Dyslipidaemia inducted by antiretroviral agents
Authors:
S. Snopková 1; K. Povolná 1; P. Husa 1; J. Jarkovský 2; T. Pavlík 2
Authors‘ workplace:
Klinika infekčních chorob Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MUDr. Petr Husa, CSc.
1; Institut biostatistiky a analýz Masarykovy univerzity Brno, ředitel doc. RNDr. Ladislav Dušek, Ph. D.
2
Published in:
Vnitř Lék 2008; 54(2): 169-177
Category:
Original Contributions
Overview
The clinical course of HIV/AIDS has been substantially modified by up-to date therapy in the recent years. The progress of the disorder has changed – today it is a chronic disease of many years course. Already in 1997 and 1998 it turned out that adverse metabolic changes which significantly affect the subsequent progress of the disease were produced by long-term HAART (highly active antiretroviral therapy). Gradually, more and more anthropometric, metabolic and coagulation changes are detected, closely resembling the changes seen in the metabolic syndrome, well known from cardiology and internal medicine - dyslipoproteinaemia, insulin resistance, abdominal obesity and so on. A combination of these disorders is clinically significant due to their role in the development of atherosclerosis and their, by no means negligible, involvement in the onset of ischaemic heart disease. In view of the much lower average age of HIV- positive individuals the earlier mentioned complications should be expected in much lower age categories than with HIV- negative individuals. Plasma lipid fractions (total cholesterol, triglycerides, LDL-cholesterol, HDL-cholesterol, apoA-I, apoB, LDL/HDL, apoA-I/apoB) have been investigated in 69 HIV infected subjects and the changes of these parameteres in the course of progression of HIV/AIDS due to cumulative time of exposure to HAART were explored. Significant increase of the level of proatherogenic plasma lipid fractions with tendency to develop at time course was found. These disturbances are observed in the course of very good immunological stabilization and viral suppression. No unambiguous data and results of long term studies are available, that would confirm the increase of cardiovascular risk in HIV infected subjects. Nevertheless, this increase is required and anticipated.
Key words:
HIV - HAART - dyslipidaemia - cardiovascular risk
Sources
1. Staňková M, Skokanová V. Problematika HIV/AIDS - ohlédnutí a perspektivy. Klin mikrobiol inf lék 2004; 10: 56-60.
2. 2005 Report on the global AIDS epidemic. UNAIDS 2006.
3. Konvalinka J, Machala L. Terapie AIDS po dvaceti letech. Vesmír 2001; 6: 332-340.
4. Hoffmann C, Rockstroh J, Kamps. S HIV Medicine 2006. 1st ed. Paris: Flying Publisher 2006.
5. Carpentier A, Patterson BW, Uffelman KD et al. Mechanism of highly active anti-retroviral therapy - induced hyperlipidemia in HIV-infected individuals. Atherosclerosis 2005; 178: 165-172.
6. Barbaro G. Highly Active antiretroviral therapy and the cardiovascular system: the heart of the matter. Pharmacology 2003; 69: 177-179.
7. Mary-Krause M, Cotte L, Simon A et al. Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men. AIDS 2003; 17: 2479-2486.
8. Calza L, Manfredi R, Chiodo F. Statins and fibrates for the treatment of hyperlipidaemia in HIV-infected patients receiving HAART. AIDS 2003; 17: 851-859.
9. Broedl UC, Maugeais C, Millar JS et al. Endothelial lipase promotes the catabolism of ApoB-containing lipoproteins. Circ Res 2004; 94: 1554-1561.
10. Reeds DN, Mittendorfer B, Patterson BW et al. Alterations in lipid kinetics in men with HIV-dyslipidemia. Am J Physiol 2003; 285: 490-497.
11. Lichtenstein KA, Delaney KM, Armon C et al. Incidence of and risk factors for lipoatrophy (abnormal fat loss) in ambulatory HIV-infected patients. J Acquir Immune Defic Syndr 2003; 32: 48-56.
12. Calza L, Manfredi R, Colangeli V et al. Substitution of nevirapine or efavirenz for protease inhibitor versus lipid-lowering therapy for the management of dyslipidaemia. AIDS 2005; 19: 1051-1058.
13. Herlihy OM, Barrow BA, Grant PJ et al. Hyperglycaemic siblings of Type II (non-insulin-dependent) diabetic patients have increased PAI-1, central obesity and insulin resistance compared with their paired normoglycaemic sibling. Diabetologia 2002; 45: 635-641.
