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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Approximately 400,000 individuals in the United States are co-infected with hepatitis C virus (HCV) and human immunodeficiency virus type 1 (HIV-1) and it is likely that almost one in two of these subjects consumes alcohol. The majority of these patients suffer an accelerated course of liver disease as manifested by the onset of cirrhosis within 5 to 10 years of developing HCV infection, as well as an increased risk of developing hepatocellular carcinoma (HCC). It is thought that chronic alcohol abuse mediates liver damage as a result of increased production of free radicals and proinflammatory cytokines. In the setting of chronic HCV infection, alcohol ingestion has an additional effect of diminishing immune clearance and increasing viral burden to hasten the onset of cirrhosis and HCC. Likewise, chronic HCV and HIV-1 co-infection results in a net increase in HCV burden; higher prevalence rates of HCV transmission to sexual partners and offspring, as well as an accelerated progression to end stage liver disease as compared to individuals with HCV infection alone. Thus, the synergistic effects of alcohol abuse and HIV-1 greatly impact on the morbidity and mortality for patients with HCV coinfection. Ultimately, this cumulative disease process will require far more aggressive management with abstinence and counseling for alcohol abuse; highly active antiretroviral therapy (HAART) for HIV infection and combination anti-viral therapy for HCV infection to stem the rapid progression to end stage liver disease.
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PMID:Hepatitis C virus (HCV) and human immunodeficiency virus type 1 (HIV-1) infections in alcoholics. 1208 18

HIV-hepatitis C virus (HCV) coinfection is common and affects more than one-third of all HIV infected persons worldwide. Prevalence among risk categories varies according to shared risk factors for transmission, mainly intravenous drug use (IDU) and hemophiliacs. Chronic HCV infection seems to accelerate the course of HIV disease, resulting in a worsened clinical and immunological progression. At the same time, several studies suggest that HIV disease modifies the natural history of HCV infection, leading to a faster course of progression from active hepatitis to cirrhosis, to end stage liver disease and death. HCV infection mimics opportunistic diseases because its natural history is significantly accelerated in HIV patients. Since highly active antiretroviral therapy (HAART) has slowed the progression of HIV disease and decreased the rate of HIV associated mortality, the prognosis of HIV disease has been modified, and the need to treat HCV coinfection become a significant issue. Because of the poor response rate obtained by either interferon alone or interferon thrice weekly plus ribavirin, the combination of pegylated interferon and ribavirin will probably become the standard of care, although the clinicians should be aware of the overlapping toxicity of nucleoside analogues and ribavirin. Many selected categories of patients pose particular challenges to physicians treating HCV infection: nonresponders to interferon, cirrhotic patients, and patients infected with both HCV and HBV. Liver transplantation in HIV patients is currently under evaluation, but should become the rescue therapy for HIV patients with end stage liver disease.
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PMID:HCV chronic hepatitis in patients with HIV: clinical management issues. 1213 7

Alcohol consumption by individuals infected with HIV is an important medical management issue with significant implications for the effectiveness of antiretroviral therapy as well as an important evolving field of HIV research. Alcohol consumption is a risk factor for poor medication adherence and can modify liver drug metabolism, both of which can lead to the emergence of drug-resistant virus. Research indicates that alcohol consumption greater than 50 g/day (four or five drinks) is a risk factor for liver disease progression among patients with HIV/HCV coinfection. In addition, alcohol-induced cirrhosis can result in changes in drug metabolism in the liver through compromised liver function. More research studies are needed to elucidate the biological and molecular basis of the clinical changes induced by alcohol consumption in HIV-infected individuals and on the relationship of these changes to the effectiveness of HIV pharmacotherapy. Specifically, research areas that are of particular importance are (1) determining alcohol consumption levels and patterns and its impact on antiretroviral medication adherence, efficacy, and physician prescribing practices; (2) identifying behavioral interventions to enhance adherence to HIV medications and reduce alcohol consumption; (3) clarifying the relationships and interactions among alcohol metabolism, HIV drug metabolism, and pharmacogenetics; (4) elucidating the extent of liver toxicity due to antiretroviral therapy and drug-drug interactions in individuals who consume alcohol; and (5) delineating the contribution of alcohol consumption to end-stage organ damage, particularly in HIV/HCV coinfection.
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PMID:Alcohol use and HIV pharmacotherapy. 1216 67

