Evidence map›Paper›PMID 26356124›Full record

ReviewJournal of clinical and translational hepatology2013

Autoimmune Hepatitis: Clinical Review with Insights into the Purinergic Mechanism of Disease.

Nikhil Kapila, Jennifer T Higa, Maria Serena Longhi, Simon C Robson

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of clinical and translational hepatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017
    Review
  3. [Warfarin-induced autoimmune hepatitis: a case report].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2015
    Article
  4. Liver Diseases and Autoimmunity.Journal of clinical and translational hepatology · 2013
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Nikhil KapilaDepartment of Medicine, University of Connecticut, Farmington, CT, USA ; These authors contributed equally to this work.
Jennifer T HigaGastroenterology Division and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA ; These authors contributed equally to this work.
Maria Serena LonghiGastroenterology Division and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA ; Institute of Liver Studies, King's College London School of Medicine at King's College Hospital, Denmark Hill, London, UK.
Simon C RobsonGastroenterology Division and Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Beth Israel Deaconess Medical Center · USKing's College Hospital · GBUniversity of Connecticut · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune hepatitis (AIH) is an important disorder that predominantly results in inflammatory liver disease in genetically predisposed women. The clinicopathological picture is characterized by symptoms associated with both systemic inflammation and hepatic dysfunction, and with increased serum aminotransferases, elevated IgG, autoantibodies, and interface hepatitis on liver biopsy. AIH usually results in liver injury as a consequence of chronic hepatitis and cirrhosis. However, rarely, patients may present with fulminant liver failure. Early diagnosis is important in all instances because the disease can be highly responsive to immunosuppressive therapeutic options. Left untreated, the disease is associated with high morbidity and mortality. Here we provide an overview of the current state of knowledge on AIH and summarize the treatment options for this serious condition in adults. We also discuss the pathogenesis of the disease as a possible consequence of autoimmunity and the breakdown of hepatic tolerance. We focus on regulatory T cell impairments as a consequence of changes in CD39 ectonucleotidase expression and altered purinergic signaling. Further understanding of hepatic tolerance may aid in the development of specific and well-tolerated therapies for AIH.

Indexed as

Autoimmune hepatitisCD39ImmunologyPathogenesisPurinergicTherapeutic overview

Identifiers

PMID26356124
PMCPMC4521285
OpenAlexW2052775717

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.