Longitudinal increases in C-reactive protein (p = 0.002), alanine transaminase (p = 0.006) and gamma-glutamyl transferase (p = 0.046) levels and estimated glomerular filtration rate (p < 0.001) were seen only in the HIV-infected group.
Enzyme alanine aminotransferase (ALT) elevation which reflects hepatocellular injury is a current challenge in people infected with human immunodeficiency virus (HIV) on antiretroviral therapy (ART).
Hepatitis C virus diagnosis was assumed to be based on an elevated ALT level detected during a control visit for HIV-infected individuals, which occurred every 3 months (scenario A) or every 6 months (scenario B).
However, a single dose of alcohol plus the two HIV PIs caused a more than five-fold increase in serum ALT, a synergistic increase in alcohol-induced liver lipid accumulation and ER stress response, and a decrease of SERCA.
Of the patients, 49/255 (19.2%) developed advanced liver diseases (ALDs) (during 5.2 years): 30 patients developed clinically overt cirrhosis, 10 developed hepatocellular carcinoma and 9 developed severe reactivation of a preexisting chronic hepatitis B. Baseline CD4(+) cell count <200 cell/mm(3) (P = 0.013, OR = 6.503), baseline alanine aminotransferase (ALT) elevation (P = 0.011, OR = 14.456), and longer cumulated time with detectable HIV RNA (P = 0.008, OR = 1.814) and HBV DNA (P = 0.014, OR = 1.536) were risk factors for ALDs development, while CD4(+) cell count changes ≥150 cells/mm(3) within 3 months (P = 0.039, OR = 0.049) and the use of lamivudine-based cART (P = 0.030, OR = 0.034) were protective against ALDs development.
The study included patients who received pegylated interferon (peginterferon) alfa-2a alone (n = 166) or in combination with ribavirin (n = 1077, including 79 patients with normal alanine aminotransferase levels and 100 patients who were coinfected with human immunodeficiency virus and HCV) and whose serum samples were negative for HCV RNA (<50 IU/mL) at their final assessment.
Thirty patients were included with median values of alanine aminotransferase (ALT) levels: 80 U/L, age: 46 years, body mass index: 23 kg/m(2), HIV RNA: 200 copies/mL, CD4 count: 365/mm(3), duration of HIV infection: 13 years, and duration of treatment exposure: 118, 41, and 53 months for nucleoside reverse transcriptase inhibitors, non-nucleoside reverse transcriptase inhibitors, and protease inhibitors, respectively.
Hepatitis B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs), hepatitis C antibody (anti-HCV), alanine aminotransferase (ALT) levels, HIV viral load and CD4(+) count were also tested in all patients.
In multivariable analyses, the following factors predicted an ALT level >50 IU/mL: log10 HCV RNA (OR, 1.15; 95% CI, 1.00 to 1.32); HIV co-infection (OR, 0.48; 95% CI, 0.25 to 0.89); and having ever been treated for HCV (OR, 1.92; 95% CI, 1.16 to 3.18).
Histological abnormalities are significantly milder in patients coinfected with HIV and HCV who have persistently normal ALT levels than those found in patients with high ALT levels.
HCV genotype 3, older age, and elevated alanine aminotransferase levels are independent predictors of advanced liver fibrosis in HCV-HIV-coinfected patients.
HCV genotype distribution was associated with gender, age, source and duration of infection, alanine aminotransferase (ALT) levels, cirrhosis, alcohol consumption, hepatitis B virus (HBV) and human immunodeficiency virus (HIV) coinfection.
We examined hepatitis C virus (HCV) RNA levels in serum, peripheral blood mononuclear cells (PBMC), and the liver for 135 patients with chronic HCV infections, 44 of whom were human immunodeficiency virus (HIV) positive and treated with highly active antiretroviral therapy (group A), 66 of whom were HIV negative (group B), with abnormal serum alanine aminotransferase (ALT) values, and 25 of whom were HIV negative, with ALT values of </=1.5 times the normal value (group C).
Prevalences of HCV infection and elevated alanine aminotransferase are significantly lower in patients treated with virus-inactivated concentrates than in those exposed to non-virus-inactivated concentrates.No patients were anti-HIV positive.