Reduction of Beta-Thromboglobulin levels in diabetics controlled by artificial pancreas

Voisin, P; Rousselle, D; Streiff, F; Debry, G; Stoltz, Jean‐François; Drouin, P

doi:10.1016/0026-0495(83)90218-4

Cited by 29 publications

(11 citation statements)

References 25 publications

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“…There was no difference between the two modes of therapy. In congruence with former findings [14,15,17,19,27,28] both PF-4 and p-TG levels did not correlate with any metabolic parameter, although they tended to be lower in the 'HbAl <8.5% ' group. Since in our patients near-normal metabolic control did not achieve full restitution of the physiologi cal glucose balance, resting elevation of p-TG and PF-4 might reflect one additional aspect of inadequate metabolic control.…”

Section: Discussionsupporting

confidence: 78%

“…Voisin et al [28] showed that glucose nor malization by means of biostator led to a sig nificant decline of plasmatic (3-TG concen trations over 48 h, but Rosove et al [27] found no reduction of elevated PF-4 and p-TG levels during 4-8 weeks of improved metabolic control by CSII treatment. In con sequence, we studied high-risk patients after long-term intensive treatment for normoglycemia.…”

Section: Discussionmentioning

confidence: 99%

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Elevated Platelet Activation in Type I Diabetics with Chronic Complications under Long-Term Near-Normoglycemic Control

Tschöepe

Ostermann²,

Huebinger³

et al. 1990

Pathophysiol Haemos Thromb

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A prethrombotic state with altered, hyperactive platelets may contribute to the development of diabetic late complications. Whether increased platelet ‘in vivo’ activation can be reduced by tight metabolic control is controversial. We studied plasma markers of platelet activation in 64 long-term, microangiopathic type I diabetics after at least 18 months of intensive treatment for near-normoglycemia. Both platelet factor 4 and β-thromboglobulin proved to be significantly (p ≤ 0.05) elevated in comparison with healthy controls: 15.8 (sdf 2)/77.6 (sdf 1.9) vs. 8.9 (sdf 1.6)/45.1 (sdf 2) ng/ml (sdf = standard deviation factor). We found no significant correlations with any metabolic parameter (actual blood glucose, mean blood glucose, HbA 1 triglycerides, cholesterol) or with the duration of intensive treatment. It is therefore concluded, that platelet ‘in vivo’ activation takes place in type I diabetics even after long-term near-normoglycemic control. This deviation could be regarded as indicator of an additional risk for the development of vascular complications.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Elevated Platelet Activation in Type I Diabetics with Chronic Complications under Long-Term Near-Normoglycemic Control

Tschöepe

Ostermann²,

Huebinger³

et al. 1990

Pathophysiol Haemos Thromb

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“…Improved short-term control has been associated with reduced platelet aggregation responses to epinephrine, 30 decreased plasma fibrinogen 19 and normalized fibrinogen survival, 13 decreased whole blood and plasma viscosity, 19 increased erythrocyte deformability, 31 and reduction of plasma BTG. 6 ' 32 ' 33 Frank hypoglycemia has been associated with increased platelet aggregation responses 34 ' 35 and enhanced fibrinolytic activity. 3637 Baseline studies showed that some of our patients had elevated plasma fibrinogen, FPA, AT-III, VIIIRCoF, BTG, and platelets that were hyperresponsive to ADP, similar to findings noted in previous reports.…”

Section: Resultsmentioning

confidence: 99%

Plasma β-Thromboglobulin, Platelet Factor 4, Fibrinopeptide A, and Other Hemostatic Functions During Improved, Short-Term Glycemic Control in Diabetes Mellitus

1984

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To determine the effect of improved, short-term glycemic control on various functions of hemostasis in insulin-dependent diabetes, we measured changes in plasma fibrinogen, fibrinopeptide A (FPA), functional antithrombin III (AT-III), factor VIII:ristocetin cofactor ( VIIIRCoF ), beta-thromboglobulin (BTG), platelet factor 4 (PF4), and platelet aggregation responses to ADP and collagen in 12 patients with low or undetectable stimulated (postprandial) serum C-peptide levels during 4-8 wk (median, 6 wk) of treatment with constant subcutaneous insulin infusion. Mean plasma fibrinogen, FPA, AT-III, VIIIRCoF , and BTG at baseline were elevated compared with normal. Three patients had heightened platelet responses to ADP that did not correlate to other indicators of a hypercoagulable state; the affected patients, in fact, had significantly lower plasma BTG (25.5 +/- 5.3 [SEM] versus 44.6 +/- 4.6 ng/ml, P less than 0.05) and FPA (1.1 +/- 0.1 versus 2.5 +/- 0.5 ng/ml, P less than 0.05) than the remaining patients. Patients with clinically evident vascular disease had higher baseline plasma BTG and FPA than those without vascular disease (44.6 +/- 5.4 versus 30.2 +/- 4.6, and 2.6 +/- 0.6 versus 1.3 +/- 0.2 ng/ml, P less than 0.05, respectively). During treatment, all patients had declining blood glucose (200 +/- 18 to 102 +/- 5 mg/dl, P less than 0.001) and HbA1 (11.8 +/- 0.6 to 10.2 +/- 0.4%, P less than 0.005). No statistically significant changes in hemostatic functions were noted. During treatment, one patient had an acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…It has been shown that by using a 24-h insulin infu sion, via the artificial pancreas, improve ments in erythrocyte deformability and platelet function occur and that the changes in the red cells are due to a direct effect of insulin [5][6][7]. Approximately 5% of type II diabetics each year, initially well-controlled on sulphonylurea drugs, develop hyperglycaemia and require insulin to alleviate the symptoms of poorly controlled diabetes [8].…”

Section: Introductionmentioning

confidence: 99%

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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Reduction of Beta-Thromboglobulin levels in diabetics controlled by artificial pancreas

Cited by 29 publications

References 25 publications

Elevated Platelet Activation in Type I Diabetics with Chronic Complications under Long-Term Near-Normoglycemic Control

Elevated Platelet Activation in Type I Diabetics with Chronic Complications under Long-Term Near-Normoglycemic Control

Plasma β-Thromboglobulin, Platelet Factor 4, Fibrinopeptide A, and Other Hemostatic Functions During Improved, Short-Term Glycemic Control in Diabetes Mellitus

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

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