D. De Lucia, K. Krekora, S. Pezzella, V. Del Giudice, M. B. Donati* and L. Iacoviello*.
Institute of General Pathology and Oncology; II University of Naples. *Consorzio Mario Negri Sud, Santa Maria Imbaro Italy.

Thromboembolism is a serious complication of the Diabetic Disease in adults. Its incidence varies from 10% to 45% in the literature. The mechanism underlying this susceptibility to thrombosis involves the change in the turnover and concentrations of most plasma proteins which alters the balance between procoagulant and anticoagulant systems. Several modifications might contribute to the thrombotic tendency: increased levels of procoagulant factors such as fibrinogen and factor VIII; platelet hyperactivation, decreased concentrations of natural clotting inhibitors (ATIII, PC, and PS) and reduced fibrinolytic activity.
The variant FV Q506 responsible for the activated protein C resistance has also been show to induce an increased risk of thromboembolism.
Although the relation between FV Q 506 allele and venous thrombosis has been extensively confirmed,its role in arterial thrombosis has not so far been established.
Non-Insulin Dependent Diabetes Mellitus (NIDDM) is associated with a high incidence of arterial thrombosis. In such patients changes in haemostasic factors have been described and may contribute to the increased risk of myocardial infarction, cerebrovascular disease and peripheral vascular disease.
For this reasons, we have analyzed 147 unselected patients with NIDDM (age 65, SD 10, 83M / 64F) and 118 healthy subjects (age 58, SD 9, 68M / 50F) without a history of diabetes.
In all enrolled subjects we searched for FV Q506 allele.
In patients with NIDDM we found 12 with FV Q506 allele (95% CI 8-2%, 3.7-12.6) all heterozygous significantly higher than in our controls (2.5%, 95% CI 2.0-3.0; p<.001 Fisher exact test).
All the patients carrying the FV mutation reported a family history of Diabetes compared with only 76 (56%) of patients without the mutation (p<.002, Fished exact test).
Our results show that FV Q506 mutation is associated with NIDDM. Diabetes patients
with this mutation might be predisposed to arterial thrombosis.
There was an excess of peripheral arterial disease in the group of patients carrying the mutation (14.7% vs. 4.4%).
The authors feel that a hemostatic abnormality expressed in patients with NIDDM may have a genetic antecedent cosegregating with diabetes and suggest that FV mutation could contribute to the high frequency of arterial disease.

Home page THROMBOEMBOLISM
Home page BIOMEDICINE DATABASE
Home page MOLECULAR MEDICINE