The role of alpha-1-antitrypsin (A1AT), serine protease inhibitor, in diabetic retinopathy is not exactly defined yet. The major pathogenic factor of diabetic microangiopathy is the non-enzymatic protein glycosylation. Chronically elevated serum glucose levels can disturb the structure and function of vascular matrix proteins by cross-linking rearrangement and cause narrowing of the luminal diameter of the micro vessels in the retina, i. e. diabetic retinopathy. Fructosamine test is considered clinically useful for assessing the short-term integrated blood glucose control in the previous one to three weeks. It is based on the alkaline reducing activity of non-enzymatic glycated serum proteins as selected according to their biological half-lives and relative concentrations, e.g. albumin, IgA, apolipoproteins, haptoglobin, transferrin, alpha-2-macroglobulin and A1AT. The aim of this study was to estimate the comparison between the serum fructosamine levels and A1AT in diabetic retinopathy patients. It covered 18 patients aged between 38 and 66 years and hospitalized in the Department of Internal Diseases, Medical University of Pleven, and 20 healthy subjects. Examinations of A1AT were done after the method of rocket immunoelectrophoresis. Fructosamine was measured after Johnson colorimetric method (Roche test fructosamine). Serum A1AT levels were significantly decreased in 11 patients (61.1%) and increased in 6 ones (33.3%) as there was no difference in one patient (5.5%) when compared to the control group. Serum fructosamine levels were significantly increased in 10 patients (55.5%) and reduced in two ones (11.1%) as there was no difference between these levels and the reference ones in 5 patients (27.7%). The statistical analysis showed a significant correlation (p < 0.005) between the elevated serum fructosamine levels and the decreased A1AT ones in diabetic retinopathy patients. The non-enzymatic protein glycosylation manifested by the elevated fructosamine level corresponds with the increased proteolytic activity of the enzymes, i.e. A1AT deficiency as a pathogenic factor for the development of diabetic retinopathy.
Scripta Scientifica Medica 2012; 44(2): 45-48.
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