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Published on: October 1, 2015
Immunological status does not influence hepatitis c virus or liver fibrosis in HIV-hepatitis C virus-coinfected
Julio Collazos1, José Antonio Cartón, Víctor Asensi
1Infectious Disease Unit, Hospital de Galdácano-Usánsolo , Vizcaya, Spain.
Insights
In HIV-HCV-coinfected patients, immunological status did not impact Hepatitis C Virus (HCV) load or liver fibrosis progression. Alcohol abuse, HBsAg positivity, and platelet counts were key factors associated with liver fibrosis development.
Area of Science:
- Hepatology
- Immunology
- Infectious Diseases
Background:
- Hepatitis C virus (HCV) and Human Immunodeficiency Virus (HIV) coinfection is common.
- The impact of immunological status on liver fibrosis and HCV viral load in coinfected patients remains unclear.
Purpose of the Study:
- To investigate the association between immunological status and liver fibrosis and HCV viral load in HIV-HCV-coinfected patients.
Main Methods:
- A cohort of HIV-HCV-coinfected patients was categorized into poor (CD4 ≤200/μl) or good (CD4 ≥500/μl) immunological status groups.
- Liver fibrosis was assessed using transient elastometry and noninvasive indexes.
- Multivariate analyses were performed to identify factors associated with liver fibrosis and HCV viral load.
Main Results:
- Current or nadir CD4 counts were not associated with HCV viral load, liver fibrosis at evaluation, or fibrosis progression.
- Alcohol abuse, HBsAg positivity, and lower platelet counts were independently associated with significant, advanced fibrosis, and cirrhosis.
- Immunological status showed no association with any stage of liver fibrosis.
Conclusions:
- Immunological status does not significantly influence HCV viral load or liver fibrosis development in HIV-HCV-coinfected patients.
- Alcohol abuse, HBsAg positivity, and platelet count are crucial predictors of liver fibrosis in this population.
Abstract:
The possible effects on liver fibrosis and HCV viral load of the immunological status of HIV-HCV-coinfected patients are unclear. A cohort of HIV-HCV-coinfected patients was divided according to the current CD4 counts into poor (≤200/μl, n = 117) or good (≥500/μl, n = 441) immunological status. The groups were compared for diverse HCV- and fibrosis-related parameters. Fibrosis was evaluated by transient elastometry and other noninvasive indexes. Many variables were significantly associated with the immunological status in univariate analyses, including fibrosis parameters. However, in multivariate analyses current immunological status or nadir CD4 were not associated with HCV viral load (p = 0.8 and p = 0.3, respectively), liver fibrosis at the time of evaluation (p = 0.9 for both), or fibrosis progression over time (p = 0.98 and p = 0.8, respectively). The factors independently associated with significant fibrosis, advanced fibrosis, and cirrhosis, as compared with minimal or no fibrosis, were alcohol abuse [OR 3.57 (95% CI 1.43-8.85), p = 0.006; OR 10.10 (3.75-27.03), p < 0.0001; and OR 31.25 (10.6-90.90), p < 0.0001, respectively], HBsAg positivity [OR 9.09 (1.47-55.56), p = 0.02; OR 55.56 (9.80-333.33), p < 0.0001; and OR 43.48 (4.76-476.19), p = 0.0008, respectively], and platelet counts [OR 0.994 (0.989-0.998), p = 0.006; OR 0.990 (0.985-0.995), p = 0.0003; and OR 0.985 (0.979-0.991), p < 0.0001, respectively]. Immunological status did not associate with any fibrosis stage (significant fibrosis, p = 0.7; advanced fibrosis, p = 0.4; and cirrhosis p = 0.9). The current or past immunological status of HIV-HCV-coinfected patients does not seem to have any significant influence on HCV viral load or on the development of liver fibrosis when adjusting for important covariates.
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