Evidence map›Paper›PMID 40976583›Full record

ArticleThe Journal of clinical endocrinology and metabolism2026

Multiracial Cytokine Profiling Reveals Immune Dysregulation not Chronic Inflammation in Polycystic Ovary Syndrome.

Gabriela Pacheco-Sanchez, Rebecca Herrera, Margareta D Pisarska, Ricardo Azziz, Dequina A Nicholas, Jessica L Chan

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2026. 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
–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

5 citing papers in PubMed.

  1. Back to the Drawing Board: Rethinking Inflammation in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Gabriela Pacheco-SanchezDepartment of Molecular Biology and Biochemistry, School of Biological Sciences, University of California Irvine, Irvine, CA 92697, USA.ORCID 0000-0002-0394-0589
Rebecca HerreraDepartment of Molecular Biology and Biochemistry, School of Biological Sciences, University of California Irvine, Irvine, CA 92697, USA.
Margareta D PisarskaDepartment of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Ricardo AzzizDepartment of Health Policy, Management and Behavior, School of Public Health, University at Albany, State University of New York, Albany, NY 12222, USA.ORCID 0000-0002-3917-0483
Dequina A NicholasDepartment of Molecular Biology and Biochemistry, School of Biological Sciences, University of California Irvine, Irvine, CA 92697, USA.ORCID 0000-0003-4996-2190
Jessica L ChanDepartment of Obstetrics and Gynecology, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.ORCID 0000-0002-9423-6027

Funding

The Role of Energy Balance in Gonadotrope and Reproductive FunctionR00HD098330 · NICHD · UNIVERSITY OF CALIFORNIA-IRVINE · PI NICHOLAS, DEQUINA ANGELINA · 2021 to 2023
$816k
The Role of Energy Balance in Gonadotrope and Reproductive FunctionK99HD098330 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NICHOLAS, DEQUINA ANGELINA · 2019 to 2020
$214k
Diabetes and Digestive and Kidney Diseases U24DK132746NICHD NIH HHS K99 HD098330NICHD NIH HHS R00 HD098330NIH HHSUCLA LIFT-UP
6 · The paper itself

Abstract

contextPolycystic ovary syndrome (PCOS) is a common endocrine disorder often associated with chronic inflammation, but comprehensive characterization of immune markers across diverse patient populations is lacking.

objectiveTo determine whether PCOS exhibits a profile of chronic inflammation or immune dysregulation when analyzed across a diverse patient population.

designRetrospective cross-sectional study of samples collected between 1987 and 2010 as part of the Androgen Excess Biorepository.

settingReproductive endocrinology clinics at the University of Alabama at Birmingham in Birmingham, Alabama, and Cedars-Sinai Medical Center in Los Angeles, California, where women and adolescents presented for evaluation of androgen excess. PATIENTS: Forty premenopausal women (20 with PCOS, 20 controls) aged 18 to 45 years, categorized by race (Black and White) and PCOS diagnosis. Participants were race, age, and body mass index matched.

main outcome measuresFasted follicular phase plasma concentrations of C-reactive protein and 96 circulating immune markers, including interleukin (IL)-6, tumor necrosis factor-α (TNF-α), and IL-18, measured using a Milliplex Luminex xMAP assay.

resultsPCOS patients showed significantly lower levels of circulating immune markers (P < .05). Growth factors (vascular endothelial growth factor A, platelet-derived growth factor), proinflammatory cytokines (IL-8, TNF-α, interferon-γ), and several chemokines were reduced in PCOS patients, independent of race. Only IL-18 and C-X-C motif chemokine ligand 16 showed statistically significant differences between Black and White women.

conclusionThis study challenges the prevailing notion of PCOS as a disorder of chronic low-grade inflammation, suggesting instead that immune suppression and impaired angiogenic signaling may be factors in PCOS pathophysiology, especially in nonobese patients. Further research with larger sample sizes and inclusion of metabolic metrics is needed to confirm these findings before they can be applied in clinical practice.

Indexed as

CytokinesInflammationPolycystic Ovary SyndromeAdolescentAdultBiomarkersChronic DiseaseC-Reactive ProteinCross-Sectional StudiesFemaleHumansMiddle AgedRetrospective StudiesYoung AdultBiomarkersC-Reactive ProteinCytokineschemokinescytokinesgrowth factorsimmune dysregulationinflammationpolycystic ovary syndromerace

Identifiers

PMID40976583
PMCPMC13334484

What Socratic holds

Textmetadata
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 Socratic graph.