title: Influence of sustained viral response on the regression of fibrosis and portal hypertension in cirrhotic HCV patients treated with antiviral triple therapy.
abstract: OBJECTIVE
  The regression of liver fibrosis and portal hypertension (PH) and their influence on the natural history of compensated hepatitis C virus (HCV)-related cirrhosis has not been studied previously. Our objective was to evaluate the influence of sustained virologic response (SVR) on the portal pressure gradient (HVPG) and non-invasive parameters of PH and prognostic factors of response.
  
  
  METHODS
  Sixteen patients with compensated HCV genotype 1-related cirrhosis with PH (HVPG > 6 mmHg) without beta-blocker therapy were considered as candidates for PEGα2a + RBV + BOC (48 weeks; lead-in and accepted stopping rules). A hemodynamic study and Fibroscan® were performed at baseline, at eight weeks and, in the case of SVR, 24 weeks after treatment. In each hemodynamic study, serum samples were analyzed for inflammatory biomarkers associated with PH.
  
  
  RESULTS
  In eight cases, SVR was obtained; five patients relapsed, and treatment was stopped early for non-response to lead in (one case) and a decrease of < 3 log at week 8 (two patients). Compared to baseline, there was a significant decrease in HVPG and Fibroscan® at weeks 8 and 72 (10.31 ± 4.3 vs 9.4 ± 5.04 vs 6.1 ± 3.61 mmHg, p < 0.0001 and 21.3 ± 14.5 vs 16.2 ± 9.5 vs 6.4 ± 4.5 kPa, p < 0.0001, respectively). The average HVPG decrease in SVR was 40.8 ± 17.53%, achieving an HVPG < 6 mmHg in five patients (62.5%) and a Fibroscan® < 7.1 kPa in three patients (37.5%).
  
  
  CONCLUSIONS
  Complete hemodynamic response (HVPG < 6 mmHg) and fibrosis regression (Fibroscan® < 7.1 kPa) occur in more than half and one-third of patients achieving SVR, respectively, and must be another target in cirrhotic patients with SVR.
authors.affiliation: Aparato Digestivo/Unidad de Hepatología, Hospital Universitario Marqués de Valdecilla, España.
authors.forename: Ángela
authors.initials: Á
authors.lastname: Puente
authors.affiliation: Aparato Digestivo/Unidad de Hepatología, Hospital Universitario Marqués de Valdecilla, España.
authors.forename: Joaquín
authors.initials: J
authors.lastname: Cabezas
authors.affiliation: Hospital Universitario Marques de Valdecilla.
authors.forename: María Jesús
authors.initials: MJ
authors.lastname: López Arias
authors.affiliation: Aparato Digestivo/Unidad de Hepatología, Hospital Universitario Marqués de Valdecilla.
authors.forename: José Ignacio
authors.initials: JI
authors.lastname: Fortea
authors.affiliation: Hospital Universitario Marques de Valdecilla.
authors.forename: María Teresa
authors.initials: MT
authors.lastname: Arias
authors.affiliation: Hospital Universitario Marques de Valdecilla.
authors.forename: Ángel
authors.initials: Á
authors.lastname: Estébanez
authors.affiliation: Hospital Universitario Marques de Valdecilla.
authors.forename: Fernando
authors.initials: F
authors.lastname: Casafont
authors.affiliation: Hospital Universitario Marques de Valdecilla.
authors.forename: Emilio
authors.initials: E
authors.lastname: Fábrega
authors.affiliation: Servicio Aparato Digestivo, Hospital Universitario Marqués de Valdecilla, 39002.
authors.forename: Javier
authors.initials: J
authors.lastname: Crespo
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D015415:Biomarkers; D004359:Drug Therapy, Combination; D005260:Female; D005355:Fibrosis; D006439:Hemodynamics; D016174:Hepacivirus; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy* / Q000821:virology*; D006801:Humans; D006975:Hypertension, Portal / Q000188:drug therapy* / Q000209:etiology; D008103:Liver Cirrhosis / Q000188:drug therapy* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D011379:Prognosis
chemical_list: D000998:Antiviral Agents; D015415:Biomarkers