Severe hepatitis in patients with AIDS and haemophilia B treated with indinavir

Hepatitis B or Hepatitis C Virus Infection Is a Risk Factor for Severe Hepatic Cytolysis after Initiation of a Protease Inhibitor-Containing Antiretroviral Regimen in Human Immunodeficiency Virus-Infected Patients

“…The first cases of severe cytolysis were described in patients receiving IDV only (2,10,13,19). We did not confirm these results in our study, and we suggest that a selection bias might have occurred in previous studies, related to clinical habits for prescription.…”

“…Several cases of acute hepatitis have been reported after exposure to protease inhibitor (PI)-containing regimens (2,10,11,13,19). At least two mechanisms may be involved in drugrelated hepatitis: either a toxic effect of the PIs or other antiretroviral drugs or an enhanced inflammatory response against hepatitis B virus (HBV) or hepatitis C virus (HCV) induced by an immune reconstitution (4,18).…”

The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: A long-term retrospective cohort study

“…Another limitation was that our HIV-positive population was not reflective of the present HIV-positive population, which often receives HAART; however, this fact allows a better demonstration of a more severe liver disease induced by HIV coinfection, because HAART has been reported to worsen HCV infection despite improvement of HIV parameters 22,23 or to induce hepatotoxicity. [24][25][26][27] The long-term follow-up, up to 15 years, in this study, permitted us to confirm that HCVrelated liver disease was able to cause death, even in HIVinfected patients whose survival was not improved by new antiretroviral therapies. This observation in injection drug users is consistent with that reported in hemophiliacs.…”

Antiretroviral Therapy that Includes, Protease Inhibitors - Induced Hepatotoxicity: A Review

“…(15,16) However the most common laboratory finding in patients on indinavir is unconjugated hyperbilirubinaemia seen in upto 40% of patients. (17) This occurs due to inhibition of the enzyme uridinediphosphoglucoronoside (UDP) -Glucuronosyl transferase that is the enzyme involved in Gilbert's syndrome mutant allele.…”