[Contribution of selected cellular adhesion molecules and proinflammatory cytokines in the pathogenesis of...

Proliferative diabetic retinopathy (PDR) is caused by structural and functional disorders of the retinal vessels. Complex pathobiological mechanisms of this process have not been clearly explained so far.

To prove the role of immunological-inflammatory process in the development of the proliferative diabetic retinopathy.

Forty six patients, aged 63.97+/-9 were enrolled in the study, treated for diabetes type 2 for 12.56+/-6,87 years. In 19 patients (12 women and 7 men aged 64.63+/-8.38, treated for diabetes for 12.47+/-6.75 years) a parallel analysis of given parameters was performed in both serum and vitreous body samples. Vitrectomy, in course of which the vitreous body samples were obtained, was performed in these patients because of vitreous haemorrhage, causing traction retinal detachment in some patients. The control group consisted of 15 patients (9 women and 6 men), aged 63.00+/-14.58, who underwent the vitrectomy procedure because of reasons other than diabetic retinopathy. The concentration values of the soluble forms of ICAM-1, VCAM-1, IL-6 and TNF-alpha were estimated both in the serum and vitreous body samples on the basis of the ELISA method. The biochemical tests were performed routinely in the clinical laboratory.

Mean concentrations of the investigated parameters were significantly higher in the group of patients suffering from PDR, both in the serum and in the vitreous body samples, in comparison with the values observed in the control group. In the presence of HbAlc at the level of 9.21+/-2.17% a directly proportional correlation between the TNF-alpha either in serum or in the vitreous body samples and VCAM-1 in the vitroeus body samples was found. It is worth mentioning that the increase of the TNF-alpha concentration in the vitreous body was significantly related to the rise of the VCAM-1.

The above mention of findings prove the remarkable role of the immunological and inflammatory response in the pathogenesis of this specific vascular complication of diabetes. The research was a source of evidence which highlighted the necessity of optimal metabolic control of the disease in the prevention of vascular complications of diabetes.