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J Viral Hepat. 2019 Jan;26(1):16-24. doi: 10.1111/jvh.12990. Epub 2018 Sep 27.

Similar recovery of liver function after response to all-oral HCV therapy in patients with cirrhosis with and without HIV coinfection.

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Infectious Diseases and Microbiology Unit, Hospital Universitario de Valme, Seville, Spain.
Infectious Diseases Unit, Hospital Universitario de Gran Canaria Dr. Negrín, Gran Canaria, Spain.
Infectious Diseases and Microbiology Unit, Hospital Universitario de Puerto Real, Instituto de Investigación e Innovación en Ciencias Biomédicas de la Provincia de Cádiz (INiBICA), Puerto Real, Spain.
Infectious Diseases Unit, Hospital Juan Ramón Jiménez, Huelva, Spain.
Infectious Diseases Unit, AGS Campo de Gibraltar, Cadiz, Spain.
Infectious Diseases Unit, Hospital Universitario Álvaro Cunqueiro, Vigo, Spain.
Infectious Diseases Unit, Hospital Universitario Virgen de la Victoria, Malaga, Spain.
Infectious Diseases and Microbiology Unit, Hospital Universitario Virgen Macarena, Seville, Spain.
Instituto Maimonides de Investigación Biomedica de Córdoba (IMIBIC), Hospital Universitario Reina Sofia, Cordoba, Spain.


Among patients with cirrhosis, recovery of liver function after SVR to all-oral direct-acting antivirals (DAA) in HIV/HCV coinfection could be different to that in HCV monoinfection. Because of this, we compared the changes in several markers of liver function between HCV-monoinfected and HIV/HCV-coinfected patients with cirrhosis who achieved SVR12 to DAA combinations. In this retrospective cohort study, cirrhotics included in the HEPAVIR-DAA and GEHEP-MONO cohorts were selected if they had SVR12 to all-oral DAAs. Patients treated with atazanavir were excluded. Liver function improvement was defined as Child-Pugh-Turcotte (CPT) decrease ≥1 and/or MELD decrease ≥2 between baseline and SVR12. Liver function worsening was defined as a CPT increase ≥1 and/or MELD increase ≥2 and/or decompensations between baseline and SVR12. We included 490 patients, 270 (55%) of them with HIV coinfection. Liver function improved in 50 (56%) HCV-infected individuals and in 82 (57%) HIV/HCV-coinfected patients (P = 0.835). Liver function worsened in 33 (15%) HCV-monoinfected patients and in 33 (13%) HIV/HCV-coinfected patients (P = 0.370). Factors independently related with liver function improvement were male gender [adjusted OR (AOR) 2.1 (95% confidence interval, 95% CI: 1.03-4.2), P = 0.040], bilirubin < 1.2 mg/dL (AOR 1.8 [95% CI: 1.004-3.3], P = 0.49), and INR < 1.3 (AOR 2.4 [95% CI: 1.2-5.0], P = 0.019) at baseline. After multivariate analysis, albumin < 3.5 g/dL was associated with liver function worsening (AOR 6.1 [95% CI: 3-12.5], P < 0.001). Liver function worsening and improvement rates after responding to DAA are similar among HCV-monoinfected and HIV/HCV-coinfected cirrhotics. Gender, INR, bilirubin, and albumin levels were associated with liver function changes after response to DAAs.


HIV/HCV; Sustained virological response; cirrhosis; direct-acting antiviral agents; liver function parameters


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