indinavir-sulfate and Hepatitis-C

In the era of antiretroviral therapy, non-AIDS complications such as kidney disease are important contributors to morbidity and mortality.. To estimate the impact of hepatitis C coinfection on the risk of kidney disease in HIV patients.. Two investigators identified English-language citations in MEDLINE and Web of Science from 1989 through 1 July 2007. References of selected articles were reviewed. Observational studies and clinical trials of HIV-related kidney disease and antiretroviral nephrotoxicity were eligible if they included at least 50 subjects and reported hepatitis C status. Data on study characteristics, population, and kidney disease outcomes were abstracted by two independent reviewers.. After screening 2516 articles, 27 studies were eligible and 24 authors confirmed or provided data. Separate meta-analyses were performed for chronic kidney disease outcomes (n = 10), proteinuria (n = 4), acute renal failure (n = 2), and indinavir toxicity (n = 5). The pooled incidence of chronic kidney disease was higher in patients with hepatitis C coinfection [6.2 versus 4.0%; relative risk 1.49, 95% confidence interval (CI) 1.08-2.06]. In meta-regression, prevalence of black race and the proportion of patients with documented hepatitis C status were independently associated with the risk of chronic kidney disease. The relative risk associated with hepatitis C coinfection was significantly increased for proteinuria (1.15; 95% CI 1.02-1.30) and acute renal failure (1.64; 95% CI 1.21-2.23), with no significant statistical heterogeneity. The relative risk of indinavir toxicity was 1.59 (95% CI 0.99-2.54) with hepatitis C coinfection.. Hepatitis C coinfection is associated with a significant increase in the risk of HIV-related kidney disease.

Topics: Acute Kidney Injury; Black People; Hepacivirus; Hepatitis C; HIV Infections; HIV Protease Inhibitors; HIV-1; Humans; Indinavir; Kidney Failure, Chronic; Proteinuria; Risk

Topics: AIDS-Related Opportunistic Infections; Antiretroviral Therapy, Highly Active; Chemical and Drug Induced Liver Injury; Helicobacter Infections; Helicobacter pylori; Hepatitis C; HIV; HIV Infections; HIV Protease Inhibitors; Humans; Hyperbilirubinemia; Indinavir; Quality of Life; RNA, Viral; Viral Load

to assess the incidence and risk factors for insulin resistance (IR) in a cohort of naive HIV-infected patients 48 weeks after starting highly active antiretroviral therapy (HAART).. prospective, two centre, observational, cohort study.. One-hundred and thirty-seven patients who started HAART and maintained the same regimen for 48 weeks were included. IR was determined by the homeostasis model assessment (HOMA-IR) method. Individuals with a HOMA-IR value >3.8 were defined as insulin resistant. Independent associations with the development of IR at 48 weeks were evaluated.. Seventeen (12.4%) individuals showed a HOMA-IR value >3.8 at baseline and were excluded for incidence analyses. Fifteen patients developed IR at 48 weeks of HAART, giving an incidence of 13%. Independent predictors of the development or IR were indinavir exposure (beta-coefficient 5.45, 95% confidence interval [CI] 1.30-22.8; P=0.02), and hepatitis C virus (HCV) antibody positivity (beta-coefficient 5.22, 95% CI 1.34-20.33; P=0.01). The appearance of IR was associated with a higher BMI (beta-coefficient 1.72 for each 2 kg/m2 increase, 95% CI 1.54-1.94; P=0.02) and with the presence of lipodystrophy at 48 weeks (beta-coefficient 5.59, 95% CI 1.45-21.5; P=0.01).. HAART induces the development of IR in previously naive non-insulin-resistant HIV-infected individuals, with an incidence of 13% in the first year of therapy. Indinavir exposure, and HCV coinfection are associated with an increased risk of developing IR.

Topics: Adult; Antiretroviral Therapy, Highly Active; Female; Hepatitis C; HIV Infections; HIV Protease Inhibitors; HIV-Associated Lipodystrophy Syndrome; Humans; Incidence; Indinavir; Insulin Resistance; Male; Risk Factors

The impact of human immunodeficiency virus (HIV) protease inhibitors on hepatitis C (HCV) viremia was assessed in 19 patients infected with both HIV and HCV. HIV and HCV RNA levels were measured before and during treatment with protease inhibitors. Before treatment, mean levels of HCV RNA were 5.3 log for HCV RNA and 5.0 log for HIV RNA. CD4 lymphocyte counts were 63/mm3. After 6 weeks of treatment, a mean reduction of 2.1 log10 in HIV RNA (P < .001) and a mean (+/-SE) increase of 73 (+/-21) CD4 and 296 (+/-70) CD8 cells were observed (P < .05). In contrast, both HCV viremia (+0.4 log +/- 0.1) and alanine aminotransferase increased (P < .04). HCV RNA levels returned to baseline after 17 and 32 weeks of treatment. Thus, potent anti-HIV regimens with protease inhibitors may temporarily worsen HCV status despite improvement of HIV parameters.

