Elevation of Factor VIII coagulant activity over Factor VIII coagulant antigen in diabetic children without vascular disease. A sign of activation of the Factor VIII coagulant moiety during poor diabetes control

Muntean, W.; Borkenstein, Martin; Haas, J.

doi:10.2337/diabetes.34.2.140

Cited by 12 publications

(6 citation statements)

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“…Poor glycaemic control in type I diabetes, as assessed by Hb A | and urinary sugar excretion, has been associated with raised factor VIII:C and VIIIR:Ag concentrations [32,33] and we have confirmed a positive association of glycaemic control and factor VIII:C in the type II diabetic patients in our study. The mea surement of C-peptide allows an accurate assessment of endogenous insulin concentra tions since C-peptide is secreted from the B cell of the pancreas in equimolar amounts with insulin.…”

Section: Discussionsupporting

confidence: 76%

Effect of Insulin Therapy on Coagulation and Platelet Function in Type II (Non-Insulin-Dependent) Diabetes mellitus

Small¹,

Jacobstein²,

Lowe³

et al. 1986

Pathophysiol Haemos Thromb

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Twenty type II (non-insulin-dependent) poorly controlled diabetics had tests of coagulation and platelet function performed while receiving high-dose sulphonylurea therapy and at 1 and 3 months following their conversion to insulin. Although no overall change in glycaemic control (assessed by glycosylated haemoglobin) was noted, a reduction in thrombin generation was observed, as judged by a significant fall in fibrinopeptide A concentrations. No changes in factor VIII coagulant activity (VIII:C), factor VIII-related antigen or antithrombin III were found. Glycosylated haemoglobin concentrations showed significant correlations with antithrombin III and factor VIII:C, suggesting that improved glycaemic control might lead to an improvement of antithrombin III function and lower factor VIIl·C concentrations. No changes in platelet function were detected. The introduction of an insulin regimen that improves glycaemic control might lead to a reversal of the ‘hypercoagulable state’ found in type II diabetes.

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Section: Discussionsupporting

confidence: 76%

Effect of Insulin Therapy on Coagulation and Platelet Function in Type II (Non-Insulin-Dependent) Diabetes mellitus

Small¹,

Jacobstein²,

Lowe³

et al. 1986

Pathophysiol Haemos Thromb

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“…This suggests that fVIII was more activated in the depressed patients. The same phenomenon has been reported in diabetic children [8]. It is possible that the rise in fVIII activity at the end of the insulin infusions resulted from the activation of fVIII by thrombin [9].…”

Section: Discussionsupporting

confidence: 59%

Activation of blood coagulation in patients with major depressive disorder during euglycemic hyperinsulinemia

Horne¹,

Merryman²,

Cullinane³

et al. 2007

Thrombosis Research

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Because hyperinsulinemia and major depressive disorder (MDD) are both associated with an increased risk of cardiovascular mortality, we hypothesized that experimental hyperinsulinemia would activate coagulation, particularly in patients with MDD [1-5]. To test this hypothesis we measured markers of coagulation activation and fibrinolytic potential in MDD patients and in controls during euglycemic insulinemia [6]. Our observations are reported here. MATERIALS AND METHODS Experimental Subjects This study was conducted under a protocol approved by the Institutional Review Board of the National Institute of Mental Health. Study subjects were required to be between the ages of 18 and 65 years, with or without depression, to have no significant underlying illnesses (eg., diabetes mellitus, cardiovascular disease), and to be taking no medications, including antidepressants. The diagnosis of depression was based upon the criteria of the American Psychiatric Association (DSM-IV) [7]. Subjects were screened with a complete history and physical examination as well as routine laboratory tests (complete blood counts, serum chemistries, thyroid function tests, lipid profile, pregnancy test). All gave signed, informed consent to participate. Experimental Design Subjects were admitted to the Warren G. Magnuson Clinical Center the night before they were studied and remained fasting after 10 PM (except for water). On the morning of the study a 20 gauge intravenous cannula was placed in one arm and connected to a four-way parallel port for the administration of glucose (20% dextrose in water), insulin (400 mU/ml), potassium phosphate (0.7 mEq/ml), and normal saline. A 20 gauge intravenous cannula was placed in the opposite arm for blood sampling. Samples for bedside glucose monitoring were collected every 5 minutes and the glucose infusion adjusted to maintain a plasma level of ~90 mg/dl. Samples

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“…Previously, we had demonstrated elevated von Willebrand factor concentrations in paediatric patients with insulin-dependent diabetes mellitus without vascular disease, 30,31 re¯ecting initial endothelial cell dysfunction. 32 Since it has been shown that multiple cardiovascular risk factors can be associated with atherosclerotic lesions even in childhood, 7 we suggest that the observed correlation between insulin and vWF-Ag in the present study might re¯ect initial endothelial alterations.…”

Section: Discussionmentioning

confidence: 99%

Determinants of haemostatic risk factors for coronary heart disease in obese children and adolescents

Gallistl¹,

Sudi

Borkenstein³

et al. 2000

Int J Obes

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OBJECTIVE: To investigate the contribution of serum lipids, parameters of glucose metabolism, body composition and cardiovascular ®tness to the variance of several haemostatic risk factors for coronary heart disease (CHD) in obese children and adolescents. SUBJECTS AND MEASUREMENTS: Forty-two healthy, obese children and adolescents (20 male, 22 female, age 12.6 AE 3.2 y; body mass index (BMI), 30.4 AE 5.3 kgam 2 ), were screened for haemostatic and metabolic risk factors for CHD. Thirty-®ve of the participants (18 male, age 13.5 AE 2.9 y; BMI, 29.9 AE 4.5 kgam 2 ; 17 female, age 12.8 AE 2.1 y, BMI, 31.1 AE 5.3 kgam 2 ) were assessed for cardiovascular ®tness by means of incremental cycle ergometer exercise. RESULTS: After adjustment for age, fat mass correlated signi®cantly with plasminogen activator inhibitor-1 antigen (PAI-1-Ag) in boys and girls and factor VIIc only in girls. Children with lower power output ( 2.77 Wakg) showed signi®cantly higher values for factor VIIc, ®brinogen and tissue-type plasminogen activator antigen (tPA-Ag). Neither body composition nor cardiovascular ®tness contributed independently to the variance of the determined haemostatic risk factors, except PAI-1-Ag, which has been shown to be determined by fat mass. In multiple linear regression analysis, triglycerides and PAI-1-Ag explained signi®cant independent proportions of the variance of tPA-Ag. Factor VIIc was explained by C-peptide, insulin and ®brinogen. Von Willebrand factor antigen (vWF-Ag) was signi®cantly related to glucose and insulin. CONCLUSION: The results suggest that in obese children and adolescents the haemostatic risk factors factor VIIc, vWF-Ag and tPA-Ag are mainly determinated by plasma insulin and triglyceride concentrations, but are primarily independent of body composition and cardiovascular ®tness.

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Elevation of Factor VIII coagulant activity over Factor VIII coagulant antigen in diabetic children without vascular disease. A sign of activation of the Factor VIII coagulant moiety during poor diabetes control

Cited by 12 publications

References 0 publications

Effect of Insulin Therapy on Coagulation and Platelet Function in Type II (Non-Insulin-Dependent) Diabetes mellitus

Effect of Insulin Therapy on Coagulation and Platelet Function in Type II (Non-Insulin-Dependent) Diabetes mellitus

Activation of blood coagulation in patients with major depressive disorder during euglycemic hyperinsulinemia

Determinants of haemostatic risk factors for coronary heart disease in obese children and adolescents

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