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A Randomized trial to assess whether portal pressure guided therapy to prevent variceal rebleeding improves survival in cirrhosis.
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A Randomized trial to assess whether portal pressure guided therapy to prevent variceal rebleeding improves survival in cirrhosis.

Hepatology. 2017 Jan 18;:

Authors: Villanueva C, Graupera I, Aracil C, Alvarado E, Miñana J, Puente Á, Hernandez-Gea V, Ardevol A, Pavel O, Colomo A, Concepción M, Poca M, Torras X, Reñe JM, Guarner C

Abstract
Monitoring the hemodynamic response of portal pressure to drug therapy accurately stratifies the risk of variceal rebleeding. We assessed whether guiding therapy with HVPG-monitoring may improve survival in the prevention of variceal rebleeding. Cirrhotic patients with controlled variceal bleeding were randomized to a HVPG-guided-therapy group (N= 84) or to a control group (N= 86). In both groups, HVPG and acute β-blocker response were evaluated at baseline and HVPG measurements were repeated at 2-4-weeks to determine chronic response. In the HVPG-guided group, acute responders were treated with nadolol and acute non-responders with nadolol+nitrates. Chronic non-responders received nadolol+prazosin and had a third HVPG study. Ligation sessions were repeated until response was achieved. The control group was treated with nadolol+nitrates+ligation. Between-group baseline characteristics were similar. During long-term follow-up (median of 24 months) mortality was lower in the HVPG-guided-therapy group than in the control group (29% vs 43%; HR= 0.59, 95%CI= 0.35-0.99). Rebleeding occurred in 19% vs 31% of patients, respectively (HR= 0.53, 95%CI= 0.29-0.98), and further decompensation of cirrhosis occurred in 52% vs 72% (HR= 0.68, 95%CI= 0.46-0.99). The survival probability was higher with HVPG-guided-therapy than in controls, both in acute (HR= 0.59, 95%CI= 0.32-1.08) and chronic non-responders (HR= 0.48, 95%CI= 0.23-0.99). HVPG-guided patients had a greater reduction of HVPG and a lower final value than controls (P< 0.05).
CONCLUSION: HVPG-monitoring, by stratifying risk and targeting therapy, improves the survival achieved with currently recommended treatment to prevent variceal rebleeding using β-blockers and ligation. HVPG-guided-therapy achieved a greater reduction in portal pressure, which may have contributed to reduce the risk of rebleeding and of further decompensation of cirrhosis, thus contributing to a better survival. This article is protected by copyright. All rights reserved.

PMID: 28100019 [PubMed - as supplied by publisher]




What is the benefit of early follow-up after hospitalization for patients with cirrhosis?
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What is the benefit of early follow-up after hospitalization for patients with cirrhosis?

Hepatology. 2017 Jan 18;:

Authors: Driver R, Rowe IA

PMID: 28100009 [PubMed - as supplied by publisher]




Is Moderate Alcohol Use in Non-Alcoholic Fatty Liver Disease Good or Bad? A Critical Review.
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Is Moderate Alcohol Use in Non-Alcoholic Fatty Liver Disease Good or Bad? A Critical Review.

Hepatology. 2017 Jan 18;:

