Background : Progressive vascular disease of the large and small vessels is characteristic of the diabetic state. Several studies have shown that hyperhomocysteinemia (HHcy) is related to both micro- and macrovascular disease in diabetes. Von Willebrand factor is a marker for endothelial dysfunction, and qualitative and quantitative abnormalities of vWF have been reported in diabetic patients. Objectives : The aim of the present study is to investigate homocysteine (Hcy) and von Willebrand factor in NIDDM, and their role as determinants (or markers) in the development of micro- and macrovascular complications in NIDDM, also to elucidate a link between HHcy and endothelial dysfunction marker, vWF antigen, in this cohort. Methods : We measured Hcy and vWF in 70 type 2 diabetic patients, 10 patients had diabetes without evidence of micro- or macrovascular complications (group II), 30 patients had microvascular complications only (group III), 30 patients had macrovascular complications with or without microvascular complications (group IV). Ten healthy subjects were included as control group (group I). Results: Hcy and vWF were significantly higher in both uncomplicated (II group) and complicated (III and IV groups) type 2 diabetic patients as compared with non-diabetic control subjects (group I). VWF values were significantly higher in complicated diabetic groups (III and IV) as compared with uncomplicated diabetic patients (group II); however, there was no significant difference in Hcy values between complicated and uncomplicated diabetic patients. There was no significant correlation between Hcy and vWF values in any of our studied groups.Conclusion: In conclusion, HHcy in type 2 diabetic patients suggests a possible synergistic role of Hcy and hyperglycemia in inducing vascular damage. High vWF in type 2 diabetic patients indicate a role of endothelial dysfunction in the development of diabetic complications. However, a link between HHcy and vascular disease in type 2 diabetic patients cannot readily be explained by endothelial dysfunction as reflected by plasma vWF concentration and alternative mechanisms may be operative.