Liver fibrosis in patients with chronic hepatitis C and persistently normal liver enzymes: Influence of HIV infection
Infectious Diseases Department, Hospital Carlos III, Madrid, Spain. Journal of Viral Hepatitis
(Impact Factor: 3.91).
04/2009; 16(11). DOI: 10.1111/j.1365-2893.2009.01133.x
Liver fibrosis progress slowly in patients with chronic hepatitis C and persistently normal alanine aminotransferase (PNALT) compared to subjects with elevated aminotransferases. Differences in liver fibrosis according to human immunodeficiency virus (HIV) status in this population have not been examined. All patients with serum hepatitis C virus (HCV)-RNA and PNALT who underwent liver fibrosis assessment using elastometry since 2004 at three different European hospitals were evaluated. Patients previously treated with interferon were excluded. PNALT was defined as ALT below the upper limit of normality in at least three consecutive determinations within the last 12 months. Fibrosis stage was defined as mild (Metavir F0–F1) if stiffness ≤7.1 kPa; moderate (F2) if 7.2–9.4 kPa; severe (F3) if 9.5–14 kPa, and cirrhosis (F4) if >14 kPa. A total of 449 HIV-negative and 133 HIV-positive patients were evaluated. HIV-negative patients were older (mean age 51.8 vs 43.5 years) and more frequently females (63% vs 37%) than the HIV counterparts. Mean serum HCV-RNA was similar in both the groups (5.9 vs 5.8 log IU/mL). Overall, 78.8% of the HIV patients were on HAART and their mean CD4 count was 525 (±278) cells/μL. In HIV-negatives, liver fibrosis was mild in 84.6%; moderate in 8.7%, severe in 3.3% and cirrhosis was found in 3.3%. In HIV patients, these figures were 70.7%, 18.8%, 6%, and 4.5%, respectively. In the multivariate logistic regression analysis, older age (odds ratio or OR: 1.04; 95% confidence interval or CI: 1.02–1.07; P < 0.001) and being HIV+ (OR: 2.6; 95% CI: 1.21–5.85; P < 0.01) were associated with severe liver fibrosis or cirrhosis (F3–F4). Thus, severe liver fibrosis and cirrhosis are seen in 6.6% of the HCV-monoinfected and in 10.5% of HCV-HIV co-infected patients with PNALT. Some degree of liver fibrosis that justifies treatment is seen in 15% of the HCV-monoinfected but doubles to nearly 30% in HIV-HCV co-infected patients with PNALT.
Figures in this publication
Available from: Andrea Kovacs
- "Another meta-analysis of 27 studies among 7666 individuals found that co-infected individuals had a twofold increased rate of cirrhosis compared to monoinfected . Severe liver fibrosis and cirrhosis were also found in 10% to 25% of co-infected HCV viremic patients with normal alanine aminotransferase (ALT) levels [34, 35]. A 20-year prospective study found increased risk of hepatitis/liver-related deaths despite HAART among co-infected drug users (DUs) compared to HCV-monoinfected DUs, providing further support that HIV accelerates liver disease in the HAART era . "
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ABSTRACT: World-wide, hepatitis C virus (HCV) accounts for approximately 130 million chronic infections, with an overall 3% prevalence. Four to 5 million persons are co-infected with HIV. It is well established that HIV has a negative impact on the natural history of HCV, including a higher rate of viral persistence, increased viral load, and more rapid progression to fibrosis, end-stage liver disease, and death. Whether HCV has a negative impact on HIV disease progression continues to be debated. However, following the introduction of effective combination antiretroviral therapy, the survival of coinfected individuals has significantly improved and HCV-associated diseases have emerged as the most important co-morbidities. In this review, we summarize the newest studies regarding the pathogenesis of HIV/HCV coinfection, including effects of coinfection on HIV disease progression, HCV-associated liver disease, the immune system, kidney and cardiovascular disease, and neurologic status; and effectiveness of current anti-HIV and HCV therapies and proposed new treatment strategies.
Current HIV/AIDS Reports 03/2011; 8(1):12-22. DOI:10.1007/s11904-010-0071-3 · 3.80 Impact Factor
Available from: ncbi.nlm.nih.gov
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ABSTRACT: Liver disease is a leading cause of mortality among HIV-infected persons in the United States and Europe. However, data regarding the effects of HIV and antiretroviral therapy (ART) on liver disease in Africa are sparse.