Mothers with hepatitis C virus (HCV) and HIV coinfection are the major source of HCV/HIV coinfection in infancy and childhood. There is no known intervention capable of interrupting HCV spread from mother to child, while the majority of infant HIV infections occurring in the developed world can be prevented by antiretroviral prophylaxis in the mother and child, elective caesarean section, and formula-feeding. In the era preceding treatment of HIV infection with highly active antiretroviral therapy, HCV coinfection was of little concern because the short-term survival of patients with HIV infection prevented the slowly developing consequences of chronic hepatitis C. As the life expectancy of patients with HIV infection increased with therapy, HCV has emerged as a significant pathogen. Several lines of evidence in adult patients suggest that liver disease may be more severe in patients coinfected with HIV and that progression of HIV disease may be accelerated by HCV coinfection. Whether coinfected children may share these clinical patterns remains a matter of speculation. Chronic hepatitis C in otherwise healthy children is usually a mild disease; liver damage may be sustained and fibrosis may increase over the years, suggesting slow progression of the disease. Interferon-alpha has been the only drug used in the past decade to treat hepatitis C in children and adolescents, with average response rates of 20%. Preliminary results of treatment with interferon-alpha and ribavirin suggest that the efficacy would be greater with combined therapy. These treatment protocols have not yet been applied to children coinfected with HIV, but the increasing number of long-term survivors will probably prompt further investigation in the near future. At present, treating HIV disease and monitoring HCV infection and hepatotoxicity induced by antiretroviral drugs seem to be the more reasonable approach to HCV/HIV coinfection in childhood.
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PMID:Hepatitis C virus infection in children coinfected with HIV: epidemiology and management. 1217 72

Coinfection with HIV and hepatitis B virus (HBV) is more common than that with HIV and hepatitis C virus (HCV), although more attention has been given to HCV coinfection as a result of its higher frequency of chronic disease. Natural history studies with HIV-HCV coinfection have also shown more rapid progression of liver disease, and end-stage liver disease due to hepatitis C is now a leading cause of death in HIV-infected patients. Like HCV infection, HBV infection can also be associated with significant morbidity and mortality in patients with HIV infection. Fortunately, treatment options of hepatitis B are expanding and may have a clinical impact on slowing disease progression. A case study of a patient with severe HBV-HIV coinfection is presented to illustrate what is known about this increasingly problematic disease state.
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PMID:Case report. Hepatitis B virus and HIV coinfection. 1240 2

The biochemical, virologic, and histologic spectrum of hepatitis C virus (HCV) in 66 consecutive patients with HIV-HCV coinfection and 119 HCV controls was compared: 86% of coinfected patients had CD4 counts >200 cells/mm3, 51% had a normal alanine aminotransferase (ALT) value, the mean HCV RNA titer was 5.7 log IU/mL, 92% of coinfected patients were of genotype 1, and the mean histologic activity index was 6.86 with advanced fibrosis in 32% of patients. The biochemical, virologic, and histologic findings of HCV in coinfected patients were similar to those observed in HCV controls. For both groups of patients, no clinical, biochemical, or virologic factors could reliably identify patients with advanced fibrosis or cirrhosis, underscoring the importance of liver biopsy in the evaluation of these patients. The spectrum of liver disease in coinfection includes a significant proportion of patients with normal ALT values, and excluding these patients from previous studies has led to an overestimation of HCV disease severity.
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PMID:The clinical spectrum of hepatitis C virus in HIV coinfection. 1251 11

Both chronic hepatitis C and nevirapine (NVP) use are risk factors for transaminase elevation under highly active antiretroviral therapy. NVP is metabolized in the liver and its clearance could be altered in the presence of chronic hepatitis C virus (HCV) infection, enhancing the risk of liver toxicity. We examined NVP plasma levels in 70 HIV-infected subjects receiving NVP-containing triple combinations. The median (range) NVP plasma trough concentrations were similar in 32 HCV antibody-positive and 38 HCV antibody-negative patients (5.8 [0.7-29] vs. 6.1 [0.9-9.6] microg/ml). Thus, HCV coinfection itself does not seem to influence significantly the pharmacokinetics of NVP in HIV-infected subjects.
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PMID:Short communication: interactions between nevirapine plasma levels, chronic hepatitis C, and the development of liver toxicity in HIV-infected patients. 1268 10

