Anti-hepatitis C virus treatment may prevent the progression of liver fibrosis in non-responder human immunodeficiency virus/hepatitis C virus coinfected patients

Sagnelli, Caterina; Uberti-Foppa, Caterina; Galli, Laura; Pasquale, Giuseppe; Coppola, Nicola; Albarello, Luca; Doglioni, C.; Lazzarin, Adriano

doi:10.1016/j.bjid.2013.06.005

Cited by 10 publications

(10 citation statements)

References 26 publications

(34 reference statements)

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“…One hundred sixty-eight consecutive anti-HIV-positive patients with anti-HCV/HCV RNA-positive asymptomatic chronic hepatitis for 18-36 months were enrolled at the time they underwent their first liver biopsy (LB), from 1993 to 2008, at one of the two participating infectious disease units. These two centers have cooperated in numerous clinical investigations applying the same clinical and laboratory approach [3][4][5].…”

Section: Patientsmentioning

confidence: 99%

“…The introduction of highly active antiretroviral therapy (HAART) has increased the average life expectancy of HIVinfected individuals by at least 20 years, but HCV infection has become the most frequent cause of comorbidity in HIV population, and liver-related mortality is the second cause of death in this setting [1]. HIV infection unfavourably influences the natural history of HCV infection because it speeds up the progression to cirrhosis, induces liver decompensation and liver failure and favours the development of hepatocellular carcinoma [2][3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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Impact of PNPLA3 variants on liver histology of 168 patients with HIV infection and chronic hepatitis C

Sagnelli

Merli

Uberti-Foppa

et al. 2016

Clinical Microbiology and Infection

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This study analysed the impact of PNPLA3 variants on liver histology of 168 HIV/hepatitis C virus (HCV)-coinfected patients who were naïve for HCV treatment. A athologist unaware of the patients' condition graded liver fibrosis and necroinflammation (Ishak) and steatosis (Kleiner). Patients were tested for PNPLA3 variants and genotyped for the PNPLA3 rs738409 C to G variant underlying the I148M substitution. All were hepatitis B surface antigen negative and stated no alcohol abuse. The mean age was 40.6 (37.6-44.1) years, 72.6% were males, 42% had HCV genotype 3, 38.9% HCV genotype 1 and 79.2% were receiving highly active antiretroviral therapy. The 79 patients with the PNPLA3 p.148I/M or M/M variants more frequently showed severe steatosis (score 3-4) than the 89 with PNPLA3 p.148I/I (43% vs. 24.7%, p 0.001), whereas no difference was observed in the degree of necroinflammation or fibrosis. Compared with 112 patients with lower scores, 56 with severe steatosis showed higher body mass index (p 0.03), higher rate of HCV genotype 3 (55.6% vs. 35.2%, p 0.01), PNPLA3 p.148I/M or M/M (60.7% vs. 39.3%, p 0.01) and lower CD4(+) cells/mm(3) (514.00 (390.5-673.0) vs. 500.00 (399.0-627.0); p 0.002). At multivariate analysis, body mass index (p 0.01), HCV genotype 3 (p 0.006), CD4(+) cell count (p 0.005) and PNPLA3 p.148I/M or M/M variants (p 0.01) were found to be independent predictors of severe liver steatosis. The PNPLA3 p.148 I/M or M/M variants and CD4(+) cell count were the only independent predictors of severe steatosis in patients with HCV non-3 genotypes. This is the first study to show that among HIV/HCV-coinfected patients the PNPLA3 p.148I/M or M/M variant have substantially less impact on steatosis for those with HCV genotype 3 than non-genotype 3.

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Section: Patientsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Impact of PNPLA3 variants on liver histology of 168 patients with HIV infection and chronic hepatitis C

Sagnelli

Merli

Uberti-Foppa

et al. 2016

Clinical Microbiology and Infection

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“…One hundred and sixty-six consecutive anti-HIV-positive patients with HCV RNA-positive chronic hepatitis C and 186 consecutive HCV-monoinfected patients were enrolled in the study from 1993 to 2008 at the time at which they underwent their first liver biopsy at one of the two participating Units of Infectious Diseases, one in Milan and the other in Naples. These two centres have cooperated for a decade in numerous clinical investigations, applying the same clinical approach and laboratory methods [8,18,[23][24][25][26][27][28].…”

Section: Patientsmentioning

confidence: 99%

“…A modifying Kleiner's scoring system for nonalcoholic fatty liver disease (NAFLD) [32], was used to assess liver steatosis, assigning a score of 1 to fatty deposition in 1-10% of hepatocytes, a score of 2 to that in 11-31%, a score of 3 to that in 31-60% and a score of 4 to that in > 60%. [24][25][26][27][28].…”

Section: Histopathological Assessment Of Liver Biopsiesmentioning

confidence: 99%

In vivo evidence that the cannabinoid receptor 2–63 RR variant is associated with the acquisition and/or expansion of HIV infection

et al. 2018

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“…At present HCV infection is one of the most frequent causes of comorbidity and mortality in the HIV population, and liver-related mortality is now the second highest cause of death in HIV-positive patients [13][14][15] . HIV infection unfavorably influences the natural history of HCV infection by increasing the rate of acute hepatitis C that progresses to chronicity, thus favoring the development of liver cirrhosis, hepatocellular carcinoma (HCC), liver decompensation and liver failure [13][14][15][16][17][18][19][20] . Therefore, optimized ART should be applied to reduce the unfavorable influence of HIV on HCV-related diseases.…”

Section: Introductionmentioning

confidence: 99%

Treatment of chronic hepatitis C in patients with HIV/HCV coinfection

Coppola

Martini

Pisaturo

et al. 2015

WJV

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frequent causes of comorbidity and mortality in the human immunodeficiency virus (HIV) population, and liver-related mortality is now the second highest cause of death in HIV-positive patients, so HCV infection should be countered with adequate antiviral therapy. In 2011 began the era of directly acting antivirals (DAAs) and the HCV NS3/4A protease inhibitors telaprevir and boceprevir were approved to treat HCV-genotype-1 infection, each one in combination with pegylated interferon alfa (Peg-IFN) + ribavirin (RBV). The addition of the first generation DAAs, strongly improved the efficacy of antiviral therapy in patients with HCVgenotype 1, both for the HCV-monoinfected and HIV/ HCV coinfected, and the poor response to Peg-IFN + RBV in HCV/HIV coinfection was enhanced. These treatments showed higher rates of sustained virological response than Peg-IFN + RBV but reduced tolerability and adherence due to the high pill burden and the several pharmacokinetic interactions between HCV NS3/ 4A protease inhibitors and antiretroviral drugs. Then in 2013 a new wave of DAAs arrived, characterized by high efficacy, good tolerability, a low pill burden and shortened treatment duration. The second and third generation DAAs also comprised IFN-free regimens, which in small recent trials on HIV-positive patients have shown comforting preliminary results in terms of efficacy, tolerability and adherence.

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Anti-hepatitis C virus treatment may prevent the progression of liver fibrosis in non-responder human immunodeficiency virus/hepatitis C virus coinfected patients

Cited by 10 publications

References 26 publications

Impact of PNPLA3 variants on liver histology of 168 patients with HIV infection and chronic hepatitis C

Impact of PNPLA3 variants on liver histology of 168 patients with HIV infection and chronic hepatitis C

In vivo evidence that the cannabinoid receptor 2–63 RR variant is associated with the acquisition and/or expansion of HIV infection

Treatment of chronic hepatitis C in patients with HIV/HCV coinfection

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