Evidence map›Paper›PMID 30247160›Full record

ArticleThe American journal of surgical pathology2018

Inflammation, Active Fibroplasia, and End-stage Fibrosis in 172 Biliary Atresia Remnants Correlate Poorly With Age at Kasai Portoenterostomy, Visceral Heterotaxy, and Outcome.

Kevin E Bove, Andrew D Thrasher, Robert Anders, Catherine T Chung, Oscar W Cummings, Milton J Finegold, Laura Finn, Sarangarajan Ranganathan, Grace E Kim, Mark Lovell and 9 more

Abstract readMulticenter Study
In one paragraph

Article in The American journal of surgical pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

5 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Biliary Atresia Animal Models: Is the Needle in a Haystack?International journal of molecular sciences · 2022
    Review
  3. Article
  4. Article
  5. In Utero Extrahepatic Bile Duct Damage and Repair: Implications for Biliary Atresia.Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society
    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

19 authors at 13 institutions in 2 countries.

Kevin E BoveDivision of Pathology and Laboratory Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Andrew D ThrasherDivision of Pathology and Laboratory Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.
Robert AndersDepartment of Pathology, Johns Hopkins School of Medicine, Baltimore, MD.
Catherine T ChungDivision of Pathology, The Hospital for Sick Children, Toronto, ON, Canada.
Oscar W CummingsDepartment of Pathology, Indiana University School of Medicine, Indianapolis, IN.
Milton J FinegoldDepartment of Pathology, Texas Children's Hospital, Houston, TX.
Laura FinnDepartment of Laboratories, Seattle Children's Hospital, Seattle, WA.
Sarangarajan RanganathanDepartment of Pathology, Children's Hospital of Pittsburgh of UPMC, Pittsburgh.
Grace E KimDepartment of Anatomic Pathology, University of California, San Francisco, CA.
Mark LovellDepartment of Pathology, Children's Hospital Colorado, Aurora, CO.
Margret S MagidDepartment of Pathology, Kravis Children's Hospital, Mount Sinai Medical Center, New York, NY.
Hector Melin-AldanaDepartment of Pathology, Ann & Robert H. Lurie Children's Hospital, Chicago, IL.
Pierre RussoDepartment of Pathology and Laboratory Medicine, the Children's Hospital of Philadelphia, Philadelphia, PA.
Bahig ShehataDepartment of Pathology, Children's Healthcare of Atlanta, Atlanta, GA.
Larry WangDepartment of Pathology, Children's Hospital Los Angeles, Los Angeles, CA.
Francis WhiteDepartment of Pathology and Immunology, Washington University School of Medicine, St Louis, MO.
Zhen ChenQuest Diagnostics, Health Informatics, Madison, NJ.
Catherine SpinoSchool of Public Health.
John C MageeDepartment of Surgery, University of Michigan, Ann Arbor, MI.
Cincinnati Children's Hospital Medical Center · USIndiana University School of MedicineHospital for Sick Children · CAJohns Hopkins University · USChildren's Healthcare of Atlanta · USChildren's Hospital of Los Angeles · USChildren's Hospital of Philadelphia · USChildren's Hospital of Pittsburgh · USJohns Hopkins Medicine · USMount Sinai Medical Center · USSeattle Children's Hospital · USTexas Children's Hospital · USWashington University in St. Louis · US

