Spontaneous platelet aggregation, VWF-AG and fibrin as risk factors for new vascular occlusions in type I and II diabetes

Breddin, H. K.; Krzywanek, H. J.; Althoff, P. H.; Kirchmaier, C. M.; Rosak, C.; Schepping, M.; Weichert, W; Ziemen, M.; Schöffling, Κ.; Überla, K

doi:10.1016/0049-3848(86)91651-8

Cited by 7 publications

(7 citation statements)

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“…In diabetes mellitus particularly, the interaction of platelets with the endothelial lining is disturbed 34,[45][46][47] and the clinical significance of platelet hyperactivity may be derived from the data reported by the "Platelet Aggregation as a Risk of Diabetes Study" (PARD) showing that the incidence of macrovascular endpoints in male diabetic patients was strongly related to the degree of spontaneous platelet aggregation at study entry. 48 In general, changes toward an enhanced thrombotic potential have been found at all levels of the platelet system:…”

Section: Platelet Pathways Of Diabetic Angiopathymentioning

confidence: 99%

Platelets in Diabetes: The Role in the Hemostatic Regulation in Atherosclerosis

Tschöepe

Roesen²,

Schwippert³

et al. 1993

Semin Thromb Hemost

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Vascular diseases and related complications still represent the main cause of death in diabetic patients. Neuropathy, nephropathy, retinopathy, and disturbed nutritive tissue perfusion may result from reduced capillary microcirculation. These disturbances are diabetes specific. Macroangiopathy does not differ structurally from atherosclerotic lesions of nondiabetic subjects, but leads to accelerated cerebral, coronary, and peripheral artery disease. Occurrence of life-terminating thrombotic events, which are superimposed on those vascular lesions, are increased. Thus, morbidity and mortality of diabetics depend mainly on vascular complications. Normal blood flow is a prerequisite of adequate organ perfusion and results from vasomotion, plasma components, corpuscular blood elements, vascular architecture, and the undisturbed interaction of these components at the endothelial interface. Functional thromboresistance of the endothelial layer is reduced in the diabetic state. Increased intravascular thrombin generation, reduced fibrinolytic potential, and hyperactive platelets lead to a prethrombotic state. This thrombotic diathesis increases the permanent danger of acute flow interruption. Activated platelets operate by three mechanisms: (1) Microembolization of the capillaries; (2) local progression of preexisting vascular lesions by secretion of constrictive, mitogenic, and oxidative substances; (3) trigger of the prognosis-limiting arterial thrombotic event. We were able to show that the increased functional properties of diabetic platelets result from the primary release of larger platelets with enhanced thromboxane formation capacity and increased numbers of functional glycoprotein receptors GPIb and GPIIb/IIIa, which are synthesized in the megakaryocytes. The megakaryocyte-platelet system is turned on in diabetes mellitus. It could be demonstrated with the Duesseldorf III method of flow cytometric activation marker testing (CD62, CD63, thrombospondin) that predominantly large platelets circulate in an activated state in diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Platelet Pathways Of Diabetic Angiopathymentioning

confidence: 99%

Platelets in Diabetes: The Role in the Hemostatic Regulation in Atherosclerosis

Tschöepe

Roesen²,

Schwippert³

et al. 1993

Semin Thromb Hemost

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“…Enhanced spontaneous platelet aggregation (2, 14), increased plasma levels for factor VIII C (I, 2,3,11) and raised plasma concentrations of on Willebrand factor have been reported by many authors (1, 2, 3,11). aur results did not differ from these findings.…”

Section: Discussionmentioning

confidence: 92%

“…Although many alterations in the coagulation and fibrinolytic system have been reported for adult type I and type 11 diabetes, only a few studies have been carried out on diabetic children without vascular disease (review 11, 1,2,5,6,7,9,12,13,14). Furthermore, contlicting reports have appeared in the literature, especially concerning the fibrinolytic system (3,5, 6,11,12).…”

