Evidence map›Paper›PMID 17983936›Full record

ReviewEndocrinology and metabolism clinics of North America2007

Interferon alpha treatment and thyroid dysfunction.

Yaron Tomer, Jason T Blackard, Nagako Akeno

Open access · greenAbstract readReview
In one paragraph

Review in Endocrinology and metabolism clinics of North America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 3 pooled it
4.9field-weighted citation impact, top 4% 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

65 citing papers in PubMed, 3 syntheses or guidelines pooled it, 145 citations in OpenAlex.

  1. KASL clinical practice guidelines: management of hepatitis C.Clinical and molecular hepatology · 2016
    Guideline
  2. KASL clinical practice guidelines: management of hepatitis C.Clinical and molecular hepatology · 2014
    Guideline
  3. Pooled it
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. ZBED2 is an antagonist of interferon regulatory factor 1 and modifies cell identity in pancreatic cancer.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  15. Anticancer Drug-induced Thyroid Dysfunction.European endocrinology · 2020
    Review
  16. Review
  17. Article
  18. Regulation ofFrontiers in immunology · 2019
    Article
  19. Article
  20. International journal of endocrinology · 2019
    Article

5 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Yaron TomerDivision of Endocrinology, Cincinnati VA Medical Center, USA. yaron.tomer@uc.edu
Jason T Blackard
Nagako Akeno
University of Cincinnati Medical Center · USCincinnati VA Medical Center · US

Funding

Mapping Autoimmune Diabetes and Thyroiditis GenesR01DK067555 · NIDDK · UNIVERSITY OF CINCINNATI · PI MIHAELA STEFAN LIFSHITZ, YARON TOMER · 2005 to 2026
$5.8M
Identifying Genes Linked to Autoimmune Thyroid DiseasesR01DK061659 · NIDDK · UNIVERSITY OF CINCINNATI · PI TOMER, YARON · 2002 to 2017
$4.1M
Extrahepatic Replication and Viral Evolution of HCV During HCV/HIV Co-infectionR21DA022148 · NIDA · UNIVERSITY OF CINCINNATI · PI BLACKARD, JASON T · 2006 to 2007
$348k
NIDA NIH HHS DA022148NIDA NIH HHS R21 DA022148NIDDK NIH HHS DK067555NIDDK NIH HHS DK61659NIDDK NIH HHS R01 DK061659NIDDK NIH HHS R01 DK067555
6 · The paper itself

Abstract

Interferon alpha (IFN alpha) is the cornerstone therapeutic agent for chronic hepatitis C virus (HCV) infection. Prospective studies have shown that up to 15% of HCV patients receiving IFN alpha develop clinical thyroid disease, and up to 40% become thyroid antibody positive. In some cases IFN-induced thyroiditis (IIT) may result in discontinuation of interferon therapy; thus, IIT represents a major clinical problem for hepatitis C patients receiving IFN alpha therapy. Recently, the mechanisms leading to the development of IIT have begun to be unraveled. It is now clear that HCV itself plays a role in the disease. Moreover, recent data suggest the IFN alpha precipitates thyroiditis by both immune modulatory mechanisms and direct thyroid toxic effects. Genetic factors also play a major role in the etiology of IIT. IIT can manifest both as clinical autoimmune thyroiditis (ie, Hashimoto's thyroiditis and Graves' disease) and as nonautoimmune thyroiditis (ie, destructive thyroiditis). Early detection and therapy of these conditions are important to avoid complications of thyroid disease such as cardiac arrhythmias. This article reviews the epidemiology and clinical manifestations of IIT and the mechanisms causing IIT, focusing on the role of HCV.

Indexed as

Antiviral AgentsGenetic Predisposition to DiseaseHepacivirusHepatitis CHumansImmunity, InnateInterferon-alphaThyroiditisVirus ReplicationAntiviral AgentsInterferon-alpha

Identifiers

PMID17983936
PMCPMC2134787
OpenAlexW2085737748

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.