Funding

Childhood Liver Disease Research Network Data Coordinating CenterU01DK062456 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MAGEE, JOHN C, MERION, ROBERT M · 2002 to 2019
$36.8M
Childhood Liver Disease Research Network Data Coordinating CenterU24DK062456 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI JOHN C MAGEE · 2019 to 2026
$18.9M
Etiology and Treatment of Biliary Atresia and INHU01DK062453 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI RONALD J. SOKOL · 2002 to 2026
$13.5M
Clinical Center for Cholestatic Liver Disease in ChildrenU01DK062497 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Alexander Miethke · 2002 to 2026
$13.2M
VCU-Atlanta Center for the Childhood Liver Disease Research Network (ChiLDReN)U01DK062470 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI SAUL J. KARPEN · 2005 to 2026
$12.7M
Mid-Atlantic BANH Consortium SiteU01DK062481 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI Binita Maya Kamath, Kathleen Mary Loomes · 2002 to 2026
$9.2M
Macrophage Cell Subset Specific Biomarkers for Disease Prognosis in Biliary AtresiaU01DK062436 · NIDDK · LURIE CHILDREN'S HOSPITAL OF CHICAGO · PI ALONSO, ESTELLA M. · 2002 to 2023
$7.0M
The Pittsburgh Cholestatic Liver Disease ConsortiumU01DK062466 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HORSLEN, SIMON · 2002 to 2023
$6.3M
Continuation of ChiLDReN, the Childhood Liver Disease Research Network: Indiana UniversityU01DK084536 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI MOLLESTON, JEAN PAPPAS · 2009 to 2023
$5.9M
Continuation of the Childhood Liver Disease Research Network Seattle Clinical CenterU01DK084575 · NIDDK · SEATTLE CHILDREN'S HOSPITAL · PI Pamela Valentino · 2009 to 2026
$5.2M
Clinical Center for ChiLDREN: Pathogenesis, Biomarkers, and Antifibrotic TherapyU01DK103149 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI BENJAMIN L SHNEIDER · 2014 to 2026
$4.8M
Limited Competition for the Continuation of the Childhood Liver Disease Research Network (ChilLDRen) Clinical Centers.U01DK084538 · NIDDK · CHILDREN'S HOSPITAL OF LOS ANGELES · PI KOHLI, ROHIT · 2009 to 2023
$4.8M
NIDDK NIH HHS U01 DK062436NIDDK NIH HHS U01 DK062445NIDDK NIH HHS U01 DK062452NIDDK NIH HHS U01 DK062453NIDDK NIH HHS U01 DK062456NIDDK NIH HHS U01 DK062466NIDDK NIH HHS U01 DK062470NIDDK NIH HHS U01 DK062481NIDDK NIH HHS U01 DK062497NIDDK NIH HHS U01 DK062500NIDDK NIH HHS U01 DK062503NIDDK NIH HHS U01 DK084536NIDDK NIH HHS U01 DK084538NIDDK NIH HHS U01 DK084575NIDDK NIH HHS U01 DK103149NIDDK NIH HHS U24 DK062456
6 · The paper itself

Abstract

Published histologic studies of the hilar plate or entire biliary remnant at the time of Kasai portoenterostomy (KHPE) have not provided deep insight into the pathogenesis of biliary atresia, relation to age at surgery, prognosis or the basis for successful drainage. We report detailed histologic findings in 172 centrally reviewed biliary remnants with an average of 6 sections per subject. Active lesions were classified as either necroinflammatory (rare/clustered in a few subjects) or active concentric fibroplasia with or without inflammation (common). Inactive lesions showed bland replacement by collagen and fibrous cords with little or no inflammation. Heterogeneity was common within a given remnant; however, relatively homogenous histologic patterns, defined as 3 or more inactive or active levels in the hepatic ducts levels, characterized most remnants. Homogeneity did not correlate with age at KHPE, presence/absence of congenital anomalies at laparotomy indicative of heterotaxy and outcome. Remnants from youngest subjects were more likely than older subjects to be homogenously inactive suggesting significantly earlier onset in the youngest subset. Conversely remnants from the oldest subjects were often homogenously active suggesting later onset or slower progression. More data are needed in remnants from subjects <30 days old at KHPE and in those with visceral anomalies. Prevalence of partially preserved epithelium in active fibroplastic biliary atresia lesions at all ages suggests that epithelial regression or injury may not be a primary event or that reepithelialization is already underway at the time of KHPE. We hypothesize that outcome after KHPE results from competition between active fibroplasia and reepithelialization of retained, collapsed but not obliterated lumens. The driver of active fibroplasia is unknown.

Indexed as

Portoenterostomy, HepaticAge FactorsBiliary AtresiaBiopsyCholangitisDatabases, FactualFemaleHeterotaxy SyndromeHumansInfantInfant, NewbornLiver Cirrhosis, BiliaryMaleNorth AmericaRisk FactorsSeverity of Illness Index

Identifiers

PMID30247160
PMCPMC6637020
OpenAlexW2893787117

What OpenQuestion holds

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LicenceTDM
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.