#PAGE_PARAMS# #ADS_HEAD_SCRIPTS# #MICRODATA#

HIV lipodystrophy


Authors: S. Snopková 1;  M. Matýšková 2;  K. Povolná 1;  P. Polák 1;  P. Husa 1
Authors place of work: Klinika infekčních chorob Lékařské fakulty MU a FN Brno, pracoviště Bohunice, přednosta prof. MU Dr. Petr Husa, CSc. 2 Oddělení klinické hematologie FN Brno, pracoviště Bohunice, přednosta prof. MU Dr. Miroslav Penka, CSc. 1
Published in the journal: Vnitř Lék 2010; 56(12): 1217-1222
Category: Reviews

Summary

Combined antiretroviral therapy results in extraordinary decrease of morbidity and mortality of HIV- infected patients and in an essential change of the HIV/ AIDS disease prognosis. However, long‑term intake of antiretroviral medicaments is related to occurrence of metabolic and morphological abnormalities, of which some have been combined into a new syndrome –  the so called HIV lipodystrophy. The HIV lipodystrophy syndrome covers metabolic and morphological changes. Metabolic changes include dyslipidaemia with hypercholesterolaemia and/ or hypertriglyceridaemia, insulin resistance with hyperinsulinaemia and hyperlaktataemia. Morphological changes have the nature of lipoatrophia (loss of subcutaneous fat –  on the cheeks, on extremities, on buttocks and marked prominence of surface veins) or lipohypertrophia (growth of fat tissue –  on the chest, in the dorsocervical area, lipomatosis of visceral tissues and organs, fat accumulation in the abdominal area). Several HIV lipodystrophy features are very similar to the metabolic syndrome of the general population. That is why this new syndrome represents a prospective risk of premature atherosclerosis and increase of the cardiovascular risk in young HIV positive individuals. The article mentions major presented studies dealing with the relation of antiretroviral treatment and the cardiovascular risk. The conclusions of the studies are not unequivocal –  this is, among others, given by the reason that their length is short from the viewpoint of atherogenesis. The major risk of subclinical atherosclerosis acceleration seems to be related to the deep immunodeficiency and low number of CD4+ lymphocytes and florid, uncontrolled HIV infection with a high number of HIV‑ 1 RNA copies actually circulating in the plasma. The question, whether metabolic and morphological changes related to HIV and cART carry a similar atherogenic potential as in the general population, remains open for future.

Key words:
antiretroviral therapy –  HIV lipodystrophy –  atherogenesis –  cardiovascular risk


Zdroje

1. Staňková M, Skokanová V. Dvacet pět let od objevu viru lidské imunodeficience (HIV). Prakt Lék 2008; 88, 11: 627– 629.

2. Sedláček D. Nové léky pro léčbu infekce HIV/ AIDS a revize evropské klasifikace HIV/ AIDS. Prakt Lék 2008; 88: 643– 647.

3. Boccara F. Cardiovascular complications and atherosclerotic manifestations in the HIV‑ infected population: type, incidence and associated risk factors. AIDS 2008; 22 (Suppl 3): S19– S26.

4. Hammer SM, Saag MS, Schechter M et al. Treatment for adult HIV infection: 2006 recommendations of the International AIDS Society‑ USA panel. JAMA 2006; 296: 827– 843.

5. Lohse N, Hansen AB, Pedersen G et al. Survival of persons with and without HIV infection in Denmark, 1995– 2005. Ann Intern Med 2007; 146: 87– 95.

6. Martinez E, Visnegarwala F, Grund B et al. The effects of intermittent, CD4- guided antiretroviral therapy on body composition and metabolic parameters. AIDS 2010; 24: 353– 363.

7. Balasubramanyam A, Sekhar RV, Jahoor Fet al. Pathophysiology of dyslipidemia and increased cardiovascular risk in HIV lipodystrophy: a model of “systemic steatosis”. Curr Opin Lipidol 2004; 15: 59– 67.

8. Grinspoon S, Carr A. Cardiovascular risk and body‑ fat abnormalities in HIV‑ infected individuals. N Engl J Med 2005; 352: 48– 62.

9. McDermott AY, Terrin N, Wanke C et al. CD4+ cell count, viral load, and highly active antiretroviral therapy use are independent predictors of body composition alterations in HIV‑ infected adults: a longitudinal study. Clin Infect Dis 2005; 41: 1662– 1670.