14. Hadigan C, Meigs JB, Corcoran C et al. Metabolic abnormalities and cardiovascular disease risk factors in adults with human immunodeficiency virus infection and lipodystrophy. Clin Infect Dis 2001; 32: 130-139.
15. Addy CL, Gavrila A, Tsiodras S et al. Hypoadiponectinemia is associated with insulin resistance, hypertriglyceridemia and fat redistribution in human immunodeficiency virus-infected patients treated with highly active antiretroviral therapy. J Clin Endocrionol Metab 2003; 88: 627-636.
16. Cotter BR. Endothelial dxsfunction in HIV infection. Curr HIV/AIDS Rep 2006; 3: 126-131.
17. Mu H, Chai H, Lin PH et al. Current update on HIV-associated vascular disease and endothelial dysfunction. World J Surg 2007; 31: 632-643.
18. Hurlimann D, Weber R, Enseleit F et al. HIV infection, antiretroviral therapy and endothelium. Herz 2005; 30: 472-480.
19. Grinspoon SK. Metabolic syndrome and cardiovascular disease in patients with human immunodeficiency virus. Am J Med 2005; 118: 23S-28S.
20. Barbaro G. Highly active antiretroviral therapy-associated metabolic syndrome: pathogenesis and cardiovascular risk. Am J Ther 2006; 13: 248-260.
21. Balasubramanyam A, Sekhar RV, Jahoor F et al. Pathophysiology of dyslipidemia and increased cardiovascular risk in HIV lipodystrophy: a model of „systemic steatosis“. Curr Opin Lipidol 2004; 15: 59-67.
22. Bartlett JG, Gallant JE. Medical management of HIV Infection 2004. Johns Hopkins University School of Medicine Baltimore, Health Publishing Business Group, 2004: 93-98.
23. Nolan D. Metabolic complications associated with HIV protease inhibitor therapy. Drugs 2003; 63: 2555-2574.
24. Perret B, Ferrand C, Bonnet E et al. Lipoprotein metabolism in HIV-positive patients. E J Med Res 2003; 8: Suppl. II: 6-7.
25. De Gaetano Donati K, Rabagliati R, Iacoviello L et al. HIV infection, HAART, and endothelial adhesion molecules: current perspectives. Lancet Infect Dis 2004; 4: 213-222.
26. Shahmanesh M, Das S, Stolinski M et al. Antiretroviral treatment reduces very-low-density lipoprotein and intermediate-density lipoprotein apolipoprotein B fractional catabolic rate in Human Immunodeficiency Virus-infected patients with mild dyslipidemia. J Clin Endocrinol Metab 2005; 2: 755-760.
27. Calza L, Manfredi R, Chiodo F. Statins and fibrates for the treatment of hyperlipidaemia in HIV-infected patients receiving HAART. AIDS 2003; 17: 851-859.
28. The Writing Committee of the DAD Study Group. Cardio- and cerebrovascular events in HIV-infected persons. AIDS 2004; 13: 1811-1817
29. Soška V. Poruchy metabolizmu lipidů - diagnostika a léčba. Praha: Grada Publishing 2001.
30. Soška V. Dyslipidemie u metabolického syndromu. Vnitř Lék 2005; 1: 77-81.
31. Češka R. Jak dosáhnout cílových hodnot LDL-cholesterolu? Místo ezetimibu v moderní léčbě hypercholesterolemie. Cor Vasa 2004; 46: 452-456.
32. Racek J et al. Klinická biochemie. Praha: Galén 2006.
33. Frohlich J, Vrablík M. Apolipoprotein B v diagnostice a léčbě dyslipidemií. KF 2006; 4: 7-9.
34. Barbado G. Pathogenesis of HIV-associated heart disease. AIDS 2003; 17: 12-20.
Labels
Diabetology Endocrinology Internal medicineArticle was published in
Internal Medicine
2008 Issue 2
Most read in this issue
- Peripheral arterial disease of extremities – guidelines for diagnostic and treatment
- Current Use of Magnetic Resonance Imaging in Cardiology
- Monitoring of anti-tumour cell-mediated response in patients with renal cell carcinoma, disturbance of T cell proliferation
- The scintigraphic 99mTc-MAA imaging quantification of the right-to-left shunt in a patients with multiple pulmonary arteriovenous malformation and familial teleangiectasis