Coinfection with HIV and the hepatitis C virus (HCV) or hepatitis B virus (HBV) is a growing public health concern. Because the diseases are spread in similar ways--notably through shared use of needles to inject drugs and sexual activity--many people are coinfected with HIV and HCV, HIV and HBV, or even all three viruses. Hepatitis C and hepatitis B are viral infections of the liver; over time they can lead to serious consequences including liver cirrhosis and liver cancer. Most studies show that HIV infection leads to more aggressive hepatitis C or hepatitis B and a higher risk of liver damage. Studies of how HCV and HBV affect HIV disease are less clear. Most research shows that HCV does not accelerate HIV disease progression, but HIV/HCV coinfection may impair immune system recovery after starting antiretroviral therapy. Coinfection can complicate treatment. People with liver damage due to chronic hepatitis are more likely to experience hepatotoxicity (liver toxicity) related to anti-HIV drugs. In addition, drugs used to treat HIV and hepatitis can interact and side effects may be exacerbated. Most experts recommend that HIV should be controlled first before a person begins HCV treatment. With careful management, most people with HIV/HCV or HIV/HBV coinfection can be successfully treated for both diseases. In fact, several recent studies suggest that HIV/HCV-coinfected people with well-controlled HIV disease and relatively high CD4 cell counts may do as well as those with HCV alone.
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PMID:HIV and hepatitis C coinfection. 1269 Oct 36

Chronic hepatitis C virus (HCV) is an independent risk factor for antiretroviral-related hepatotoxicity, but little is known about the frequency of severe liver toxicity in patients with HIV-HCV coinfection first treated for HCV (pretreated). The aim of this prospective study of 105 patients was to compare the incidence of progression to severe antiretroviral-related liver toxicity in 66 patients pretreated (36 with interferon-alpha [IFNalpha], 30 with IFNalpha plus ribavirin), and 39 patients not pretreated. The subjects could choose whether to receive anti-HCV therapy. Severe liver toxicity was defined as alanine aminotransferase (ALT) level > or =5-times the upper limit of normal in patients with normal baseline levels and > or =3.5-times in those with increased baseline levels. The authors also estimated the hepatotoxicity-related risk of discontinuing antiretroviral therapy. During antiretroviral therapy, 10 subjects (9.5%) experienced severe hepatotoxicity: 4 of 66 pretreated patients and 6 of 39 untreated patients (24-month survival: 94% +/- 2.9% vs. 85% +/- 5.8%). After adjusting for baseline CD4 cell counts, ALT levels, histologic scores, HCV and HIV viremia, HCV genotype (genotype 1 in 29% of pretreated patients and 20% of patients not pretreated), and previous anti-HCV therapy, the risk of discontinuing anti-HIV treatment was significantly higher in the anti-HCV untreated patients (RR = 10.4; 95% CI: 1.6-66; p =.0127) and in those with increased baseline ALT levels (RR = 1.014; 95% CI: 1.006-1.021; p =.0005). The authors' data suggest that previous treatment of chronic active HCV is an independent factor associated with a decrease of severe liver toxicity as the result of a subsequent antiretroviral regimen. The authors also confirm that the baseline level of ALT is an important prognostic factor for increased liver damage during antiretroviral therapy.
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PMID:Pretreatment of chronic active hepatitis C in patients coinfected with HIV and hepatitis C virus reduces the hepatotoxicity associated with subsequent antiretroviral therapy. 1279 46

To compare the impact of hepatitis C virus (HCV) coinfection on progression of HIV infection in the eras before and after the introduction of highly active antiretroviral therapy (HAART), the authors conducted a retrospective cohort study. One hundred twenty-five HCV+ patients and 1076 HCV- patients were studied; 83% of HCV+ patients were injection drug users. HCV+ subjects experienced no clear benefit from HAART. The adjusted hazard ratios (HRs) of opportunistic infection, death, and hospitalization were 0.74 (95% CI: 0.31-1.78), 1.78 (95% CI: 0.59-5.37), and 2.1 (95% CI: 0.90-4.90), respectively, comparing the post-HAART era with the pre-HAART era. In contrast, HCV- subjects experienced rate reductions for all outcomes. Comparable HRs for opportunistic infection, death, and hospitalization were 0.49 (95% CI: 0.37-0.64), 0.28 (95% CI: 0.19-0.41), and 0.51 (95% CI: 0.38-0.67), respectively. HCV+ subjects remained at increased risk for death and hospitalization post-HAART even after additional adjustment for antiretroviral use and time-updated CD4 cell and viral load measures. Deaths and hospitalizations in HCV+ patients were primarily for non-AIDS-defining infections and complications of injection drug use. HCV coinfection and comorbidity associated with injection drug use are preventing the realization of substantial health benefits associated with HAART.
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PMID:The impact of hepatitis C virus coinfection on HIV progression before and after highly active antiretroviral therapy. 1284 48


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