The role of disorders of the endothelial function in the development and progression of diabetic distal symmetric polyneuropathy depending on genetic factors

Abstract

Background. The purpose was to examine indicators of endothelial functional status in patients with diabetic distal symmetric polyneuropathy (DDSP) on the background of type 2 diabetes mellitus (DM), which depends on the polymorphism of the endothelial nitric oxide synthase gene (eNOS). Materials and methods. One hundred and ten patients with DDSP on the background of type 2 DM were examined and composed the basic group. The average age of patients was 54.2 years (from 38 to 72 years). The patients were distributed according to DDSP severity: the first group consisted of 32 (29.1 %) patients with the initial manifestations of DDSP; the second group included 58 (52.7 %) patients with moderate degree; the third group consisted of 20 (18.2 %) patients with severe DDSP. All patients underwent neurological examination using the scale of neuropathic symptomatic and neuropathic functional counting. The endothelial function was investigated by the content of stable metabolites of NO in the blood and the number of circulating endothelial cells in the blood. G894T polymorphism in eNOS gene was detected by polymerase chain reaction. Results. According to the data, most patients (78.5 %) presented with decreased amount of NO2– - NO3–.The number of desquamated endothelial cells was significantly increased in all examined patients compared to control. Comparing endothelial function parameters depending on G894T polymorphism in the eNOS gene, 43.6 % patients with a homozygous genotype for rare T allele were found to have a significant reduction of NO2– - NO3– content compared to control group (p < 0.05). Conclusions. There were significantly more pronounced disorders of the endothelial function in patients with moderate to severe DDSP on the background of type 2 DM. The results of the investigation showed the probable effect of G894T polymorphism of eNOS gene on the formation of a phenotype predisposing to the development of microangiopathies.