Topics: Anti-HIV Agents; Drug Therapy, Combination; Female; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Male; Reverse Transcriptase Inhibitors; Ritonavir; Saquinavir; Viremia

HIV infection accelerates natural course of HCV infection, but impact of antiretroviral treatment on HCV infection is not well known. The aim of this study is to compare the change of HCV viral load in patients on combination of 2 nucleoside analogues and in patients on combination of 2 nucleoside analogues and protease inhibitor. HCV and HIV viral load, lymphocyte CD4 counts, alanine aminotransferase (ALT) and aspartate amino transferase (AST) were measured before and 3 months after starting treatment in 2 groups: Group 1 (n = 15) treated with 2 nucleoside analogues and Group 2 (n = 15) treated with 2 nucleoside analogues and a protease inhibitor. Results show a significant increase in lymphocyte and a significant decrease in HIV viral load in the both group but no significant change in HCV viral load and in ALT and AST. In conclusion efficiency of anti-HIV therapy (combination of 2 nucleoside analogues with or without a protease inhibitor) doesn't seem to have any impact on the course of HCV viremia in HIV-coinfected patients.

Topics: Adult; AIDS-Related Opportunistic Infections; Alanine Transaminase; Anti-HIV Agents; Aspartate Aminotransferases; CD4 Lymphocyte Count; Disease Progression; Drug Therapy, Combination; Female; Hepacivirus; Hepatitis C; HIV; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Male; Reverse Transcriptase Inhibitors; Substance Abuse, Intravenous; Treatment Outcome; Viral Load; Viremia

HIV-associated vasculitis is an infrequent entity, and only few data about its long-term evolution is available.. We report the long-term outcome of a patient with central nervous system HIV-associated periarteritis nodosa and then discuss the therapeutic options for this class of vasculitis.. This observation highlights the role of HAART in the treatment of HIV-associated vasculitis. Persistent remission can be obtained when viral replication is under control.

Topics: Adult; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Central Nervous System Infections; Female; Follow-Up Studies; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Polyarteritis Nodosa; Stavudine; Time Factors; Treatment Outcome; Virus Replication; Zalcitabine

Ten severely immunocompromised HIV-HCV co-infected patients were enrolled in a quantifiable HCV-RNA assay. Serum alanine aminotransferase, HCV-RNA levels and HIV viral loads were determined at baseline, at month three and at month six after initiation of a highly active antiretroviral therapy including an HIV protease inhibitor. HCV genotypes were determined using a line probe assay kit. Our results suggested that this therapy did not result in lower HCV viraemia, whatever the HCV genotypes, and probably had no effect on the outcome of chronic viral hepatitis C. As our patients were severely immunocompromised and their mean increase of CD4 cell counts was less than 50/mm(3), we cannot reach any conclusions about the impact of the improvement of immune status on the HCV-RNA load.

Topics: Antiretroviral Therapy, Highly Active; CD4 Lymphocyte Count; Hepacivirus; Hepatitis C; HIV; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Reverse Transcriptase Inhibitors; Ritonavir; RNA, Viral; Viral Load; Viremia; Virus Replication

Topics: Acute Disease; Adult; Alcoholism; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Male; Porphyria Cutanea Tarda

Indinavir is a well-known cause of crystal-induced acute renal failure, dysuria and flank pain, and nephrolithiasis. Recently a more insidious tubulointerstitial lesion has been recognized as secondary to the drug. We report a case of a hepatitis C-positive patient on long-term indinavir therapy for human immunodeficiency virus (HIV) who developed a slowly progressive rise in serum creatinine. Renal biopsy revealed a diffuse interstitial infiltrate with numerous eosinophils and scarring. The tubules showed focal necrosis and dilation with elongated crystals present within their lumina. The elevated serum creatinine decreased to a new baseline over several months with the discontinuation of indinavir. We review the literature of renal syndromes associated with indinavir focusing on chronic progressive tubulointerstitial injury and speculate on risk factors and potential mechanisms of indinavir-induced renal injury.

