Antiviral Therapy Decreases Hepatic Venous Pressure Gradient in Patients with Chronic Hepatitis C and Advanced Fibrosis

Rincón, Diego; Ripoll, Cristina; Iacono, Oreste Lo; Salcedo, Magdalena; Catalina, María Vega; Álvarez, E.; Núñez, Óscar; Matilla, Ana; Clemente, G.; Bañares, Rafael

doi:10.1111/j.1572-0241.2006.00743.x

Cited by 144 publications

(82 citation statements)

References 34 publications

(32 reference statements)

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“…These data are also supported by other studies in which the achievement of virological response following antiviral therapy was associated with a significant decrease of HVPG values, 21,22 fibrosis regression, 23,24 and reduction of portal hypertension-related complications in patients with similar clinical characteristics. 25,26 This study failed to identify a reliable predictor associated with high risk for early EV development.…”

Section: Discussionsupporting

confidence: 78%

Sustained virologic response prevents the development of esophageal varices in compensated, Child-Pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study

et al. 2010

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The incidence of de novo development of esophageal varices (EV) in patients with compensated liver cirrhosis has been determined by few studies in the short term and never in the long term. The aims of the present study were to determine the incidence and the risk factors associated with the development of EV and to assess whether antiviral treatment and achievement of sustained virologic response (SVR) may prevent de novo EV development in patients with HCV-induced cirrhosis. We studied 218 patients with compensated EVfree, HCV-induced cirrhosis consecutively enrolled between 1989 and 1992 at three referral centers in Milan, Italy. Endoscopic surveillance was performed at 3-year intervals according to international guidelines. SVR was defined as undetectable serum HCV-RNA 24 weeks after treatment discontinuation. During a median follow-up of 11.4 years, 149/ 218 (68%) patients received antiviral treatment and 34 (22.8%) achieved SVR. None of the SVR patients developed EV compared with 22 (31.8%) of the 69 untreated subjects (P < 0.0001) and 45 (39.1%) of the 115 non-SVR patients (P < 0.0001). On multivariate analysis, HCV genotype 1b (hazard ratio [HR] 2.40; 95% confidence interval [CI] 1.17-4.90) and baseline model for end-stage liver disease (MELD) score (HR 1.20; 95% CI 1.07-1.35 for 1 point increase) were independent predictors of EV. Conclusion: In the long term, the achievement of SVR prevents the development of EV in patients with compensated HCV-induced cirrhosis. Therefore, in these patients, endoscopic surveillance can be safely delayed or avoided. Genotype 1b infection and MELD score identify the subset of patients at higher risk of EV development who need tailored endoscopic surveillance.

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Section: Discussionsupporting

confidence: 78%

Sustained virologic response prevents the development of esophageal varices in compensated, Child-Pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study

et al. 2010

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“…There were 25 pressure evaluations (18 patients) that fulfilled our definition of potentially discrepant results with respect to the expected fibrosis stage or HVPG. The median biopsy length of the entire "discrepant" group was 22 mm (range, [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] and the number of fragments was 3.5 (range, 2-8) similar to the population as a whole. In the discrepant group, 56% of biopsies did not show severe nodularity/cirrhosis with 4 (range, 1-9) complete portal tracts and 8 (range, 2-13) partial portal tracts.…”

Section: Total Cohortmentioning

confidence: 85%

“…2) (expressed as difference between the last and first measurement) had a weak correlation with changes in fibrosis score (r ϭ 0.30, P ϭ 0.045). However, no significant correlation was found between change in grade and HVPG (P ϭ 0.042) and median HVPG did not change (5 mmHg; range, [1][2][3][4][5][6][7][8][9][10][11][12][13][14]. Regarding the whole paired group, the mean of the first evaluations for HVPG was 5.31 Ϯ 2.9 vs. 6.29 Ϯ 4.5 for the last (P ϭ 0.82); when evaluating those with PHT at first measurement, a better correlation was found, with mean first HVPG at 8.4 Ϯ 2.3 vs. 10 Ϯ 5 for the last HVPG (P ϭ 0.076).…”

