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.
"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 . "
[Show abstract][Hide abstract] 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
[Show abstract][Hide abstract] ABSTRACT: In the last two centuries, physical, chemical, and biological alterations of Lake Champlain have resulted in the loss of two species, addition of 15 fish species, and listing of 16 species as endangered, threatened or of special concern. The lake currently supports 72 native fish species; lake trout (Salvelinus namaycush) and Atlantic salmon (Salmo salar) were extirpated by 1900, American eel (Anguilla rostrata) and lake sturgeon (Acipenser fulvescens) populations are extremely low, and walleye (Sander vitreum) are declining. Dams on several rivers, and ten causeways constructed in the mid 1800s to early 1900s, cut off access to critical spawning areas and may have limited fish movements. Siltation and sediment loading from agricultural activity and urban growth have degraded substrates and led to noxious algal blooms in some bays. A commercial fishery targeting spawning grounds of lake whitefish (Coregonus clupeaformis), lake trout, and walleye probably reduced numbers of these species prior to its closure in 1912. Non-native species introductions have had ecosystem-wide impacts. Sea lamprey (Petromyzon marinus) populations were very high prior to successful control, possibly as a consequence of ecological imbalance and habitat changes. A paucity of historic survey data or accurate species accounts limits our understanding of the causes of current fish population trends and status; in particular, the effects of habitat fragmentation within the lake and between the lake and its watershed are poorly understood. Holistic, ecosystem management, including pollution reduction and examination of habitat impacts, is necessary to restore the general structure of native biological assemblages.
Journal of Great Lakes Research 01/2012; 38. DOI:10.1016/j.jglr.2011.09.007 · 1.75 Impact Factor
[Show abstract][Hide abstract] 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.
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