Evidence map›Paper›PMID 18220286›Full record

ArticleHepatology (Baltimore, Md.)2008

Low circulating levels of dehydroepiandrosterone in histologically advanced nonalcoholic fatty liver disease.

Michael Charlton, Paul Angulo, Naga Chalasani, Ralph Merriman, Kimberly Viker, Phunchai Charatcharoenwitthaya, Schuyler Sanderson, Samer Gawrieh, Anuradha Krishnan, Keith Lindor

Open access · greenAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 3 pooled it
6.8field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 137 citations in OpenAlex.

  1. Pooled it
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  16. Observational
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  19. Adrenal Insufficiency in Cirrhosis.Journal of the Endocrine Society · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

Michael CharltonDivision of Gastroenterology and Hepatology, Mayo Clinic and Foundation, Rochester, MN 55905, USA.
Paul Angulo
Naga Chalasani
Ralph Merriman
Kimberly Viker
Phunchai Charatcharoenwitthaya
Schuyler Sanderson
Samer Gawrieh
Anuradha Krishnan
Keith Lindor
Mayo Clinic · USIndiana University – Purdue University Indianapolis · USMedical College of Wisconsin · USUniversity of California, San Francisco · US

Funding

ZESTRIL VS. VERAPAMIL IN THE TREATMENT OF HYPERTENSIONM01RR000585 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 1985 to 2006
$30.4M
Pathophysiology and Characterisation of NAFLDR01DK069757 · NIDDK · MAYO CLINIC ROCHESTER · PI CHARLTON, MICHAEL R · 2005 to 2009
$1.5M
NCRR NIH HHS M01 RR000585NCRR NIH HHS RR00585NIDDK NIH HHS R01 DK069757
6 · The paper itself

Abstract

unlabelledThe biological basis of variability in histological progression of nonalcoholic fatty liver disease (NAFLD) is unknown. Dehydroepiandrosterone (DHEA) is the most abundant steroid hormone and has been shown to influence sensitivity to oxidative stress, insulin sensitivity, and expression of peroxisome proliferator-activated receptor alpha and procollagen messenger RNA. Our aim was to determine whether more histologically advanced NAFLD is associated with low circulating levels of DHEA. Serum samples were obtained prospectively at the time of liver biopsy in 439 patients with NAFLD (78 in an initial and 361 in validation cohorts) and in controls with cholestatic liver disease (n = 44). NAFLD was characterized as mild [simple steatosis or nonalcoholic steatohepatitis (NASH) with fibrosis stage 0-2] or advanced (NASH with fibrosis stage 3-4). Serum levels of sulfated DHEA (DHEA-S) were measured by enzyme-linked immunosorbent assay. Patients with advanced NAFLD had lower plasma levels of DHEA-S than patients with mild NAFLD in both the initial (0.25 +/- 0.07 versus 1.1 +/- 0.09 microg/mL, P < 0.001) and validation cohorts (0.47 +/- 0.06 versus 0.99 +/- 0.04 microg/mL, P < 0.001). A "dose effect" of decreasing DHEA-S and incremental fibrosis stage was observed with a mean DHEA-S of 1.03 +/- 0.05, 0.96 +/- 0.07, 0.83 +/- 0.11, 0.66 +/- 0.11, and 0.35 +/- 0.06 microg/mL for fibrosis stages 0, 1, 2, 3, and 4, respectively. All patients in both cohorts in the advanced NAFLD group had low DHEA-S levels, with the majority in the hypoadrenal range. The association between DHEA-S and severity of NAFLD persisted after adjusting for age. A relationship between disease/fibrosis severity and DHEA-S levels was not seen in patients with cholestatic liver diseases.

conclusionMore advanced NAFLD, as indicated by the presence of NASH with advanced fibrosis stage, is strongly associated with low circulating DHEA-S. These data provide novel evidence for relative DHEA-S deficiency in patients with histologically advanced NASH.

Indexed as

AdiponectinAdultBiomarkersBiopsyBlood GlucoseCohort StudiesC-Reactive ProteinDehydroepiandrosteroneDehydroepiandrosterone SulfateFatty LiverFemaleHumansLeptinLiverLiver CirrhosisMaleAdiponectinBiomarkersBlood GlucoseC-Reactive ProteinDehydroepiandrosteroneDehydroepiandrosterone SulfateLeptinResistin

Identifiers

PMID18220286
PMCPMC2906146
OpenAlexW1964974443

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.