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Hepatic steatosis in patients with HIV-Hepatitis C Virus coinfection: is it associated with antiretroviral therapy and more advanced hepatic fibrosis?

Verma S, Goldin RD, Main J - BMC Res Notes (2008)

Bottom Line: Hepatic steatosis is associated with more advanced hepatic fibrosis in the HIV-HCV coinfected population.HAART only therapy (rather than NRTIs only or sequential therapy) appears to be associated with a lower prevalence of hepatic steatosis.This may be one of the mechanisms by which HAART could attenuate hepatic fibrosis in such a cohort.

View Article: PubMed Central - HTML - PubMed

Affiliation: Hepatology Section, Department of Medicine, Imperial College at St Mary's Hospital, London, UK. s.verma@bsms.ac.uk

ABSTRACT

Background and aims: Patients with HIV and hepatitis C virus (HCV) coinfection are at increased risk of developing hepatic steatosis. The aims of this study were to assess the prevalence of steatosis in a cohort with HIV-HCV coinfection, and to determine an association, if any, between steatosis, antiretroviral therapy (ART), and advanced hepatic fibrosis.

Patients and methods: HIV-HCV coinfected patients were retrospectively identified from the HIV clinic. ART was classified as none, nucleoside reverse transcriptase inhibitors (NRTIs) only, highly active antiretroviral therapy (HAART) only, and sequential therapy (initial NRTIs followed by HAART). Fibrosis stage and necroinflammation grade were assessed by the modified HAI (Ishak) scoring method. Steatosis was graded as 0-3.

Results: Sixty patients were identified. The overall prevalence of hepatic steatosis was 58%. Those that received HAART only had a lower prevalence of steatosis (41%) compared to those on NRTIs only (70%) or sequential therapy (82%). Independent predictors of hepatic steatosis were absence of HAART only therapy, OR 2.9, p = 0.09, and presence of cirrhosis, OR 4.6, p = 0.044. Forty five percent of the patients had advanced fibrosis (fibrosis stage >/= 3). NI grade (OR 1.9, p = 0.030), and steatosis grade (OR 3.6, p = 0.045), were independent predictors of advanced fibrosis.

Conclusion: Hepatic steatosis is associated with more advanced hepatic fibrosis in the HIV-HCV coinfected population. HAART only therapy (rather than NRTIs only or sequential therapy) appears to be associated with a lower prevalence of hepatic steatosis. This may be one of the mechanisms by which HAART could attenuate hepatic fibrosis in such a cohort.

No MeSH data available.


Related in: MedlinePlus

Box plot showing fibrosis progression rates/year in those with (yes) and without (no) hepatic steatosis.
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Figure 3: Box plot showing fibrosis progression rates/year in those with (yes) and without (no) hepatic steatosis.

Mentions: Duration of stavudine (44.9 ± 21.5 vs. 24.8 ± 20.6) and didanosine (34.0 + 22.1 vs. 11.7 ± 10.4) were longer in those with fibrosis stage ≥ 3, though the differences did not achieve statistical significance (p value = 1.0 and 0.80 respectively). Factors that were significantly associated with fibrosis stage ≥ 3 on univariate analysis (p ≤ 0.1) (HIV diagnosed before or after 1996, cholestrol/HDL ratio, platelet count, grade of hepatic steatosis, necroinflammatory grade, and CD4 counts at time of the biopsy) were then entered into a step wise logistic regression model. The following were independently associated with advanced fibrosis: grade of necroinflammation (OR 1.9 (95% CI 1.1–3.3, p = 0.030), and grade of hepatic steatosis (OR 3.6 (95% CI 1.0–12.7), p = 0.045). There were 15 patients who had both a necroinflammatory grade ≥ 4 (mean grade in the whole group) and steatosis. Prevalence of cirrhosis in this group was 40%, compared to 13% in those without any of these two factors (p = 0.02). Fig 3 shows the fibrosis progression rates/year (FPR) in those with and without hepatic steatosis. The FPR was faster in the former though the differences did not achieve statistical significance, probably due to the small sample size.


