María‐Vega Catalina

Hospital General Universitario Gregorio Marañón

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Rafael Bañares

Hospital General Universitario Gregorio Marañón

Diego Rincón

Hospital General Universitario Gregorio Marañón

Cristina Ripoll

Jena University Hospital

Luis Ibáñez

Hospital General Universitario Gregorio Marañón

Agustı́n Albillos

Hospital Universitario Ramón y Cajal

Helena Masnou

Hospital Universitari Germans Trias i Pujol

Virginia Hernández–Gea

Universitat de Barcelona

José Luis Mundi

Instituto de Investigación Biosanitaria de Granada

Manuel Romero‐Gómez

Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas

Wim Laleman

KU Leuven

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Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas

101

Instituto de Salud Carlos III

Hospital General Universitario Gregorio Marañón

Centro de Investigación Biomédica en Red

Universitat de Barcelona

Universidad Complutense de Madrid

Consorci Institut D'Investigacions Biomediques August Pi I Sunyer

Hospital Clínic de Barcelona

Inserm

University College London

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Respiratory infection in patients with cirrhosis and acute varicealbleeding on antibiotic prophylaxis: A multicenter observational study of 2138 patients

Jorge Martínez Luís Téllez Virginia Hernández–Gea Bogdan Procopeț Álvaro Giráldez-Gallego

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Risk factors for developing de novo autoimmune hepatitis associated with anti-glutathione S-transferase T1 antibodies after liver transplantation

Liver Transplantation (2009)

Óscar Len Margarita Rodríguez‐Mahou Carmen Rodríguez-Sáinz Diego Rincón Emilio Álvarez

De novo autoimmune hepatitis (de novo AIH) is a rare form of graft dysfunction that develops after liver transplantation (LT) in patients transplanted for conditions other than autoimmune disorders. Although characterized by biochemical, serological, and histological features of AIH, de novo AIH is sometimes associated with atypical serum autoantibodies, many of which are directed against glutathione S-transferase T1 (anti-GSTT1). GSTT1 donor/recipient genotype mismatch has been suggested as a necessary condition for the appearance of autoantibodies and de novo AIH. However, clinically evident disease is not observed in all patients with anti-GSTT1 antibodies. We examined the incidence of de novo AIH and its conditioning (risk) factors in patients with anti-GSTT1 antibodies. Anti-GSTT1 autoantibodies were detected in 29 of 419 [6.9%; 95% confidence interval (CI), 4.9–9.8] consecutive adult LT recipients with donor/recipient GSTT1 mismatch. Twenty of 27 assessable patients (74%) developed de novo AIH after a median follow-up of 26 months (95% CI, 19.2–32.8). The probability of de novo AIH was 11%, 44%, and 60% 12, 24, and 36 months after LT, respectively. No relationship emerged between de novo AIH and recipient gender, donor and recipient age, rejection episodes, immunosuppressive regime, allelic GSTT1 expression, human leukocyte antigen distribution, or cytomegalovirus infection. Multivariate analysis identified male donor [hazard ratio (HR), 3.3; 95% CI, 1.18–9.26; P = 0.018], nonalcoholic etiology (HR, 4.67; 95% CI, 1.64–13.3; P = 0.002), and high anti-GSTT1 titer (HR, 2.98; 95% CI, 1.04–8.57; P = 0.035) as independent predictors of de novo AIH. Most patients with anti-GSTT1 antibodies and donor/recipient GSTT1 mismatch developed clinically evident de novo AIH after LT. The risk of developing the disease was increased by male donor gender, nonalcoholic etiology of original liver disease, and a high anti-GSTT1 titer. Liver Transpl 15:530–539, 2009. © 2009 AASLD.

Autoimmune Hepatitis

Glutathione S-transferase

Glutathione transferase

Transferase

10.1002/lt.21721

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Citations (55)

130 Applicability and safety of extracorporeal liver support using albumin dialysis (MARS) in the setting of liver transplantation

Journal of Hepatology (2006)

María‐Vega Catalina Cristina Ripoll G. Clemente M. Salcedo Diego Rincón

Extracorporeal

Artificial liver

10.1016/s0168-8278(06)80131-5

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Prognostic Markers in Patients Who Have Recovered from an Acute Variceal Bleeding: Role of HVPG Measurement

Disease Markers (2011)

Rafael Bañares María‐Vega Catalina Cristina Ripoll Diego Rincón

10.1155/2011/472689

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Citations (4)

A meta-analysis of transjugular intrahepatic portosystemic shunt versus paracentesis for refractory ascites

Journal of Hepatology (2005)

Agustı́n Albillos Rafael Bañares Mónica González María‐Vega Catalina Luis-Miguel Molinero

Hepatic Encephalopathy

Paracentesis

Spontaneous bacterial peritonitis

10.1016/j.jhep.2005.06.005

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Citations (160)