Topics: Adult; Biomarkers; Blood Urea Nitrogen; Creatinine; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Kidney Diseases; Male

Topics: Adult; Anti-HIV Agents; Drug Therapy, Combination; Hepatitis C; HIV Seropositivity; Humans; Indinavir; Lamivudine; Male; Opioid-Related Disorders; Porphyria Cutanea Tarda; Remission, Spontaneous; Stavudine

A HIV-1 patient database was scanned in March 1998, and 750 patients were identified who had received HAART including indinavir. Of these, 28 cases had nephrolithiasis; and 85 asymptomatic indinavir-treated patients were randomly selected as controls. The characteristics of cases and controls were compared by analysis of variance for quantitative parameters and by Fisher's exact test for classes.. We observed a significant increase in the incidence of nephrolithiasis in patients co-infected with HIV-1 and either hepatitis C virus (HCV) (HCV RNA-positive) or hepatitis B virus (HBV) (HBs antigen-positive) (odds ratio and 95% confidence intervals: 2.8 and 1.1-7.7), whereas no significant differences were demonstrated between cases and controls with regard to age (42.4 +/- 8.0 versus 39.8 +/- 9.8 years), sex (male patients 70.4 versus 74.1%), duration of HIV-1 infection (8.6 +/- 3.1 versus 7.7 +/- 4.0 years), duration of indinavir treatment (16.1 +/- 5.8 versus 14.1 +/- 5.4 months), AST increase > or = 1.25 of normal (29.6 versus 25.9%), or ALT increase > or = 1.25 of normal (33.3 versus 22.4%). In co-infected patients, ALT increase (> or = 1.25 of normal), but not AST increase, at the time of indinavir initiation was statistically related to the occurrence of nephrolithiasis.. We found a significant increase of nephrolithiasis incidence in patients co-infected with HIV-1 and HCV or HBV, which suggests that underlying multifactorial hepatic damage may limit liver catabolism of indinavir, and consequently increase its renal excretion and the risk of nephrolithiasis. Caution is therefore advised when initiating indinavir treatment in HIV patients with evidence of HBV or HCV infection.

Topics: Adult; Anti-HIV Agents; Case-Control Studies; Databases, Factual; Drug Therapy, Combination; Female; Hepatitis B; Hepatitis C; HIV Infections; HIV Protease Inhibitors; HIV-1; Humans; Incidence; Indinavir; Kidney Calculi; Male; Middle Aged; Reverse Transcriptase Inhibitors

Effective antiretroviral therapy leads to rapid decrease in plasma HIV-1 RNA, frequently followed by an increase in CD4 T-helper cell counts. The improvement of immune function during highly active antiretroviral therapy has important impact on natural history of AIDS-related opportunistic disorders. Here we describe cases of unusual clinical inflammatory syndromes in CMV retinitis, hepatitis C, and atypical mycobacteriosis in HIV-1 infected patients associated with the initiation of antiretroviral therapy. Pathogenetic implications and therapeutic management of these new immunopathologic syndromes are discussed.

Topics: Acquired Immunodeficiency Syndrome; Adult; AIDS-Related Opportunistic Infections; Anti-HIV Agents; Antiretroviral Therapy, Highly Active; Cytomegalovirus Retinitis; Female; Hepatitis C; HIV Protease Inhibitors; HIV-1; Humans; Indinavir; Lamivudine; Male; Middle Aged; Mycobacterium avium-intracellulare Infection; Reverse Transcriptase Inhibitors; Zidovudine

Topics: Adult; Antiretroviral Therapy, Highly Active; CD4 Lymphocyte Count; Female; Follow-Up Studies; Hepatitis B; Hepatitis C; HIV Infections; HIV Protease Inhibitors; HIV-1; Humans; Indinavir; Liver Function Tests; Male; Ritonavir

Topics: Adult; Age Factors; Aged; Aged, 80 and over; Anti-HIV Agents; Antiviral Agents; Bacterial Vaccines; Blood Donors; Clinical Trials as Topic; Drug Therapy, Combination; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Interferons; Lamivudine; Middle Aged; Multicenter Studies as Topic; Pneumonia, Pneumococcal; Randomized Controlled Trials as Topic; Ribavirin; Streptococcus pneumoniae; Transfusion Reaction; Zidovudine

Topics: AIDS-Related Opportunistic Infections; Hepacivirus; Hepatitis C; HIV Protease Inhibitors; Humans; Immunity; Indinavir; Retrospective Studies; Ritonavir; Saquinavir

Topics: Adult; AIDS-Related Opportunistic Infections; Anti-HIV Agents; Drug Therapy, Combination; Hepatitis C; HIV Protease Inhibitors; HIV-1; Humans; Indinavir; Lamivudine; Male; Necrosis; Red-Cell Aplasia, Pure; Reverse Transcriptase Inhibitors; Zidovudine

