fibrinopeptide-a and Hyperglycemia

fibrinopeptide-a has been researched along with Hyperglycemia* in 4 studies

Other Studies

4 other study(ies) available for fibrinopeptide-a and Hyperglycemia

ArticleYear
The role of hyperglycaemia-induced alterations of antithrombin III and factor X activation in the thrombin hyperactivity of diabetes mellitus.
    Diabetic medicine : a journal of the British Diabetic Association, 1990, Volume: 7, Issue:4

    Factor X concentration and factor X activation, antithrombin III anti-Xa activity and plasma concentration, and fibrinopeptide A were measured in 20 diabetic patients and 20 normal subjects. Although factor X activation (81.3 +/- 2.2 vs 97.3 +/- 2.1%, p less than 0.01; mean +/- SE) and antithrombin III activity (76.5 +/- 2.2 vs 96.3 +/- 1.8%, p less than 0.01) were reduced in the diabetic patients, fibrinopeptide A concentration was increased (3.7 +/- 0.4 vs 1.7 +/- 0.2 ng ml-1, p less than 0.01). The ratio of factor X activation to antithrombin III anti-factor Xa activity was increased in the diabetic patients (1.10 +/- 0.01 vs 1.01 +/- 0.02, p less than 0.01). Induced hyperglycaemia was able to mimic all these abnormalities, without changing factor X or antithrombin III concentration. The results suggest that in vivo hyperglycaemia produces a decrease of factor X activation, but at the same time increases fibrinopeptide A formation due to a greater decrease of antithrombin III anti-Xa activity.

    Topics: Adult; Antithrombin III; Blood Glucose; Diabetes Mellitus, Type 1; Factor X; Factor Xa; Female; Fibrinopeptide A; Humans; Hyperglycemia; Male; Reference Values; Thrombin

1990
Evidence for a hyperglycaemia-dependent decrease of antithrombin III-thrombin complex formation in humans.
    Diabetologia, 1990, Volume: 33, Issue:3

    In the presence of increased levels of fibrinopeptide A, decreased antithrombin III biological activity, and thrombin-antithrombin III complex levels are seen in diabetic patients. Induced-hyperglycaemia in diabetic and normal subjects decreased antithrombin III activity and thrombin-antithrombin III levels, and increased fibrinopeptide A plasma levels, while antithrombin III concentration did not change; heparin was shown to reduced these phenomena. In diabetic patients, euglycaemia induced by insulin infusion restored antithrombin III activity, thrombin-antithrombin III complex and fibrinopeptide A concentrations; heparin administration had the same effects. These data stress the role of a hyperglycaemia-dependent decrease of antithrombin III activity in precipitating thrombin hyperactivity in diabetes mellitus.

    Topics: Adult; Antithrombin III; Blood Glucose; Diabetes Mellitus, Type 1; Female; Fibrinopeptide A; Heparin; Humans; Hyperglycemia; Kinetics; Male; Peptide Hydrolases; Reference Values

1990
Hyperglycemia may determine fibrinopeptide A plasma level increase in humans.
    Metabolism: clinical and experimental, 1989, Volume: 38, Issue:12

    The effects of hyperglycemia on plasma fibrinopeptide A (FPA) levels in normal subjects are reported. An increase of FPA concentration parallel to sustained hyperglycemia was observed; when the glycemia returned to basal values, FPA showed values in normal range. Heparin infusion was able to significantly decrease the hyperglycemia-induced augment of FPA levels. Isovolumic-isotonic NaCl solution infusion produced a slight (NS) increase in FPA levels; however, mild hyperglycemia, achieved by glucagon, was also able to produce a significant increase in FPA concentration. These data demonstrate the direct role of hyperglycemia in conditioning FPA level, and suggest that hyperglycemia, by itself, is a sufficient stimulus to produce thrombin activation in humans.

    Topics: Adult; Blood Glucose; Fibrinogen; Fibrinopeptide A; Glucagon; Glucose; Heparin; Humans; Hyperglycemia; Infusions, Intravenous; Male; Thrombin; Time Factors

1989
Acute changes in blood glucose concentration do not promote thrombin generation or fibrin breakdown in type 1 diabetes.
    Diabetic medicine : a journal of the British Diabetic Association, 1988, Volume: 5, Issue:9

    To investigate the effect of blood glucose concentration on thrombin generation and fibrinolytic activity, six Type 1 patients had the blood glucose concentration maintained for 1 h at 5, 15, and 25 mmol l-1, and 8 patients underwent hypoglycaemia of 20 min duration after the blood glucose had been kept at 8 mmol l-1 for 1 h. During hyperglycaemia plasminogen activator activity rose from 214 (11-625) (median, range) to 478 (18-772) units (p less than 0.05) at a blood glucose of 5 mmol l-1 and to 511 (89-816) (p less than 0.05) and 535 (33-976) (p less than 0.05) units at a blood glucose of 15 and 25 mmol l-1, respectively. Cross-linked fibrin degradation products (FDP) were 45 and 53 micrograms l-1 at a blood glucose of 5 mmol l-1 and remained unchanged at higher glucose levels. Fibrinopeptide A was 1.3 (0.6-2.8) nmol l-1 at a blood glucose of 5 mmol l-1, and remained unchanged with hyperglycaemia, being 1.3 (0.9-1.3) nmol l-1 after 1h at 25 mmol l-1. During hypoglycaemia, plasminogen activator activity rose from 155 to 745 units (p less than 0.05) while both fibrinopeptide A and cross-linked FDP remained unchanged. The results indicate that acute fluctuations in blood glucose concentration do not lead to thrombin generation. Additionally, increased fibrinolytic activity measured in vitro is not associated with an increase in cross-linked FDP. This suggests that short-term hyper- and hypoglycaemia do not affect the end-products of the coagulation and fibrinolytic pathways.

    Topics: Blood Glucose; Diabetes Mellitus, Type 1; Fibrin; Fibrinopeptide A; Glycated Hemoglobin; Humans; Hyperglycemia; Hypoglycemia; Male; Plasminogen Activators; Thrombin

1988