Evidence map›Paper›PMID 22978414›Full record

Trial reportBMC medical genetics2012

PNPLA 3 I148M genetic variant associates with insulin resistance and baseline viral load in HCV genotype 2 but not in genotype 3 infection.

Karolina Rembeck, Cristina Maglio, Martin Lagging, Peer Brehm Christensen, Martti Färkkilä, Nina Langeland, Mads Rauning Buhl, Court Pedersen, Kristine Mørch, Gunnar Norkrans and 7 more

Open access · goldAbstract readClinical Trial, Phase IIIMulticenter StudyRandomized Controlled Trial
In one paragraph

Trial report in BMC medical genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Metabolic alterations and hepatitis C: From bench to bedside.World journal of gastroenterology · 2016
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. PNPLA3 I148M polymorphism and progressive liver disease.World journal of gastroenterology · 2013
    Review
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

17 authors at 5 institutions in 4 countries.

Karolina RembeckDepartment of Infectious Diseases/Virology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.
Cristina Maglio
Martin Lagging
Peer Brehm Christensen
Martti Färkkilä
Nina Langeland
Mads Rauning Buhl
Court Pedersen
Kristine Mørch
Gunnar Norkrans
Kristoffer Hellstrand
Magnus Lindh
Carlo Pirazzi
Maria Antonella Burza
Stefano Romeo
Johan Westin
NORDynamIC group
University of Gothenburg · SEHaukeland University Hospital · NOUniversity of Southern Denmark · DKAarhus University · DKUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatic steatosis in HCV patients has been postulated as a risk factor associated with a higher frequency of fibrosis and cirrhosis. A single genetic variant, PNPLA3 I148M, has been widely associated with increased hepatic steatosis. Previous studies of the PNPLA3 I148M sequence variant in HCV infected individuals have reported an association between this variant and prevalence of steatosis, fibrosis, and cirrhosis. To evaluate the impact of PNPLA3 I148M variant on metabolic traits and treatment response in HCV genotype 2 and 3 infected patients.

methodsThree hundred and eighty-two treatment naïve HCV genotype 2 or 3 infected patients were included in a phase III, open label, randomized, multicenter, investigator-initiated trial (the NORDynamIC study), in which pretreatment liver biopsies were mandatory. PNPLA3I148M genotyping was performed in a total of 359 Caucasian patients.

resultsIn HCV genotype 2 infected patients carrying the PNPLA3 148M allele, there was significantly increased insulin resistance (P = 0.023) and lower viral load (P = 0.005) at baseline as well as the first seven days of antiviral treatment. These results were not observed in HCV genotype 3 infected patients.

conclusionsOur results suggest a possible association between the PNPLA3 148M allele and insulin resistance as well as baseline viral load in HCV genotype 2, but not in genotype 3.

Indexed as

AcyltransferasesAdultAllelesAntiviral AgentsFatty LiverFemaleGenotypeHepacivirusHepatitis C, ChronicHumansInsulin ResistanceLipaseMaleMembrane ProteinsMiddle AgedPhospholipases A2, Calcium-IndependentAcyltransferasesAntiviral AgentsLipaseMembrane ProteinsPhospholipases A2, Calcium-IndependentPNPLA3 protein, human

Identifiers

PMID22978414
PMCPMC3495049
OpenAlexW2074492173

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.