Increased Prothrombin Fragment 1 +2 in Type I Diabetic Patients
Antonio Ceriello, Roberta Giacomello, Antonio Colatutto, Claudio Taboga, Fabio Gonano
1992
Pathophysiology of Haemostasis and Thrombosis
The pathogenesis of vascular lesions in diabetic patients has been considered to be at least partly dependent on the alterations in the hemostatic system [1]. However, the existence and the relevance of a hypercoagulable state in diabetes mellitus have been the subject of much debate [1,2]. It has been demonstrated that the conversion of the coagulation zymogen prothrombin to thrombin is associated with the prominent production of a cleavage product namely prothrombin fragment 1+2 (Fl+2) [3].
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... has been proposed recently that prothrombin Fl+2 plasma levels may be considered a very sensitive marker for hypercoagulable states in humans [4]. We evaluated prothrombin Fl+2'(ELISA) levels in 19 insulin-dependent diabetic patients without signs of vascular complications (12 males and 7 females: age 23.4 ± 1.9 years, mean ± SE; body mass index 22.8 ± 1.4; duration of diabetes 6.4 ± 1.3 years; insulin regimen 25-55 U/day, mean 32.8 ± 2.5 U/ day; all subjects had 24-hour urinary albumin excretion rates less than 30 µg/min, and no microaneurysms were detected on full fundal photographs or íluorescein fundal angiogra-phy; they had systolic blood pressures < 120 mm Hg and diastolic blood pressures < 90 mm Hg; ischemic heart disease and peripheral vascular occlusion were excluded according to local criteria) compared to 10 matched healthy normal subjects (6 males and 4 females: age 24.2 ± 1.8 years, body mass index 23.2 ± 1.3). Prothrombin Fl+2 levels were significantly elevated in diabetic patients (0.69 ± 0.11 vs. 0.27 ± 0.03 nmol/l;p < 0.01), but no correlation was found between prothrombin Fl+2 plasma levels and both fasting glycemia (r = 0.17) and glycosylated Hb A1 c (r = 0.16). Increased FPA levels have been reported in diabetes [5]. These findings were considered more suggestive of a thrombin hyperac-tivity than of an increase of thrombin production [6]. This hypothesis was sustained by the evidence of normal [7] or depressed [6] levels of thrombinantithrombin complex in the presence of increased FPA [6] and fibrin monomers [7] in diabetes.
doi:10.1159/000216291
pmid:1521827
fatcat:w3eqawqnkjgm5ims5zlqlaxrxi