Topics: AIDS-Related Opportunistic Infections; Anti-HIV Agents; Cohort Studies; Drug Therapy, Combination; Hemophilia A; Hepacivirus; Hepatitis C; HIV; HIV Protease Inhibitors; Humans; Indinavir; Lamivudine; Reverse Transcriptase Inhibitors; RNA, Viral; Saquinavir; Stavudine; Treatment Outcome; Viral Load; Zidovudine

Triple antiretroviral therapy combining reverse transcriptase and protease inhibitors modifies the prognosis of human immunodeficiency virus (HIV) infection, with dramatic improvement in immune status. The precise impact, if any, of anti-HIV triple therapy on hepatitis C virus (HCV) infection is unknown. We describe an unusual case of rapidly evolving HCV-related cirrhosis that paralleled restoration of immune status in an HIV-infected patient and discuss the possible link between such a severe course of hepatitis C and anti-HIV triple therapy.

Topics: Adult; Anti-HIV Agents; CD4 Lymphocyte Count; CD8-Positive T-Lymphocytes; Drug Therapy, Combination; Female; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Indinavir; Lamivudine; Liver Cirrhosis; Reverse Transcriptase Inhibitors; Stavudine

To report observations from case studies on the pathogenic mechanisms underlying the acute hepatitis that sometimes occurs in hepatitis C virus (HCV) and HIV coinfected patients following treatment with potent antiretroviral therapy that includes a HIV protease inhibitor.. Cases of acute hepatitis were identified from a group of 133 patients enrolled in a retrospective study of pathogen-associated inflammatory disease following the use of potent antiretroviral therapy. Data on serum alanine aminotransferase concentrations, clinical events, HCV antibodies, and liver biopsies were collected from medical records. HCV RNA assays and additional HCV antibody assays were undertaken on stored plasma or sera.. Three of the 133 patients (2%) developed symptomatic hepatitis. One was HCV antibody-positive prior to commencing antiretroviral therapy and developed hepatitis subsequent to an episode of Mycobacterium avium complex disease associated with immune restoration. However, the other two patients had previously undiagnosed HCV infection for up to 2 years prior to antiretroviral therapy, with HCV RNA detected but anti-HCV antibody repeatedly undetectable in stored plasma or sera. HCV antibody was only detectable after antiretroviral therapy-induced decrease in plasma HIV RNA and immunological reconstitution. Plasma HCV RNA increased after therapy in one of these patients, but in the other the level was not increased at a time of active hepatitis demonstrated by liver biopsy.. Hepatitis in HCV-HIV-coinfected patients following treatment with potent antiretroviral therapy may reflect restoration of anti-HCV immune responses rather than increased HCV replication or a hepatotoxic effect of antiretroviral therapy.

Topics: Adult; AIDS-Related Opportunistic Infections; Anti-HIV Agents; Female; Hepacivirus; Hepatitis C; HIV Protease Inhibitors; Humans; Indinavir; Lamivudine; Male; Retrospective Studies; Reverse Transcriptase Inhibitors; Ritonavir; Stavudine

Nephrolithiasis may be an important consequence of indinavir therapy; however little has been published on the variation in incidence between different populations of patients or the possible mechanisms of calculus formation.. To examine variation in the incidence of indinavir-associated nephrolithiasis (IAN) in HIV-positive patients in relation to hemophilia and hepatitis C virus (HCV) infection.. Clinical data were abstracted retrospectively from the medical records of all adult patients treated with indinavir from September 1995 to September 1997. Occurrence of first IAN, defined as flank pain and hematuria after initiation of therapy, was analyzed in relation to hemophilia status and HCV infection.. There were 17 episodes of IAN (22%) among 79 patients treated with indinavir. Of 10 patients with hemophilia, 50% developed IAN as compared with 17% of patients without hemophilia (P = 0.03). Median days to first IAN was 22 (range 7-110 days) for hemophiliacs and 156 (range 5-611 days) for those without hemophilia. Data for HCV status were available for 74 out of 79 patients: 10 out of 27 (37%) patients with HCV developed IAN compared with six out of 42 (14%) without HCV (P = 0.02).. Overall incidence of IAN was higher than that previously reported and was significantly greater in hemophiliacs than in non-hemophiliacs. HCV may be a contributing factor.

Topics: Adult; Anti-HIV Agents; Female; Hemophilia A; Hepatitis C; HIV Infections; HIV Protease Inhibitors; Humans; Incidence; Indinavir; Kidney Calculi; Male; Risk Factors