A total of 500 HIV-infected participants in an HIV care programme in rural Rakai, Uganda were frequency-matched by age, gender and site to 500 HIV-uninfected participants in a population cohort. All participants underwent transient elastography (FibroScan(®)) to quantify liver stiffness measurements (LSM) and identify participants with significant liver fibrosis, defined as LSM≥9.3 kPa (≈ Metavir F≥2). Risk factors for liver fibrosis were identified by estimating adjusted prevalence risk ratios (adjPRR) and 95% CI using modified Poisson multivariate regression.
The prevalence of hepatitis B coinfection in the study population was 5%. The prevalence of significant fibrosis was 17% among HIV-infected and 11% in HIV-uninfected participants (P=0.008). HIV infection was associated with a 50% increase in liver fibrosis (adjPRR 1.5, 95% CI 1.1-2.1; P=0.010). Fibrosis was also associated with male gender (adjPRR 1.4, 95% CI 1.0-1.9; P=0.045), herbal medicine use (adjPRR 2.0, 95% CI 1.2-3.3; P=0.005), heavy alcohol consumption (adjPRR 2.3, 95% CI 1.3-3.9; P=0.005), occupational fishing (adjPRR 2.5, 95% CI 1.2-5.3; P=0.019) and chronic HBV infection (adjPRR 1.7, 95% CI 1.0-3.1; P=0.058). Among HIV-infected participants, ART reduced fibrosis risk (adjPRR 0.6, 95% CI 0.4-1.0; P=0.030).
The burden of liver fibrosis among HIV-infected rural Ugandans is high. These data suggest that liver disease may represent a significant cause of HIV-related morbidity and mortality in Africa.
Antiviral therapy 01/2011; 16(3):405-11. DOI:10.3851/IMP1783 · 3.02 Impact Factor
Available from: Azucena Rodriguez-Guardado
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ABSTRACT: Reliable non-invasive methods for the evaluation of liver fibrosis are desirable, and the risk factors associated with fibrosis are not fully identified.
A cross-sectional study of a cohort of 805 HIV-HCV-coinfected patients with active HCV replication, most (95.2%) of whom were intravenous drug users, was conducted. Liver fibrosis was measured by transient elastometry with cutoff values of 7.2 kPa (significant fibrosis), 9.4 kPa (advanced fibrosis) and 14.0 kPa (cirrhosis), and by liver fibrosis indexes (LFI; APRI, Forns and FIB-4). Available liver biopsies were also evaluated.
The prevalences of significant fibrosis, advanced fibrosis and cirrhosis were 55.8%, 38.4% and 23.5%, respectively. A number of parameters were associated both in the univariate and multivariate analyses with each of the diverse fibrosis groups; however, only six of them were predictive of all stages of fibrosis: heavy alcohol intake (odds ratio [OR] 3.37, 95% confidence interval [CI] 2.02-5.59; P < 0.001), duration of HCV infection (OR 1.13, 95% CI 1.07-1.19; P < 0.001), CDC category C3 (OR 1.80, 95% CI 1.07-3.02; P=0.026), anti-HCV treatment failure (OR 4.37, 95% CI 2.24-8.55; P < 0.001), thrombocytopaenia (OR 1.015, 95% CI 1.011-1.019; P < 0.001) and increased aspartate aminotransferase (1.006, 95% CI 1.0021-1.010; P = 0.004). Furthermore, 53%, 68% and 80% of patients with significant fibrosis, advanced fibrosis and cirrhosis, respectively, had increased measures on at least one of the LFI, with the Forns index being the most sensitive. Area under the receiver operating characteristic curves of elastometry to predict histological fibrosis was 0.83 (95% CI 0.76-0.90), 0.89 (95% CI 0.83-0.95) and 0.87 (95% CI 0.80-0.94) for Metavir score ≥ F2, ≥ F3 and F4, respectively.
Elastometry constitutes a useful tool in the diagnosis and follow-up of HIV-HCV-coinfected patients. Fibrosis is associated with diverse factors, some of them treatable or preventable, which need to be addressed considering the high prevalence and course of fibrosis in these patients.
Antiviral therapy 01/2011; 16(1):27-35. DOI:10.3851/IMP1708 · 3.02 Impact Factor
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