protein C suggests that, in healthy subjects and in basal conditions, thrombin upregulates the anticoagulant protein C pathway. Thus, it is questionable whether prothrombin fragment 1+2 can directly be used as an indicator of a hypercoagulable state.

Adolescent↗