ArticleFrontiers in endocrinology2026
Thyroid autoimmunity does not delineate a cardiometabolic or androgenic phenotype in women with polycystic ovary syndrome: a pre-specified cross-sectional analysis.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Thyroid autoimmunity (TAI) is frequently reported in women with polycystic ovary syndrome (PCOS), yet its clinical relevance for cardiometabolic and androgenic severity remains uncertain. We evaluated whether TAI identifies a metabolically or androgenically more severe PCOS phenotype using pre-specified exposure definitions and cardiometabolic endpoints. Methods: This cross-sectional study included 1,300 women with confirmed PCOS in the source dataset. Thyroid autoimmunity was defined Results: TAI_A was not significantly associated with the primary endpoint (TG/HDL >3.5) (OR 0.77, 95% CI 0.21-1.67). No significant associations were observed for secondary endpoints including non-HDL-C ≥130 mg/dL (OR 1.09, 95% CI 0.61-1.76) or impaired glucose tolerance on OGTT (OR 1.27, 95% CI 0.63-2.18). Results remained directionally consistent across alternative TAI definitions and sensitivity analyzes, including restriction to euthyroid women and trimming of extreme values. In exploratory analyzes, thyroid-stimulating hormone levels differed between TAI-positive and TAI-negative women, while no androgenic or cardiometabolic parameters remained significant after false discovery rate correction. Model diagnostics did not indicate major violations of model assumptions. Conclusion: In this large cross-sectional cohort of women with PCOS, thyroid autoimmunity was not associated with an adverse cardiometabolic or androgenic phenotype. Anti-TPO positivity alone therefore does not appear to identify a metabolically high-risk PCOS subgroup under the studied conditions. Prospective studies are needed to clarify the longitudinal implications of thyroid autoimmunity in PCOS.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.