The human immunodeficiency virus has affinity not only to the cells of the immune system but also to the cells of the nervous system that have the CD4 receptor on their surface. The frequency of CNS disorders, according to the literature, ranges from 30% to 80%. This is due both to the direct effect of the virus on the nervous system and to mediated biochemical changes in human cells [1].
Due to advances in the treatment of this disease and the use of antiretroviral therapy (ART), the life expectancy of patients is increasing, which leads to an increase in the incidence of age-associated cardiovascular events, including strokes [2].
According to some studies, many antiretroviral drugs can affect the lipid spectrum and blood glucose levels, which increases the risk of strokes [3,4,5]. In particular, a decrease in the level of high-density lipoproteins (HDL) is characteristic of HIV-infected patients, and with the progression of the disease, a decrease in the level of low-density lipoproteins (LDL) as well as an increase in triglycerides and very-low-density lipoproteins (VLDL) [5,6,7,8]. In general, the available data on changes in lipid metabolism in HIV patients with strokes are insufficient and do not allow estimating the degree of risk of cerebral circulation disorders due to vascular atherosclerosis. In this regard, the purpose of this study was to study the peculiarities of changes in laboratory parameters of lipid metabolism in cerebral stroke in patients with HIV infection.
Materials and Methods. 77 patients with ischemic strokes (IS) and 32 patients with hemorrhagic strokes (HS) were examined against the background of comorbid HIV infection, they were admitted for treatment to hospitals in the Tyumen Region in 2015 - 2020. Lipid metabolism parameters were examined on "Becman Coulter AU-480" (the USA). Blood sampling was carried out on the day of admission of the patients. The levels of total cholesterol (TC), low-density lipoproteins (LDL), high-density lipoproteins (HDL), and triglycerides (TG) were assessed, the atherogenicity coefficient was calculated. The control group consisted of 116 patients (82 patients with IS and 34 with HS). The significance of the differences was determined at a bilateral significance level of p<0.05.