10. Jemsek JG, Arathoon E, Arlotti M et al. Body fat and other metabolic effects of atazanavir and efavirenz, each administered in combination with zidovudine plus lamivudine, in antiretroviral‑ naive HIV‑ infected patients. Clin Infect Dis 2006; 42: 273– 280.

11. Sabin CA, Worm SW, Weber R et al. Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV‑ infected patients enrolled in the D:A:D study: a multi‑cohort collaboration. Lancet 2008; 371: 1417– 1426.

12. Snopková S, Povolná K, Husa P. Metabolické komplikace a antiretrovirová léčba. Prakt Lék 2008; 88: 630– 634.

13. Hsue PY, Hunt PW, Schnell A et al. Role of viral replication, antiretroviral therapy, and immunodeficiency in HIV‑associated atherosclerosis. AIDS 2009; 23: 1059– 1067.

14. Souček M. Metabolický syndrom. Vnitř Lék 2009; 55: 618– 621.

15. Grunfeld C, Delaney JA, Wanke C et al. Preclinical atherosclerosis due to HIV infection: carotid intima‑ medial thickness measurements from the FRAM study. AIDS 2009; 23: 1841– 1849.

16. Kingsley LA, Cuervo‑ Rojas J, Muñoz A et al. Subclinical coronary atherosclerosis, HIV infection and antiretroviral therapy: Multicenter AIDS Cohort Study. AIDS 2008, 22: 1589– 1599.

17. Sabin CA, Worm SW, Weber R et al. Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV‑ infected patients enrolled in the D:A:D study: a multi‑cohort collaboration. Lancet 2008; 371: 1417– 1426.

18. Mangili A, Gerrior J, Tang AM et al. Risk of cardiovascular disease in a cohort of HIV‑ infected adults: a study using carotid intima‑ media thickness and coronary calcium score. Clin Infect Dis 2006; 43: 1482– 1489.

19. Murphy R, Costagliola D. Increased cardiovascular risk in HIV infection: drugs, virus and immunity. AIDS 2008; 22: 1625– 1627.

20. Kaplan RC, Kingsley LA, Gange SJ et al. Low CD4+ T‑ cell count as a major atherosclerosis risk factor in HIV‑ infected women and men. AIDS 2008; 22: 1615– 1624.

21. Hirschel B, Flanigan T. Is it smart to continue to study treatment interruptions? AIDS 2009; 23: 757– 759.

22. van Leuven SI, Franssen R, Kastelein JJ et al. Systemic inflammation as a risk factor for atherothrombosis. Rheumatology 2008; 47: 3– 7.

23. Maggiolo F, Airoldi M, Callegaro A et al. CD4 cell‑ guided scheduled treatment interruptions in HIV‑ infected patients with sustained immunologic response to HAART. AIDS 2009; 23: 799– 807.

24. Calmy A, Gayet‑ Ageron A, Montecucco F et al. STACCATO Study Group. HIV increases markers of cardiovascular risk: results from a randomized, treatment interruption trial. AIDS 2009; 23: 929– 939.

25. Maggi P, Maserati R, Antonelli G. Atherosclerosis in HIV patients: a new face for an old disease? AIDS Rev 2006; 8: 204– 209.

26. Guillevin L. Vasculitides in the context of HIV infection. AIDS 2008; 22 (Suppl 3): S27– S33.

27. Sterne JA, May M, Bucher HC et al. HAART and the heart: changes in coronary risk factors and implications for coronary risk in men starting antiretroviral therapy. J Intern Med 2007; 261: 255– 267.

28. Levy JA. HIV pathogenesis: 25 years of progress and persistent challenges. AIDS 2009; 23: 147– 160.

29. Sarkar I, Hauber I, Hauber J et al. HIV‑ 1 proviral DNA exciton using an evolved recombinase. Science 2007; 316: 1912– 1915.

Štítky
Diabetology Endocrinology Internal medicine

Článok vyšiel v časopise

Internal Medicine

Číslo 12

2010 Číslo 12
Najčítanejšie tento týždeň
Najčítanejšie v tomto čísle
Prihlásenie
Zabudnuté heslo

Zadajte e-mailovú adresu, s ktorou ste vytvárali účet. Budú Vám na ňu zasielané informácie k nastaveniu nového hesla.

Prihlásenie

Nemáte účet?  Registrujte sa

#ADS_BOTTOM_SCRIPTS#