Authors: Ajmera VH, Terrault NA, Harrison SA

Abstract
Moderate alcohol consumption in patients with nonalcoholic fatty liver disease (NAFLD) is common, yet the effects on cardiovascular and liver health are unclear. Moderate alcohol use is associated with improved insulin sensitivity and decreased cardiovascular mortality in the general population but whether similar benefits are seen in persons with NAFLD is largely unstudied. There is significant overlap in the pathogenesis of alcoholic liver disease (ALD) and NAFLD although studies of ALD have focused on pathologic alcohol intake and few mechanistic studies of moderate alcohol use in NAFLD exist. We undertook a critical review of the effect of moderate alcohol use on cardiovascular and liver disease in patients with NAFLD. A total of 7 observational studies met criteria for inclusion (one for cardiovascular endpoints and 6 for liver endpoints). There were insufficient studies to assess the association with cardiovascular outcomes. There was a positive association between moderate alcohol use and decreased NASH and fibrosis, however heavy episodic drinking may accelerate fibrosis progression and in patients with advanced fibrosis moderate alcohol use may increase the risk of hepatocellular carcinoma. Significant methodologic limitations were present including incomplete adjustment for confounders and failure to measure lifetime use or the pattern of alcohol intake. Thus, a strong recommendation of benefit of moderate alcohol use in NAFLD cannot be made. There remains a need for additional high quality longitudinal studies that evaluate both cardiovascular and liver outcomes among NAFLD patients with moderate or lesser degrees of alcohol use. This article is protected by copyright. All rights reserved.

PMID: 28100008 [PubMed - as supplied by publisher]




Race or Genetic Makeup for HCV Treatment Decisions?
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Race or Genetic Makeup for HCV Treatment Decisions?

Hepatology. 2017 Jan 18;:

Authors: O'Brien TR, Kottilil S, Feld JJ, Morgan TR, Pfeiffer RM

PMID: 28100007 [PubMed - as supplied by publisher]




The Fingerprint of Antimitochondrial Antibodies and the Etiology of Primary Biliary Cholangitis.
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The Fingerprint of Antimitochondrial Antibodies and the Etiology of Primary Biliary Cholangitis.

Hepatology. 2017 Jan 18;:

Authors: Shuai Z, Wang J, Badamagunta M, Choi J, Yang G, Zhang W, Kenny TP, Guggenheim K, Kurth MJ, Ansari AA, Voss J, Coppel RL, Invernizzi P, Leung PS, Gershwin ME

Abstract
The identification of environmental factors that lead to loss of tolerance has been coined the Holy Grail of autoimmunity. Our work has focused on the reactivity of antimitochondrial autoantibodies (AMA) to chemical xenobiotics and has hypothesized that a modified peptide within PDC-E2, the major mitochondrial autoantigen, will have been immunologically recognized at the time of loss of tolerance. Herein we successfully applied intein technology to construct a PDC-E2 protein fragment containing amino acid residues 177-314 of PDC-E2 by joining a recombinant peptide spanning residues 177 to 252 (PDC-228) with a 62 residue synthetic peptide from 253 to 314 (PP), which encompasses PDC-E2 ILD. We named this intein-constructed fragment PPL. Importantly, PPL, as well as lipoic acid conjugated PPL (LA-PPL) and xenobiotic 2-octynoic acid conjugated PPL (2OA-PPL), are recognized by AMA. Of great importance, AMA has specificity for the 2OA modified PDC-E2 ILD peptide backbone distinct from antibodies that react with native lipoylated PDC-E2 peptide. Interestingly, this unique AMA subfraction is of the IgM isotype and more dominant in early stage PBC, suggesting that exposure to 2OA-PPL-like compounds occurs early in the generation of AMA. To understand the structural basis of this differential recognition we analyzed PPL, LA-PPL and 2OA-PPL using electron paramagnetic resonance spectroscopy, with confirmations by ELISA, immunoblotting and affinity antibody analysis. We demonstrate that the conformation of PDC-E2 ILD is altered when conjugated with 2OA, compared to conjugation with lipoic acid. In conclusion a molecular understanding of the conformation of xenobiotic modified PDC-E2 is critical for understanding xenobiotic modification and loss of tolerance in PBC with widespread implications for a role of environmental chemicals in the induction of autoimmunity. This article is protected by copyright. All rights reserved.

PMID: 28100006 [PubMed - as supplied by publisher]




Reply to: Race or Genetic Makeup for HCV Treatment Decisions?
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Reply to: Race or Genetic Makeup for HCV Treatment Decisions?

Hepatology. 2017 Jan 18;:

Authors: Su F, Ioannou GN

PMID: 28100005 [PubMed - as supplied by publisher]