Section: Discussionmentioning

confidence: 99%

15 Parameters of Coagulation and Fibrinolysis in Children with Type I Diabetes Mellitus (Onset Period)

Koert

Nowak-Göttl²,

Kreuz³

et al. 1991

Klin Padiatr

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15 parameters of coagulation and fibrinolysis were investigated in 38 children with type I diabetes mellitus without clinical signs of diabetic angiopathy. Compared to an age matched non diabetic control group spontaneous platelet aggregation was enhanced, plasma levels for factor VIII C, von Willebrand factor, antithrombin III and C-1-inactivator were elevated, alpha-2-macroglobulin was decreased at onset of the disease. During remission (3, 6, 12 months) these changes reverted to normal. Alpha-2-antiplasmin decreased after 12 months. If, during partial remission, diabetic duration was longer than one year an increase of factor VIII C was seen again. In comparison to the controls no significant alterations were found for ristocetin cofactor, fibrinogen, plasminogen and alpha-1-antichymotrypsin. It seems likely that changes in plasmatic coagulation, fibrinolysis and platelet function during the onset period of diabetes mellitus type I are due to metabolic changes and precede diabetic angiopathy.

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“…1986 wiesen Breddin et al [30] in der PARD-Studie (Platelet Aggregation as Risk Factor in Diabetes) nach, dass die spontane Plättchenaggregation bei Diabetikern deutlich gesteigert ist. Im selben Jahr veröffentlichten Ostermann & van de Loo [31] eine umfangreiche Übersicht zu diesem Thema.…”

Section: Plättchenaktivierung Bei Diabetes Mellitusunclassified

Die Rolle der Thrombozyten bei Atherosklerose, Diabetes mellitus und chronischer Niereninsuffizienz

Maurin

2010

Med Klin

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Erythropoiesis-stimulating agents (ESA) are used to treat renal anemia. The TREAT study (Trial to Reduce Cardiovascular Events with Aranesp Ther- apy) of diabetic patients with chronic kidney disease (CKD) found that the risk of stroke was significantly higher than in the control arm. This raises the question as to what causes this phenomenon. Platelets may play a crucial role in this context. Atherogenesis involves complex interactions between platelets and monocytes (platelet-monocyte crosstalk) and with endothelial cells. Platelets are activated in cases of diabetes mellitus, especially. During atherogenesis, partial functions of platelets other than those inhibited by aspirin, as a cyclooxygenase inhibitor, or by adenosine diphosphate receptor P2Y(12)antagonists, such as thienopyridines, are of relevance. During platelet-monocyte crosstalk, specifically, an important role is played by adhesion receptors such as selectins and integrins. In addition, ESA cause platelet activation by direct and indirect mechanisms. Antagonistic thereto is a renal bleeding tendency in cases of severe CKD, due to platelet dysfunction, which can be remedied with appropriate renal replacement therapy and administration of ESA in order to reach a hemoglobin (Hb) level of 10 g/dl. However, if the Hb level exceeds 10 g/dl, the even stronger platelet activation caused by ESA, combined with the activation caused by diabetes, leads to a prothrombotic state, which in patients with severe atherosclerosis can result in acute atherothrombotic complications, in the genesis of which platelets play a key role. This would be one hypothesis for explaining the increased incidence of strokes in the TREAT study.

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Spontaneous platelet aggregation, VWF-AG and fibrin as risk factors for new vascular occlusions in type I and II diabetes

Cited by 7 publications

References 0 publications

Platelets in Diabetes: The Role in the Hemostatic Regulation in Atherosclerosis

Platelets in Diabetes: The Role in the Hemostatic Regulation in Atherosclerosis

15 Parameters of Coagulation and Fibrinolysis in Children with Type I Diabetes Mellitus (Onset Period)

Die Rolle der Thrombozyten bei Atherosklerose, Diabetes mellitus und chronischer Niereninsuffizienz

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