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Hepatitis C Virus in Patients With HIV Infection and Lipodystrophy
 
 
  Note from Jules Levin: In this letter to the Editor appearing in the current issue of the Journal of AIDS, the authors from Spain find HCV/HIV coinfected patients had a significantly higher rate of lipoatrophy than HIV-infected patients. After 1 year of following patients, 23 of 51 HCV/HIV coinfected patients had lipodystrophy compared to 11 of 246 patients who had HIV only and developed lipodystrophy.
 
As is widely reported, HIV patients frequently develop lipodystrophy. It has been hypothesized that mitochondrial toxicity caused by nucleosidic reverse transcriptase inhibitors could be involved. Hepatitis C virus can also induce mitochondrial toxicity in the liver of chronically infected patients. In addition, HIV infection is often coincident with HCV infection in the same patient. Nevertheless, the possible implication of HCV infection in HIV-infected patients with lipodystrophy has been rarely considered, and the degree of HCV replication has not been assessed. We describe the possible influence of HCV infection on the metabolic alterations developed among HIV-infected patients.
 
Of 297 HIV patients receiving highly active antiretroviral therapy (HAART), we retrospectively analyzed 51 subjects with HIV and HCV concurrent infection who were matched for sex, age, and CDC HIV category with 37 HIV-infected patients without HCV coinfection. In all individuals, adherence to antiretroviral treatment was estimated to be adequate (>95% compliance). Follow-up lasted 1 year and included baseline and determinations every 3 months of serum cholesterol and triglyceride level. In HCV/HIV-coinfected patients, quantitative polymerase chain reaction (PCR) and genotype were determined. Lipodystrophy was diagnosed when patient and doctor agreed on the presence of facial and/or limb lipoatrophy with or without increased deposit of fat in abdomen or trunk.
 
Seventy-six percent of the patients were male; mean age was 40 years (range 21-65). The two groups did not differ statistically in sex, age, CDC category, plasma HIV RNA (15,775 ± 57,886 copies/mL in HCV/HIV-coinfected patients and 14,871 ± 68,967 in subjects with HIV infection only), or CD4 cell count (414 ± 252 for HCV/HIV-coinfected patients and 502 ± 285 in subjects with HIV infection only). There were no significant differences among nucleoside reverse transcriptase inhibitors received by both groups (HCV/HIV-coinfected group: abacavir 3.9%; zidovudine 20%; stavudine 47%; didanosine 25%; lamivudine 58%; HIV infection only: abacavir 5.6%; zidovudine 22.3%; stavudine 48.4%; didanosine 21.4%; lamivudine 50%). Seventy-five percent of HCV/HIV-coinfected patients had detectable plasma HCV RNA (mean 3,528,382 copies/mL: genotype 1, 23%; genotype 3, 8%; genotype 4, 4.6%; and genotype 2, 2%; in the remaining patients genotype was not available). Lipodystrophy developed in 34 subjects (23 from the HCV/HIV-coinfected group; p = .0031). Multivariate analysis also showed a significant association between lipodystrophy and hepatitis C infection (p = .030). However, there were no significant differences between HCV/HIV-coinfected patients with or without lipodystrophy regarding plasma HCV RNA (2,702,228 ± 3,760,999 copies/mL vs. 3,342,008 ± 4,767,691, respectively; p = .638), HCV genotype, serum triglyceride levels (167 ± 220 mg/dL in HCV/HIV coinfected patients and 208 ± 286 mg/dL in patients with HIV infection only), and serum cholesterol (189 ± 52 mg/dL in HCV/HIV coinfected subjects and 212 ± 42 mg/dL in patients with HIV infection only).
 
HAART has definitely reduced morbidity and mortality for HIV infection, though it has contributed to the development of several complications, including lipodystrophy. Diverse pathogenic mechanisms have been pointed out for lipodystrophy, including the presence of some viral coinfections. Our results show a greater presence of lipodystrophy in the HCV/HIV coinfected group though not coincident with a higher HCV replication. Regarding lipid changes, some studies have affirmed that patients with HCV/HIV coinfection have lower serum cholesterol and triglyceride levels than patients with HIV infection only, which is something that has not been ascertained in our patients.
 
So we may conclude that HIV-associated lipodystrophy could be associated with concurrent HCV infection. Nevertheless, because lipodystrophy seems to be a multifactorial problem, new studies will be needed to analyze the possible role of HCV infection in its genesis.
 
JAIDS Journal of Acquired Immune Deficiency Syndromes 2003; 32(3):348-349 Azucena Rodriguez-Guardado; Jose Antonio Maradona; Victor Asensi; Jose Antonio Cart—n; Luis Casado Infectious Diseases Unit. Hospital Central de Asturias
 
 
 
 
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