Hepatic steatosis in patients with HIV-Hepatitis C Virus coinfection: is it associated with antiretroviral therapy and more advanced hepatic fibrosis?

Verma S, Goldin RD, Main J - BMC Res Notes (2008)

Box plot showing fibrosis progression rates/year in those with (yes) and without (no) hepatic steatosis.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2527001&req=5

Figure 3: Box plot showing fibrosis progression rates/year in those with (yes) and without (no) hepatic steatosis.
Mentions: Duration of stavudine (44.9 ± 21.5 vs. 24.8 ± 20.6) and didanosine (34.0 + 22.1 vs. 11.7 ± 10.4) were longer in those with fibrosis stage ≥ 3, though the differences did not achieve statistical significance (p value = 1.0 and 0.80 respectively). Factors that were significantly associated with fibrosis stage ≥ 3 on univariate analysis (p ≤ 0.1) (HIV diagnosed before or after 1996, cholestrol/HDL ratio, platelet count, grade of hepatic steatosis, necroinflammatory grade, and CD4 counts at time of the biopsy) were then entered into a step wise logistic regression model. The following were independently associated with advanced fibrosis: grade of necroinflammation (OR 1.9 (95% CI 1.1–3.3, p = 0.030), and grade of hepatic steatosis (OR 3.6 (95% CI 1.0–12.7), p = 0.045). There were 15 patients who had both a necroinflammatory grade ≥ 4 (mean grade in the whole group) and steatosis. Prevalence of cirrhosis in this group was 40%, compared to 13% in those without any of these two factors (p = 0.02). Fig 3 shows the fibrosis progression rates/year (FPR) in those with and without hepatic steatosis. The FPR was faster in the former though the differences did not achieve statistical significance, probably due to the small sample size.

Bottom Line: Hepatic steatosis is associated with more advanced hepatic fibrosis in the HIV-HCV coinfected population.HAART only therapy (rather than NRTIs only or sequential therapy) appears to be associated with a lower prevalence of hepatic steatosis.This may be one of the mechanisms by which HAART could attenuate hepatic fibrosis in such a cohort.

View Article: PubMed Central - HTML - PubMed

Affiliation: Hepatology Section, Department of Medicine, Imperial College at St Mary's Hospital, London, UK. s.verma@bsms.ac.uk

ABSTRACT

Background and aims: Patients with HIV and hepatitis C virus (HCV) coinfection are at increased risk of developing hepatic steatosis. The aims of this study were to assess the prevalence of steatosis in a cohort with HIV-HCV coinfection, and to determine an association, if any, between steatosis, antiretroviral therapy (ART), and advanced hepatic fibrosis.

Patients and methods: HIV-HCV coinfected patients were retrospectively identified from the HIV clinic. ART was classified as none, nucleoside reverse transcriptase inhibitors (NRTIs) only, highly active antiretroviral therapy (HAART) only, and sequential therapy (initial NRTIs followed by HAART). Fibrosis stage and necroinflammation grade were assessed by the modified HAI (Ishak) scoring method. Steatosis was graded as 0-3.

Results: Sixty patients were identified. The overall prevalence of hepatic steatosis was 58%. Those that received HAART only had a lower prevalence of steatosis (41%) compared to those on NRTIs only (70%) or sequential therapy (82%). Independent predictors of hepatic steatosis were absence of HAART only therapy, OR 2.9, p = 0.09, and presence of cirrhosis, OR 4.6, p = 0.044. Forty five percent of the patients had advanced fibrosis (fibrosis stage >/= 3). NI grade (OR 1.9, p = 0.030), and steatosis grade (OR 3.6, p = 0.045), were independent predictors of advanced fibrosis.

Conclusion: Hepatic steatosis is associated with more advanced hepatic fibrosis in the HIV-HCV coinfected population. HAART only therapy (rather than NRTIs only or sequential therapy) appears to be associated with a lower prevalence of hepatic steatosis. This may be one of the mechanisms by which HAART could attenuate hepatic fibrosis in such a cohort.

No MeSH data available.


Related in: MedlinePlus