Hamostaseologie 2015; 35(01): 25-33
DOI: 10.5482/HAMO-14-09-0039
Review
Schattauer GmbH

The vulnerable blood

Coagulation and clot structure in diabetes mellitusDas vulnerable BlutGerinnung und Gerinnselstruktur bei Diabetes mellitus
K. Hess
1   Department of Internal Medicine I, University Hospital Aachen, Germany
› Author Affiliations
The author is supported by the Deutsche Forschungsgemeinschaft (HE 5666/1–2).
Further Information

Publication History

received: 01 September 2014

accepted in revised form: 11 November 2014

Publication Date:
28 December 2017 (online)

Summary

Patients with diabetes are at increased risk of cardiovascular morbidity and mortality. While arteriosclerotic lesions have long been recognized as the underlying cause more recent studies suggest that alterations of the blood are also critically involved. Following plaque rupture, adherence of platelets is followed by the formation of a cross-linked fibrin clot. Patients with diabetes exhibit a prothrombotic milieu consisting of hyper reactive platelets, a tight and rigid clot structure which is due to up-regulation of coagulation factors and prolongation of clot lysis. Metabolic alterations as well as inflammatory processes, which are up–regulated in diabetes, are thought to be the main underlying causes. More recently, the complement cascade has emerged as a potential new player in this context with several complement components directly influencing both platelet function and coagulation.

This review provides an overview concerning the changes that lead to alterations of platelet function and clot structure in diabetes.

Zusammenfassung

Patienten mit Diabetes mellitus haben ein deutlich erhöhtes kardiovaskuläres Risiko. Lange Zeit galten Veränderungen der arteriosklerotischen Plaque als Ursache. Neue Studien legen nahe, dass Veränderungen des Blutes in diesem Zusammenhang ebenfalls eine entscheidende Rolle spielen. Im Rahmen der Plaque-Ruptur kommt es zur Aktivierung der Thrombozyten mit konsekutiver Bildung eines quervernetzten Fibringerinnsels. Patienten mit Diabetes mellitus weisen ein deutlich erhöhtes thrombotisches Milieu auf, das durch Thrombozytendysfunktion sowie eine deutlich dichtere und rigidere Fibringerinnselstruktur gekennzeichnet ist. Letztere kommt durch das vermehrte Vorliegen von Gerinnungsfaktoren und Inhibitoren der Fibrinolyse zustande. Insgesamt gelten metabolische Veränderungen sowie das bei Patienten mit Diabetes mellitus erhöhte inflammatorische Milieu als ursächlich. Neue Studien legen zudem eine Beteiligung des Komplementsystems in diesem Zusammenhang nahe.

Dieser Überblick erklärt die Veränderungen der Thrombozytenfunktion und der Fibringerinnsel bei Patienten mit Diabetes mellitus.

 
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