Detection of HIV-1 at between 20 and 49 copies per milliliter by the Cobas TaqMan HIV-1 v2.0 assay is associated with higher pretherapy viral load and less time on antiretroviral therapy.

New commercial techniques for determination of the viral load (VL) in plasma are able to detect as few as 20 copies of HIV-1 RNA/ml. The relevance of this new technical threshold is uncertain. Upon multivariate analysis, factors associated with detection of VLs between 20 and 49 copies/ml by the Cobas TaqMan HIV-1 v2.0 assay in an HIV clinic were the basal VL and time on antiretroviral therapy.

Transient elastography to rule out esophageal varices and portal hypertensive gastropathy in HIV-infected individuals with liver cirrhosis.

BACKGROUND/AIMS: It is recommended that patients with cirrhosis undergo endoscopic screening to rule out the presence of gastroesophageal varices: a noninvasive predictive method to identify cirrhotic patients with a very low risk of esophageal varices could potentially avoid unnecessary endoscopies. METHODS: We studied in 85 HIV-infected patients with cirrhosis the association between the absence of esophageal varices and portal hypertensive gastropathy, assessed by endoscopy, and liver stiffness measurement by transient elastography. We analyzed other parameters related to portal hypertension and hepatic function. RESULTS: Values of transient elastography and platelet count were significantly associated with absence of esophageal varices/portal hypertensive gastropathy. The area under the receiver operating characteristics curve [95% confidence interval (CI)] of transient elastography for the prediction of the absence of esophageal varices/portal hypertensive gastropathy was 0.7 (0.58-0.81). A liver stiffness measurement value less than 20 kPa was highly predictive of the absence of esophageal varices and portal hypertensive gastropathy. The combination of transient elastography (<20 kPa) and platelet count (>120 × 10 cells/l) had the highest negative predictive value (100%, CI 95% 77.2-100) for absence of esophageal varices and portal hypertensive gastropathy. CONCLUSION: Transient elastography combined with platelet count is useful for predicting the absence of esophageal varices and portal hypertensive gastropathy and, therefore, avoid unnecessary diagnostic endoscopies in HIV-infected patients with liver cirrhosis.

The natural history of liver cirrhosis in HIV-hepatitis C virus-coinfected patients.

OBJECTIVE: To provide detailed information about the natural history of HIV-hepatitis C virus (HCV)-coinfected patients with cirrhosis. METHODS: Prospective cohort including 340 HIV-HCV-coinfected patients with compensated (n = 248) or decompensated (n = 92) cirrhosis. We evaluated predictors of survival and of first hepatic decompensation. RESULTS: The mortality rate for patients with decompensated and compensated cirrhosis was 27.14 deaths per 100 person-years [95% confidence interval (CI) 18.93-35.35] and 3.98 deaths per 100 person-years (95% CI 2.42-5.54), respectively. Rate of first hepatic decompensation in patients with compensated cirrhosis was 4.62 per 100 persons-years (95% CI 2.91-6.33). In the complete cohort, permanent HAART interruption during follow-up, CD4 cell count nadir and baseline Child-Pugh score (CPS) B or C were significantly associated with shorter survival. In patients with compensated cirrhosis factors significantly associated with decreased survival were having the first hepatic decompensation during follow-up, permanent HAART discontinuation, and CPS B and C at baseline. For patients with compensated cirrhosis, time since diagnosis of HCV infection, CPS B and C and permanent HAART discontinuation were significantly associated with the risk of first hepatic decompensation. Sustained viral response to anti-HCV therapy was not independently associated with better survival in patients with compensated cirrhosis. CONCLUSION: HIV-HCV-coinfected patients with cirrhosis have a relatively good 3-year survival (87%). In contrast, 2-year survival of patients with decompensated liver cirrhosis is only 50%. Three-year survival was mostly impacted by liver-related factors and HAART maintenance.

HAART is associated with lower hepatic necroinflammatory activity in HIV-hepatitis C virus-coinfected patients with CD4 cell count of more than 350 cells/microl at the time of liver biopsy.

OBJECTIVE: To evaluate the impact of HAART on the liver damage of HIV-hepatitis C virus (HCV)-coinfected patients with relatively preserved immune status. DESIGN: Cross-sectional study of liver biopsies. METHODS: HIV-HCV-coinfected patients who underwent liver biopsies and had a CD4 cell count of at least 350 cells/microl at the time of liver biopsy were included. Exclusion criteria included positive hepatitis B surface antigen and prior anti-HCV therapy. Necroinflammatory activity and fibrosis was scored by the Scheuer fibrosis staging system. Steatosis was scored according to the percentage of hepatocytes affected. Logistic regression analysis was used to assess determinants of necroinflammatory activity of at least 3. RESULTS: One hundred and nineteen HIV-HCV coinfected patients were included. In the univariate analysis, alcohol abuse, serum alanine aminotransferase levels, steatosis and a high fibrosis score were significantly associated with higher necroinflammatory activity. In the multivariate analysis, a high level of alanine aminotransferase, advanced fibrosis and absence of HAART were associated with higher necroinflammatory activity. CONCLUSION: Use of HAART was associated with lower levels of necroinflammatory activity. Necroinflammatory activity was strongly associated with higher fibrosis scores. These results suggest that HAART might decrease hepatitis C activity in HIV-HCV-coinfected patients with CD4 cell count of more than 350 cells/microl.