Evidence map›Paper›PMID 29659906›Full record

ArticleThe Journal of clinical endocrinology and metabolism2018

Increased Chromogranin A-Positive Hormone-Negative Cells in Chronic Pancreatitis.

Abu Saleh Md Moin, Megan Cory, Jennifer Choi, Allison Ong, Sangeeta Dhawan, Sarah M Dry, Peter C Butler, Robert A Rizza, Alexandra E Butler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.6field-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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
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  9. Review
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  12. Review
  13. Pancreatic Progenitors: There and Back Again.Trends in endocrinology and metabolism: TEM · 2019
    Review
  14. Article
  15. 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

9 authors at 4 institutions in 2 countries.

Abu Saleh Md MoinDiabetes and Metabolism Research Institute, City of Hope, Duarte, California.
Megan CoryLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Jennifer ChoiLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Allison OngLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Sangeeta DhawanDiabetes and Metabolism Research Institute, City of Hope, Duarte, California.
Sarah M DryDepartment of Pathology and Laboratory Medicine, David Geffen School of Medicine at University of California Los Angeles, Los Angeles, California.
Peter C ButlerLarry L. Hillblom Islet Research Center, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California.
Robert A RizzaDivision of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, Rochester, Minnesota.
Alexandra E ButlerAnti Doping Laboratory Qatar, Doha, Qatar.
University of California, Los Angeles · USCity of Hope · USAnti-Doping Laboratory · QAMayo Clinic · US

Funding

Role of IAPP in Islet Dysfunction in DiabetesR01DK059579 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BUTLER, PETER CAWOOD · 2001 to 2019
$7.5M
Capacity and Mechanisms of Beta Cell Regeneration in HumansR01DK077967 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BUTLER, PETER CAWOOD · 2008 to 2016
$2.5M
NIDDK NIH HHS R01 DK059579NIDDK NIH HHS R01 DK077967
6 · The paper itself

Abstract

Context: Chronic pancreatitis (CP) is characterized by inflammation, fibrosis, and a loss of pancreatic acinar cells, which can result in exocrine and eventually endocrine deficiency. Pancreatitis has been reported to induce formation of new endocrine cells (neogenesis) in mice. Our recent data have implicated chromogranin A-positive hormone-negative (CPHN) cells as potential evidence of neogenesis in humans. Objective: We sought to establish if CPHN cells were more abundant in CP in humans. Design, Setting, and Participants: We investigated the frequency and distribution of CPHN cells and the expression of the chemokine C-X-C motif ligand 10 (CXCL10) and its receptor chemokine C-X-C motif receptor 3 in pancreas of nondiabetic subjects with CP. Results: CPHN cell frequency in islets was increased sevenfold in CP [2.1% ± 0.67% vs 0.35% ± 0.09% CPHN cells in islets, CP vs nonpancreatitis (NP), P < 0.01], as were the CPHN cells found as scattered cells in the exocrine areas (17.4 ± 2.9 vs 4.2 ± 0.6, CP vs NP, P < 0.001). Polyhormonal endocrine cells were also increased in CP (2.7 ± 1.2 vs 0.1 ± 0.04, CP vs NP, % of polyhormonal cells of total endocrine cells, P < 0.01), as was expression of CXCL10 in α and β cells. Conclusion: There is increased islet endogenous expression of the inflammation marker CXCL10 in islets in the setting of nondiabetic CP and an increase in polyhormonal (insulin-glucagon expressing) cells. The increase in CPHN cells in CP, often in a lobular distribution, may indicate foci of attempted endocrine cell regeneration.

Indexed as

AgedChemokine CXCL10Chromogranin AFemaleHumansIslets of LangerhansMaleMiddle AgedPancreasPancreatitis, ChronicReceptors, CXCR3Chemokine CXCL10Chromogranin ACXCR3 protein, humanReceptors, CXCR3

Identifiers

PMID29659906
PMCPMC6456995
OpenAlexW2795491923

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.