Evidence map›Paper›PMID 30558178›Full record

ReviewJournal of clinical medicine2018

Do Androgens Modulate the Pathophysiological Pathways of Inflammation? Appraising the Contemporary Evidence.

Abdulmaged Traish, Jose Bolanos, Sunil Nair, Farid Saad, Abraham Morgentaler

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 3 pooled it
10.5field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 3 syntheses or guidelines pooled it, 140 citations in OpenAlex.

  1. Pooled it
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  7. Association ofGenes · 2026
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  20. Sex as a modifier of genetic risk for type 1 diabetes.Diabetes, obesity & metabolism · 2025
    Review

38 more citing papers are in PubMed but not listed here.

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

5 authors at 5 institutions in 3 countries.

Abdulmaged TraishDepartment of Urology, Boston University School of Medicine, Boston, MA 02118, USA. atraish@bu.edu.
Jose BolanosMen's Health Boston, Chestnut Hill, MA 02467, USA. jose@menshealthboston.com.ORCID 0000-0002-2416-5315
Sunil NairDivision of Pulmonary and Critical Care Medicine, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA. ssnair84@gmail.com.
Farid SaadMedical Affairs Andrology, Bayer AG, 13353 Berlin, Germany. farid.saad@bayer.com.
Abraham MorgentalerMen's Health Boston, Beth Israel Deaconess Medical Center, Harvard Medical School, Chestnut Hill, MA 02467, USA. amorgent@yahoo.com.
Beth Israel Deaconess Medical Center · USBoston University · USChestnut Hill College · USGulf Medical University · AENew York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of testosterone in the pathophysiology of inflammation is of critical clinical importance; however, no universal mechanism(s) has been advanced to explain the complex and interwoven pathways of androgens in the attenuation of the inflammatory processes. PubMed and EMBASE searches were performed, including the following key words: "testosterone", "androgens", "inflammatory cytokines", "inflammatory biomarkers" with focus on clinical studies as well as basic scientific studies in human and animal models. Significant benefits of testosterone therapy in ameliorating or attenuating the symptoms of several chronic inflammatory diseases were reported. Because anti⁻tumor necrosis factor therapy is the mainstay for the treatment of moderate-to-severe inflammatory bowel disease; including Crohn's disease and ulcerative colitis, and because testosterone therapy in hypogonadal men with chronic inflammatory conditions reduce tumor necrosis factor-alpha (TNF-α), IL-1β, and IL-6, we suggest that testosterone therapy attenuates the inflammatory process and reduces the burden of disease by mechanisms inhibiting inflammatory cytokine expression and function. Mechanistically, androgens regulate the expression and function of inflammatory cytokines, including TNF-α, IL-1β, IL-6, and CRP (C-reactive protein). Here, we suggest that testosterone regulates multiple and overlapping cellular and molecular pathways involving a host of immune cells and biochemical factors that converge to contribute to attenuation of the inflammatory process.

Indexed as

chronic inflammatory diseasesC-reactive proteininterleukin-1 betainterleukin-6testosteronetumor necrosis factor-alpha

Identifiers

PMID30558178
PMCPMC6306858
OpenAlexW2904342773

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.