Section: Total Cohortmentioning

confidence: 99%

“…10 Other studies have correlated HVPG both with severity and etiology of cirrhosis, 3,7,11 with only 1 study documenting a difference between HCV and alcoholic cirrhosis. 12 A significant correlation has been shown between antiviral response and HVPG changes in HCV chronic hepatitis, 13,14 and between HVPG and histological features of cirrhosis. 15 HVPG Ͼ10 mmHg predicts the development of complications of HCV cirrhosis.…”

mentioning

confidence: 98%

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Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

et al. 2007

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Progression of fibrosis following recurrent hepatitis C virus (HCV) infection is frequent after liver transplantation (LT).Histology remains the gold standard to assess fibrosis, but the value of hepatic venous pressure gradient (HVPG) is being explored. We evaluated patients with recurrent HCV infection after LT to assess whether HVPG correlates with liver histology, particularly fibrosis. A total of 90 consecutive patients underwent 170 HVPG measurements concomitant with transjugular liver biopsy (TJB), with 31.5 (range, 6-156) months of follow up. Median biopsy length was 22 mm and total portal tract count was 12 (complete 6, partial 6). Median HVPG was 4 mmHg: 38% of patients Ն6 mmHg (portal hypertension, PHT), 13% Ն10 mmHg. HVPG correlated with Ishak stage (r ϭ 0.73, P Ͻ 0.001) for mild (0-3) and severe fibrosis (4-6), and grade score (r ϭ 0.47, P Ͻ 0.001), but neither correlated with interval from LT nor biopsy length. HVPG was Ն10 mmHg in 15 patients: 12 had stage 5 or 6, and 3 severe portal expansion. HVPG was repeated in 49, between 7 and 60 months with weak correlation to fibrosis score (r ϭ 0.30, P ϭ 0.045). A total of 12 patients with HVPG Ն6 mmHg had fibrosis score Յ3, while 8 patients had normal HVPG but fibrosis stage Ն4. These discrepancies were mostly associated with specific histological features such as perisinusoidal fibrosis rather than errors in measuring HVPG. In 29 with HVPG Ͻ6 mmHg at 1 yr, none decompensated compared to 4 of 13 (31%) with PHT. In conclusion, HVPG correlates with fibrosis and its progression, due to recurrent HCV infection, assessed in TJB. Liver Transpl 13:1305Transpl 13: -1311Transpl 13: , 2007 The severity of portal hypertension (PHT) correlates with the severity of liver disease and cirrhosis, both functionally and histologically 1 and also with the Model for End-Stage Liver Disease, 2 such that it has independent prognostic value separate from clinical and laboratory assessment. 2,3 Hepatic vein catheterisation 4 was modified by Groszmann et al. 5 using a balloon catheter. The measurement of hepatic venous pressure gradient (HVPG) (the difference between wedge hepatic venous pressure [WHVP] Ϫ free hepatic venous pressure) is reproducible 6 and is the preferred technique for evaluating PHT, correlating 1:1 with the direct measurement of portal vein pressure in patients with sinusoidal and postsinusoidal causes of cirrhosis, 7,8 particularly alcoholic and viral-related cirrhosis. Normally HVPG ranges from 1 to 5 mmHg; pressures Ն6 mmHg indicate PHT. 6 WHVP increases with progression of chronic hepatitis and PHT, before histologically detectable cirrhosis. 9 A gradient Ͼ5 mmHg was always associated with significant changes in liver biopsy in 1 study, although a normal gradient did not completely rule out cirrhosis, 10 suggesting that WHVP could provide supplementary information to liver biopsy, with a higher predictive value for assessing stage and activity of chronic liver disease, than routine biochemical tests. 10 Other studies have correlated HVPG both with severit...

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“…HVPG has been shown to correlate well with the severity of advanced liver disease in HCV infection [38]. It has been even shown to be helpful in assessing reversal of fibrosis following antiviral therapy [48]. Recently, a correlation between HVPG and histologic stages of liver disease has been shown in a study in patients with chronic liver disease due to HBV infection [49].…”

Section: Safety and Complications Of Hvpgmentioning

confidence: 99%

Liver fibrosis: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL)

et al. 2008

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Antiviral Therapy Decreases Hepatic Venous Pressure Gradient in Patients with Chronic Hepatitis C and Advanced Fibrosis

Abstract: AVT reduces HVPG in compensated patients with advanced hepatitis C (fibrosis stage 3 or 4) and portal hypertension.

Cited by 144 publications

References 34 publications

Sustained virologic response prevents the development of esophageal varices in compensated, Child-Pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study

Sustained virologic response prevents the development of esophageal varices in compensated, Child-Pugh class A hepatitis C virus-induced cirrhosis. A 12-year prospective follow-up study

Hepatic venous pressure gradient to assess fibrosis and its progression after liver transplantation for HCV cirrhosis

Liver fibrosis: consensus recommendations of the Asian Pacific Association for the Study of the Liver (APASL)

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