P0135 : Impact of vasopressin AVP1A receptor gene polymorphisms on mortality and renal failure in patients with acute decompensation of chronic liver disease

Journal of Hepatology (2015)

Jelte J. Schaapman A.C. Kerbert J.J. van der Reijden Àlex Amorós Navarro Marco Pavesi

Decompensation

10.1016/s0168-8278(15)30355-x

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Effect of Eradication of HCV on Hepatic Venous Pressure Gradient in HIV-Infected Patients With Compensated HCV-Related Cirrhosis

JAIDS Journal of Acquired Immune Deficiency Syndromes (2015)

Matilde Sánchez‐Conde Leire Pérez‐Latorre Diego Rincón Pilar Miralles María‐Vega Catalina

To the Editors: Coinfection by hepatitis C virus (HCV) is frequent in patients infected with human immunodeficiency virus (HIV) because both viruses share routes of transmission.1 Progression of chronic hepatitis C to cirrhosis and end-stage liver disease is more frequent and rapid among HIV-infected individuals than in those not infected by HIV.2 The major determinants of this accelerated fibrogenesis in HIV/HCV-coinfected patients are immunosuppression and alcohol consumption, although direct action of HIV may also be a contributing factor.3 Therefore, liver disease is a leading cause of hospital admissions and death after the introduction of combination antiretroviral therapy in areas where the prevalence of HIV/HCV coinfection is high.4 Decompensation in cirrhosis results primarily from portal hypertension, which is defined as a pathologic increase in the hepatic venous pressure gradient (HVPG), that is, the pressure gradient between the portal vein and the inferior vena cava.5 HVPG is the most accurate predictor of liver decompensation and hepatocellular carcinoma in patients with compensated cirrhosis.6 In addition, HVPG is an independent predictor of death in patients with decompensated cirrhosis.7 Therefore, HVPG is considered the best surrogate marker of the natural history of cirrhosis. Sustained virologic response (SVR) after anti-HCV therapy has been associated with improvements in liver fibrosis and with reversion of cirrhosis in one-third to half of patients with baseline cirrhosis included in randomized clinical trials of interferon plus ribavirin with pretreatment and posttreatment liver biopsies.8 SVR has also been associated with improved survival and reduced liver decompensation and hepatocellular carcinoma in patients with chronic hepatitis C with or without HIV infection.9,10 Although these findings support the notion that eradication of HCV can reduce HVPG in patients with HCV-related cirrhosis, this area has received little attention,11 particularly in coinfected patients. Our objective was to assess the effect of eradication of HCV after anti-HCV therapy on HVPG in HIV-infected patients with compensated HCV-related cirrhosis. The study population comprised all HIV/HCV-coinfected patients with compensated liver cirrhosis whose HVPG was measured before and after anti-HCV therapy between 2007 and 2012. HVPG was measured after an overnight fast as described elsewhere.12 The HVPG was calculated as the wedged hepatic venous pressure minus the free hepatic venous pressure. All patients signed an informed consent document before the portal hemodynamic study. Transient elastography (TE) was performed immediately before the determination of HVPG using a FibroScan device (Echosens, Paris, France). The median value [expressed in kilopascals (kPa)] of 10 successful acquisitions was considered the representative measurement of liver stiffness.13 We considered a cutoff value of liver stiffness ≥14 kPa as diagnostic of liver cirrhosis.14 Between 2007 and 2012, determination of HVPG and TE was performed in 60 HIV/HCV–coinfected patients with compensated cirrhosis confirmed by liver biopsy and/or TE. During this period, 27 of these 60 patients were treated with pegylated interferon (Peg-IFN) alpha-2a or alpha-2b plus ribavirin (programmed for 48 weeks), whereas 33 were not. A total of 15 treated patients achieved SVR, defined as undetectable HCV-RNA in serum at 24 weeks after discontinuation of anti-HCV therapy. The median [interquartile range (IQR)] baseline HVPG was 13 (10–15) mm Hg for untreated patients, 15 (10–18) mm Hg for treated patients with SVR, and 10 (9–14) mm Hg for nonresponders. The median (IQR) baseline liver stiffness was 30.4 (15.7–43.9) kPa for untreated patients, 23.9 (15.1–38.0) kPa for treated patients with SVR, and 14.6 (12.2–24.6) kPa for nonresponders. Eight of the 15 patients with SVR consented to have a second determination of HVPG and are the focus of this study. All 8 patients had clinically significant portal hypertension (HVPG ≥ 10 mm Hg), and 6 had severe portal hypertension (HVPG > 12 mm Hg). The second HVPG and TE determinations were performed a median of 18 (10–26) months after the discontinuation of anti-HCV therapy. The median (IQR) HVPG was 15.50 (11.25–17.62) mm Hg at baseline and 8.75 (6.25–12.00) mm Hg after SVR (P = 0.01) (Figure 1). After SVR, 7 patients experienced a reduction in HVPG from baseline of ≥20%, and all 7 had HVPG values ≤12 mm Hg. Likewise, the median (IQR) liver