Hepatotoxicity but not clinical hepatitis was common in HIV-1-infected patients receiving nevirapine-containing regimens and the incidence steadily increased over time. Prolonged exposure to any antiretroviral therapy, coinfection with hepatitis C virus and abnormal baseline levels of alanine aminotransferase identified patients at a higher risk.
Current antiretroviral therapy has lead to longer survival in patients infected with HIV, but it is also associated with new and important problems. Body fat redistribution and metabolic abnormalities, the so-called lipodystrophy syndrome, are among the most prevalent and worrisome ones. While an increasing number of patients infected with HIV are becoming affected by this syndrome, the pathogenesis of this syndrome and how to prevent and treat the problem all remain largely unknown. Body fat changes stigmatise the bodies of patients infected with HIV giving them a similar look to that seen in patients some years ago when the wasting syndrome was more prevalent and HIV infection was ultimately fatal. The psychological impact of body fat changes may be severe enough to affect a patients' desire to continue with antiretroviral therapy. Metabolic abnormalities, probably with the exception of symptomatic diabetes mellitus and hypertriglyceridaemia-induced pancreatitis, do not have an immediate impact on the quality of the lives of patients with HIV. However, their potential long term cardiovascular and bone consequences may increase the morbidity and the mortality of patients infected with HIV through noninfectious diseases. The impact of lipodystrophy on patients infected with HIV is not readily captured with the classic instruments used to measure quality of life and hence it is necessary to modify them urgently. Though treating lipodystrophy seems fully justified, there is no proven treatment for this problem, although a number of treatments have been used with varying success. Despite the recognition that lipodystrophy may have important psychological repercussions, the best psychological approach for this problem is not known at present. Although lipodystrophy has its own peculiarities, existing knowledge about how to psychologically help other patients with deforming body changes might be of help for patients infected with HIV, or at least may act as a starting point.
We prospectively followed 20 consecutive patients with human immunodeficiency virus type 1 (HIV-1) with viral loads of <200 RNA copies/mL. These patients had been treated with 2 nucleoside reverse transcriptase inhibitors and> or =1 HIV-1 protease inhibitor for > or =3 months; they developed body changes consistent with lipodystrophy and requested they be switched from protease inhibitor to efavirenz. At baseline and every 3 months, we assessed the following: body mass index, waist-to-hip ratio, regional fat thickness (assessed by sonography), fasting total and high-density lipoprotein cholesterol, triglycerides, glucose, insulin, CD4(+) cells, and viral load. At baseline, hypertriglyceridemia (> or =200 mg/dL) was present in 17 (85%) patients, hypercholesterolemia (> or =200 mg/dL) in 14 (70%), and impaired fasting glucose (> or =110 mg/dL) in 8 (40%); CD4(+) T cells were 280x10(6) cells/L (range, 64-942x10(6) cells/L). HIV-1 RNA had been at <200 copies/mL for a median of 14 months (range, 3-24 months). Six months after switching to efavirenz, there was a reduction in triglyceride levels (a decrease of 31%; P=.03) and fasting insulin resistance index (a decrease of 28%; P=.03), but total and high-density lipoprotein cholesterol and glucose did not change. Waist-to-hip ratio decreased from 0.92 to 0.87 (P=.06). Subcutaneous fat thickness did not change. CD4(+) cells remained stable (363x10(6) cells/L; range, 102-741x10(6) cells/L; P=.65). Nineteen patients (95%) had HIV-1 RNA levels that remained at <200 copies/mL. Although CD4(+) response and viral suppression remained preserved after 6 months of switching from protease inhibitor to efavirenz, the benefits of this approach on the evolution of lipodystrophy were limited, and our findings do not support its routine recommendation to treat lipodystrophy.
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