Evidence map›Paper›PMID 26877604›Full record

ReviewWorld journal of gastroenterology2016

Anti-rods/rings autoantibody generation in hepatitis C patients during interferon-α/ribavirin therapy.

Gerson Dierley Keppeke, S John Calise, Edward K L Chan, Luis Eduardo C Andrade

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of gastroenterology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Observational
  7. Article
  8. Infinite Assembly of Folded Proteins in Evolution, Disease, and Engineering.Angewandte Chemie (International ed. in English) · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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 1 institution in 2 countries.

Gerson Dierley KeppekeGerson Dierley Keppeke, Luis Eduardo C Andrade, Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP 04023-062, Brazil.
S John CaliseGerson Dierley Keppeke, Luis Eduardo C Andrade, Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP 04023-062, Brazil.
Edward K L ChanGerson Dierley Keppeke, Luis Eduardo C Andrade, Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP 04023-062, Brazil.
Luis Eduardo C AndradeGerson Dierley Keppeke, Luis Eduardo C Andrade, Rheumatology Division, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP 04023-062, Brazil.
University of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammation associated with hepatitis C virus (HCV) infection can lead to disabling liver diseases with progression to liver cirrhosis and hepatocellular carcinoma. Despite the recent availability of more effective and less toxic therapeutic options, in most parts of the world the standard treatment consists of a weekly injection of pegylated interferon α (IFN-α) together with a daily dose of ribavirin. HCV patients frequently present circulating non-organ-specific autoantibodies demonstrating a variety of staining patterns in the indirect immunofluorescence assay for antinuclear antibodies (ANA). Between 20% to 40% of HCV patients treated with IFN-α and ribavirin develop autoantibodies showing a peculiar ANA pattern characterized as rods and rings (RR) structures. The aim of this article is to review the recent reports regarding RR structures and anti-rods/rings (anti-RR) autoantibody production by HCV patients after IFN-α/ribavirin treatment. Anti-RR autoantibodies first appear around the sixth month of treatment and reach a plateau around the twelfth month. After treatment completion, anti-RR titers decrease/disappear in half the patients and remain steady in the other half. Some studies have observed a higher frequency of anti-RR antibodies in relapsers, i.e., patients in which circulating virus reappears after initially successful therapy. The main target of anti-RR autoantibodies in HCV patients is inosine-5'-monophosphate dehydrogenase 2 (IMPDH2), the rate-limiting enzyme involved in the guanosine triphosphate biosynthesis pathway. Ribavirin is a direct IMPDH2 inhibitor and is able to induce the formation of RR structures in vitro and in vivo. In conclusion, these observations led to the hypothesis that anti-RR autoantibody production is a human model of immunologic tolerance breakdown that allows us to explore the humoral autoimmune response from the beginning of the putative triggering event: exposure to ribavirin and interferon.

Indexed as

Antibodies, AntinuclearAntiviral AgentsAutoimmunityDrug Therapy, CombinationHepatitis C, ChronicHumansImmunity, HumoralIMP DehydrogenaseInterferon-alphaProtein ConformationRibavirinSelf ToleranceTime FactorsTreatment OutcomeAntibodies, AntinuclearAntiviral AgentsIMP DehydrogenaseIMPDH2 protein, humanInterferon-alphaRibavirinAutoantibodiesHepatitis CInterferon-αRibavirinRods and rings

Identifiers

PMID26877604
PMCPMC4726672
OpenAlexW2441583716

What OpenQuestion holds

Textmetadata
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.