Evidence map›Paper›PMID 29534101›Full record

Observational studyPloS one2018

Stagnation of histopathological improvement is a predictor of hepatocellular carcinoma development after hepatitis C virus eradication.

Hiroyuki Motoyama, Akihiro Tamori, Shoji Kubo, Sawako Uchida-Kobayashi, Shigekazu Takemura, Shogo Tanaka, Satoko Ohfuji, Yuga Teranishi, Ritsuzo Kozuka, Etsushi Kawamura and 5 more

Erratum issuedAbstract readObservational Study
In one paragraph

Observational study in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Article
  3. Article
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Hiroyuki MotoyamaDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Akihiro TamoriDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Shoji KuboDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Sawako Uchida-KobayashiDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Shigekazu TakemuraDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Shogo TanakaDepartment of Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Satoko OhfujiDepartment of Public Health, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Yuga TeranishiDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Ritsuzo KozukaDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Etsushi KawamuraDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Atsushi HagiharaDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Hiroyasu MorikawaDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Masaru EnomotoDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Yoshiki MurakamiDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.
Norifumi KawadaDepartment of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) develops in some patients who achieve sustained virological response (SVR) against hepatitis C virus (HCV) infection via anti-HCV therapy. To examine the pathogenesis of HCC development after HCV eradication, histopathological changes and clinical markers were evaluated in SVR patients.

methodsOf 654 SVR patients treated with interferon (IFN)-based therapies, 34 patients who had undergone liver biopsy before initiating IFN therapy and after SVR achievement were enrolled: 11 patients with HCC and 23 patients without HCC (male/female, 9/2 and 8/15, respectively: age, 58 ± 5 and 54 ± 11 years, respectively). We compared the clinical and histopathological factors between the two groups. Immunohistochemistry for Cytoglobin (CYGB) and α smooth muscle actin (α-SMA) was also performed.

resultsAt baseline, prior to initiating the IFN-based therapy, there were significant differences between the SVR-non-HCC and SVR-HCC groups in the male gender, HBc antibody positivity, prothrombin activity, and histological inflammatory grade. Histopathological evaluation, using the new Inuyama classification system, revealed an improvement in the inflammatory grade, from 2.1 ± 0.6 to 1.0 ± 0.6 (p < 0.0001), whereas the fibrosis stage remained unchanged, from 2.3 ± 0.9 to 2.0 ± 1.2 (p = 0.2749), during the 97 ± 72-month observation period in the SVR-HCC group. Both the grade and stage scores were significantly improved in the SVR-non-HCC group. The area of collagen deposition, evaluated using Sirius red staining, showed a marked decrease, from 18.6 ± 7.6% to 7.7 ± 4.6%, in the SVR-non-HCC group, with no change in the SVR-HCC group. CYGB- and α-SMA-positive hepatic stellate cells (HSCs), indicative of the HSC activated phenotype, remained in the fibrotic tissue of livers among patients in the SVR-HCC group.

conclusionStagnation of fibrosis regression is associated with a high risk for HCC after SVR. HSC activation may inhibit improvement in fibrosis after SVR and potentially contribute to hepatocarcinogenesis.

Indexed as

AdultAntineoplastic AgentsAntiviral AgentsCarcinoma, HepatocellularCollagenCytoglobinFemaleFibrosisGlobinsHepacivirusHepatitis CHumansInterferonsLiverLiver NeoplasmsMaleAntineoplastic AgentsAntiviral AgentsCollagenCYGB protein, humanCytoglobinGlobinsInterferons

Identifiers

PMID29534101
PMCPMC5849339

What OpenQuestion holds

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Registered trials

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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.