Risk Assessment for the Development of Metabolic Syndrome in Patients with AIDS After the First Year of Antiretroviral Therapy

Miloš N Pejković; Vladislava Stojić; Biljana Popovska-Jovičić

doi:10.5937/mp70-17921

Miloš N Pejković Faculty of Medical Sciences, University of Kragujevac
Vladislava Stojić Faculty of medical Sciences, University of Kragujevac
Biljana Popovska-Jovičić Faculty of medical Sciences, University of Kragujevac

DOI: https://doi.org/10.5937/mp70-17921

Abstract

Introduction: Antiretroviral therapy (ART) in the treatment of HIV infection has allowed maximum control of viral replication and reconstruction of the immune system, which has contributed to the long-term survival. However, it has been observed that a long-term use of ART can lead to cumulative toxicity and metabolic abnormalities.

Aim: The aim of this study was to determine whether there is a difference in lipidogram, glycemia and body mass index (BMI) before and after the initiation of ART, and to determine in which of the antiretroviral drugs the changes in the values of the measured variables were most common.

Material and methods: The research was conducted at the Clinic for Infectious Diseases, Clinical Center of Kragujevac, as a prospective study involving 40 patients diagnosed with HIV infection. Biochemical parameters and BMI calculation were performed before the initiation of ART and one year after.

Results: The analysis of the observed variables indicated a statistically significant difference in total cholesterol (p = 0.001), HDL (p = 0.002), LDL (p = 0.003), triglycerides (p < 0.001), glucose (p < 0.001) and BMI (p = 0.002). By analyzing the administered АRT therapy, statistical significance was achieved in the measured triglyceride values after the administration of ritonavir and lopinavir, while the highest BMI values, compared to initial ones, were observed after the administration of ritonavir, but without achieving statistical significance.

Conclusion: The results of the study showed that АRТ therapy has effect on the development of hyperlipidemia, which may be associated with an increased risk of developing cardiovascular disease and protease inhibitors of the older generation are highlighted, in particular. АRT therapy in HIV-infected cells contributes to the development of a metabolic syndrome involving dyslipidemia, lipodystrophy and insulin resistance.

Keywords: HIV, antiretroviral therapy, cardiovascular disease, protease inhibitors, hyperlipidemia

Author Biographies

Miloš N Pejković, Faculty of Medical Sciences, University of Kragujevac

student, VI year of medicine, Faculty od Medical Sciencies, University of Kragujevac

Vladislava Stojić, Faculty of medical Sciences, University of Kragujevac

assistant at Medical statistics and informatics, Faculty of medical Sciences, University of Kragujevac

Biljana Popovska-Jovičić, Faculty of medical Sciences, University of Kragujevac

assistant Prof. at Indectious diseases, Faculty of medical Sciences, University of Kragujevac

infectologist, Clinic for infectious diseases, department for HIV, Clinical centre Kragujevac

References

Volberding P, Greene W, Lange JMA, Gallant JE, Sewankambo N. Sande’s HIV/AIDS Medicine: Medical Management of AIDS 2013: Second Edition. Elsevier Inc., 2012. 580 p. https://doi.org/10.1016/B978-1-4557-0695-2.00048-1

Arts EJ, Hazuda DJ. HIV-1 Antiretroviral Drug Therapy. Cold Spring Harb Perspect Med. 2012 Apr; 2(4): a007161.

Boccara F, Lang S, Meuleman C, Ederhy S, Mary-Krause M, Costagliola D, et al. HIV and Coronary Heart Disease: time for a better understanding. J Am Coll Cardiol. 2013;61(5):511-23.

Baker JV, Lundgreen JD. Cardiovascular implications from untreated human immunodeficiency virus infection. Eur Heart J 2011; 32: 945-51

Jevtović Dj, Dragović G, Salemović D, Ranin J, Djurković-Djaković O. The metabolic syndrome, an epidemic among HIV-infected patients on HAART. Biomed. Pharmacother, 2009; 63: 337e342.

Worm SW, Sabin C, Weber R, Reiss P, El-Sadr W, et al. Risk of myocardial infarction in patients with HIV infection exposed to specific individual antiretroviral drugs from 3 major drug classes: thee data collection on adverse events of anti-HIV drugs (D:A:D) study. J Infect Dis 2010; 201(3): 318-30.

Quiros-Roldan E, Magoni M, Raffetti E, et al. The burden of chronic diseases and cost-of-care in subjects with HIV infection in a Health District of Northern Italy over a 12-year period compared to that of the general population. BMC Public Health 2016;16:1146.

Bavinger C, Bendavid E, Niehaus K, Olshen RA, Olkin I, Sundaram V, et al. Risk of cardiovascular disease from antiretroviral therapy for HIV: a systematic review. PLoS One 2013; 8(3):e59551.

Raposeiras-Roubin S, Triant V. Ishemic heart disease in HIV: An In-depth Look at Cardiovasular Risk. Rev Esp Cardiol (Engl Ed). 2016;69(12):1204-1213.

Currier JS, Lundgren JD, Carr A, Klein D, Sabin CA, Sax PE, et al. Epidemiological evidence forcardiovascular disease in HIV-infected patients and relationship to highly active antiretroviral therapy. Circulation 2008; 118: 29–35.

Boccara F. Cardiovascular complications and atherosclerotic mani-festations in the HIV-infected population: type, incidence and associated risk factors. AIDS 2008; 22 Suppl 3:19–26.

Lang S, Boccara F, Mary-Krause M, Cohen A. Epidemiology of coronary heart disease in HIV-infected versus uninfected individuals in developed countries; Arch Cardio Dis 2015; 108 (3): 206-215.

Shlay JC, Bartsch G, Peng G, Wang J, Grunfeld C, Gibert CL, et al. Long-term body composition and metabolic changes in antiretroviral naive persons randomized to protease inhibitor-, nonnucleoside reverse transcriptase inhibitor-, or protease inhibitor plus nonnucleoside reverse transcriptase inhibitor-based strategy. J Aequir Immune Dific Syndr 2007; 54: 506-17.

Baker JV, Lundgren JD. Cardiovascular implications from untreated human immunodeﬁciency virus infection. Eur Heart J 2011; 32:945–51.

Eugenin EA, Morgello S, Klotman ME, Mosoian A, Lento PA et al. Human immunode-ﬁciency virus (HIV) infects human arterial smooth muscle cells in vivo and in vitro: implications for the pathogenesis of HIV-mediated vascular disease. Am J Pathol 2008; 172:1100