Role of adhesion molecules in vascular complications of type 2 diabetes mellitus

The present study was undertaken to evaluate the plasma levels of soluble adhesion molecules [intercellular adhesion molecule-1 [ICAM-1] and vascular cell adhesion molecule-1 [VCAM-l] in type 2 DM to elucidate its potential involvement in pathogenesis of diabetic vascular complications and its association with other independent risk factors for diabetic atherosclerosis. The study was conducted on 60 patients with type 2 DM [27 with vascular complications Vs. 33 without vascular complications, assessed by fundus examinations] and 20 healthy controls, at Al-Azhar University Hospitals between March 2004 to August 2004. Serum levels of ICAM-l and VCAM-l in association with fasting blood sugar, fasting insulin and insulin resistance were measured, as wall as lipid profile, plasminogen activator inhibitor [PAl] and factor VII. Serum levels of ICAM-1 and VCAM-1 were significantly higher in type 2 diabetic patients with vascular complication than those without vascular complications, but no significant changes in their levels were found between patients without vascular complications and controls. Serum levels of ICAM- 1 and VCAM- I were significantly correlated with other studied parameters in patients with and without vascular complications except fasting serum insulin levels. Serum levels of insulin resistance [IR] and lipid profile were significantly higher in patients with type 2 DM than controls and in patients with vascular complications than those without vascular complications. Serum levels of fasting blood glucose, factor VII and PAl were significantly higher in diabetic patients with and without vascular complications than controls, on the other hand no significant changes was found between patients with and those without vascular complications. The present study suggested that the levels of soluble adhesion molecules in type 2 DM with dyslipidaemia, hyperinsulinemia and hypercoagulable state may be a marker of endothelial cell activation or dysfunction and may be related to the activity of multiple cell types in atherosclerotic lesion. Serum levels of ICAMs were closely related to vascular diabetic complications. Furthermore, they may serve as a tool for monitoring the impact of prevention and intervention on vascular damage

Apoptosis and arterial thrombosis: expression of CD31 and CD146 in recent and old thrombotic disorders

Apoptosis [programmed cell death] of vascular lining endothelium is one of the causes of increased thrombogenicity. The Luminal release of apoptotic endothelium-derived microparticles can cause activation of tissue factor [TF], the most potent known inhibitor of the blood clotting system. The study was carried out at Al-Azhar University Hospitals on 70 cases of arterial thrombosis above the age of 25 years: Group 1: consisted of 15 apparently healthy subjects as a control group. Group 11: including 32 patients of recent thrombosis; 13 with cerebral infarction, 12 with acute myocardial in farction [MI] and 7 patients with peripheral arterial thrombosis. Group 111: including 38 patients with old thrombosis; 12 with cerebral infarction, 18 with MI and 8 patients with old peripheral arterial thrombosis. Endothelial-derived CD31 and CD146 were statistically higher in patients with recent and old arterial thrombosis than controls [p<0.005, p< 0.01] respectively and statistically higher in old than in recent arterial thrombosis [p<0.05]. Hypertension DM, smoking and lipid profile have no significant effect on CD31 and CD146. Finally, endothelial microparticle detection among cases of arterial thrombosis may indicate the persistence of the danger of re-thrombosis. Patients with acute and chronic ischemia have altered response of endothelial cells. It remains to be determined whether the reduction of the increased activity of CD31 and CD146 could provide an effective rationale for acute arterial thrombosis therapy