stiffness was 27.75 (18.20–38.60) kPa at baseline and 12.80 (7.30–17.05) kPa after SVR (P = 0.01) (Figure 1). After a median follow-up time of 60 months, all 8 patients were alive and free from decompensation and hepatocellular carcinoma.FIGURE 1: A, Median and IQR values and individual values of HVPG at baseline and after SVR. B, Median and IQR values and individual TE values at baseline and after SVR.The effect of anti-HCV therapy on HVPG in patients with HCV-related cirrhosis has received little attention hitherto. In one study, HVPG was measured in 5 patients immediately before and immediately after the discontinuation of a 48-week course of interferon monotherapy and in 5 control patients.15 In treated patients, HVPG decreased from a mean of 13.8 mm Hg at baseline to 11.1 mm Hg at the end of therapy, whereas in controls, it increased from a mean of 13.2 to 14.6 mm Hg; neither of these changes was statistically significant.15 In a second study, HVPG measurements were performed immediately before and immediately after discontinuation of Peg-IFN plus ribavirin in 20 patients with compensated chronic hepatitis C and portal hypertension, defined as an HVPG > 5 mm Hg.16 The authors found a greater reduction in HVPG in patients who achieved end-of-treatment virologic response than in nonresponders. The effect of SVR on portal pressure in 33 patients with HCV-related cirrhosis was assessed at baseline and after 6 months of treatment-free follow-up in 33 patients with cirrhosis by Roberts et al,11 who found that after treatment, there was a significant decrease in HVPG in sustained responders (from a mean of 9.0 mm Hg to a mean of 6.9 mm Hg) compared with relapsers and primary nonresponders. Our findings and those of others bring a pathophysiological correlate to the observation of clinical benefits obtained with SVR in patients with HCV-related compensated liver cirrhosis with or without HIV infection.9,10 It is important to remark that the achievement of an adequate reduction in HVPG after pharmacological treatment of portal hypertension in patients with variceal bleeding reduces not only the probability of recurrent bleeding but also the probability of developing other severe manifestations of end-stage liver cirrhosis such as spontaneous bacterial peritonitis, hepatorenal syndrome, and even death.17 This adequate reduction in portal pressure has been estimated as a decrease in HVPG of ≥20% from baseline or an absolute reduction of HVPG to ≤12 mm Hg.17 We found that 7 of the 8 patients met both these requirements for reduction of portal pressure and, therefore, were at less risk of decompensation and death. The remaining patient had a reduction of 10% in HVPG from baseline, and his HVPG value after SVR was 13.5 mm Hg. However, he was also the patient with the shortest interval between drug discontinuation and the second HVPG determination (only 7 months). Roberts et al11 found that among patients with portal hypertension, a higher proportion of responders achieved a ≥20% reduction in HVPG compared with nonresponders (71% vs. 20%, respectively). According to our experience and that of others, most patients with HCV-related compensated cirrhosis and portal hypertension achieve adequate reductions in HVPG after SVR following anti-HCV therapy, although a small fraction do not achieve that goal. These patients probably remain at risk of developing complications related to portal hypertension despite eradication of HCV.10,18 HVPG determinations or even TE19 could help to identify patients with HCV-related cirrhosis who remain at risk for decompensation or hepatocellular carcinoma despite having achieved SVR. This issue should be addressed in prospective studies. The main limitation of this study is the small sample size and the lack of a control group comprising HIV-infected patients with HCV-related cirrhosis who are nonresponders to anti-HCV therapy and whose HVPG was determined before and after treatment. However, a key strength of our study is the long interval (18 months) between the discontinuation of interferon and ribavirin and the determination of the second portal pressure measurement. Previous studies on the subject addressed the effect of antiviral therapy on HVPG but not that of SVR on HVPG15,16 or they determined changes in portal pressure 6 months after treatment discontinuation11; therefore, the question of whether the reduction of portal pressure after SVR was maintained in the long term remains unresolved. In conclusion, the results of our study support the notion that eradication of HCV is associated with a marked and clinically significant reduction in portal pressure in most—but not all—HIV-infected patients with HCV-related cirrhosis.

Decompensation

Hepatitis C

Liver disease

10.1097/qai.0000000000000639

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Citations (3)

La insuficiencia hepática crónica reagudizada: un nuevo concepto para una complicación clásica

Gastroenterología y Hepatología (2014)

María‐Vega Catalina Luis Ibáñez Rafael Bañares

10.1016/j.gastrohep.2013.11.004

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Citations (1)