Abstract
Subjects infected with human immunodeficiency virus (HIV) treated with combined antiretroviral therapy (cART) show a greater predisposition to metabolic disturbances compared to the general population. The aim of the study was to assess the effect of cART on the level of selected parameters related to carbohydrate and lipid metabolism, cardiovascular diseases and inflammation in the plasma of HIV-infected patients against the uninfected. The levels of irisin (IRS), myostatin (MSTN), peptide YY (PYY), glucagon-like peptide-1 (GLP-1), dipeptidyl peptidase IV (DPP-4), fetuin A (FETU-A), pentraxin 3 (PTX 3), chemokine stromal cell-derived factor 1 (SDF-1), and regulated on activation normal T cell expressed and secreted (RANTES) in the plasma of HIV-infected patients and the control group were measured by immunoassay methods. HIV-infected patients were analyzed in terms of CD4+ T cells and CD8+ T cell count, HIV RNA viral load, and the type of therapeutic regimen containing either protease inhibitors (PIs) or integrase transfer inhibitors (INSTIs). The analysis of HIV-infected patients before and after cART against the control group showed statistically significant differences for the following parameters: IRS (p = 0.02), MSTN (p = 0.03), PYY (p = 0.03), GLP-1 (p = 0.03), PTX3 (p = 0.03), and RANTES (p = 0.02), but no significant differences were found for DPP-4, FETU-A, and SDF-1. Comparing the two applied therapeutic regimens, higher levels of all tested parameters were shown in HIV-infected patients treated with INSTIs compared to HIV-infected patients treated with PIs, but the differences were not statistically significant. The obtained results indicated significant changes in the expression of selected parameters in the course of HIV infection and cART. There is need for further research on the clinical usefulness of the selected parameters and for new information on the pathogenesis of HIV-related comorbidities to be provided. The obtained data may allow for better monitoring of the course of HIV infection and optimization of therapy in order to prevent the development of comorbidities as a result of long-term use of cART.