Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (628 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A condition caused by the excessive secretion of androgens from the adrenal cortex; the ovaries; or the testes. The clinical significance in males is negligible. In women, the common manifestations are hirsutism and virilism as seen in patients with polycystic ovary syndrome and adrenocortical hyperfunction.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Where it fits in the MeSH classification
- Broader topics
- 46, XX Disorders of Sex Development; Adrenogenital Syndrome
- See also
- Hirsutism; Virilism
Related concepts
- Androgens
- Adrenal Cortex
- Ovary
- Testis
- Hirsutism
- Virilism
- Polycystic Ovary Syndrome
- Adrenocortical Hyperfunction
Research landscape
PubMed indexes 2,787 records tagged with the MeSH heading “Hyperandrogenism” (counts retrieved 2026-10-29). 775 of them (27.8%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 1,021 records.
Reviews account for 757 records (27.2%) and meta-analyses for 46. Randomized controlled trials number 106 (3.8%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 328 |
| 2000-2009 | 663 |
| 2010-2019 | 1,021 |
| 2020 onward | 775 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 757 | 27.2% |
| Meta-analyses | 46 | 1.7% |
| Randomized controlled trials | 106 | 3.8% |
Method: PubMed query "Hyperandrogenism"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in rare and inherited diseases
Rare conditions are difficult to study: few patients means small studies, case reports and registries are common, and randomized trials are the exception. Small samples limit precision and can exaggerate effects, and cases reported in the literature may be the most severe or unusual. Evidence from many small studies is best read together. Check how patients were identified, how many were included and how long they were followed.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Insulin resistance in polycystic ovary syndrome across various tissues: an updated review of pathogenesis, evaluation, and treatment [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic ovulation dysfunction and overabundance of androgens; it affects 6-20% of women of reproductive age.
- Closing excerpt
- In addition, the review provides a comprehensive overview of the current progress in the efficacy of insulin sensitization therapy in the management of PCOS, providing the latest evidence for the clinical treatment of women with PCOS and IR.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (152 words)
Polycystic ovary syndrome (PCOS) is a common endocrine disorder characterized by chronic ovulation dysfunction and overabundance of androgens; it affects 6-20% of women of reproductive age. PCOS involves various pathophysiological factors, and affected women usually have significant insulin resistance (IR), which is a major cause of PCOS. IR and compensatory hyperinsulinaemia have differing pathogeneses in various tissues, and IR varies among different PCOS phenotypes. Genetic and epigenetic changes, hyperandrogenaemia, and obesity aggravate IR. Insulin sensitization drugs are a new treatment modality for PCOS. We searched PubMed, Google Scholar, Elsevier, and UpToDate databases in this review, and focused on the pathogenesis of IR in women with PCOS and the pathophysiology of IR in various tissues. In addition, the review provides a comprehensive overview of the current progress in the efficacy of insulin sensitization therapy in the management of PCOS, providing the latest evidence for the clinical treatment of women with PCOS and IR.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36631836 · DOI · PMC9832677
11-Oxygenated C19 Steroids Are the Predominant Androgens in Polycystic Ovary Syndrome [2]
Abstract reading summary — source excerpts
- Opening excerpt
- ContextAndrogen excess is a defining feature of polycystic ovary syndrome (PCOS), but the exact origin of hyperandrogenemia remains a matter of debate.
- Closing excerpt
- ResultsAs expected, serum concentrations of the classic androgens testosterone (P ConclusionsWe show that 11-oxygenated androgens represent the majority of circulating androgens in women with PCOS, with close correlation to markers of metabolic risk.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (141 words)
ContextAndrogen excess is a defining feature of polycystic ovary syndrome (PCOS), but the exact origin of hyperandrogenemia remains a matter of debate. Recent studies have highlighted the importance of the 11-oxygenated C19 steroid pathway to androgen metabolism in humans. In this study, we analyzed the contribution of 11-oxygenated androgens to androgen excess in women with PCOS.MethodsOne hundred fourteen women with PCOS and 49 healthy control subjects underwent measurement of serum androgens by liquid chromatography-tandem mass spectrometry. Twenty-four-hour urinary androgen excretion was analyzed by gas chromatography-mass spectrometry. Fasting plasma insulin and glucose were measured for homeostatic model assessment of insulin resistance. Baseline demographic data, including body mass index, were recorded.ResultsAs expected, serum concentrations of the classic androgens testosterone (P ConclusionsWe show that 11-oxygenated androgens represent the majority of circulating androgens in women with PCOS, with close correlation to markers of metabolic risk.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 27901631 · DOI · PMC5460696
Controversies in the Pathogenesis, Diagnosis and Treatment of PCOS: Focus on Insulin Resistance, Inflammation, and Hyperandrogenism [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Polycystic ovary syndrome (PCOS) is a heterogeneous and extremely common disease with symptoms that vary with the age of the patient, typically characterized by hyperandrogenism, chronic oligo-anovulation, and/or several metabolic disorders.
- Closing excerpt
- We also evaluated the advantages and disadvantages of contraceptive therapy and antiandrogens.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (144 words)
Polycystic ovary syndrome (PCOS) is a heterogeneous and extremely common disease with symptoms that vary with the age of the patient, typically characterized by hyperandrogenism, chronic oligo-anovulation, and/or several metabolic disorders. The syndrome includes various phenotypes, and the pathogenesis is multifactorial, often involving insulin resistance. This feature is closely related to ovarian dysfunction, inflammation, hyperandrogenism, and metabolic disorders, which characterize and complicate the syndrome. Therapy currently considers both lifestyle improvements and medications, and must be tailored on a case-by-case basis. To date, the published studies have not arrived at a definition of the most suitable therapy for each individual case and many of the drugs used are still off-label. In this review, we discuss some controversial diagnostic and therapeutic aspects of PCOS, such as the role of insulin resistance, inflammation, and hyperandrogenism. We also evaluated the advantages and disadvantages of contraceptive therapy and antiandrogens.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 35456928 · DOI · PMC9030414
Hyperandrogenemia Induces Trophoblast Ferroptosis and Early Pregnancy Loss in Patients With PCOS via CMA-Dependent FTH1 Degradation [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Polycystic ovary syndrome (PCOS) patients with hyperandrogenemia exhibit an increased risk of early pregnancy loss; however, the underlying mechanisms remain poorly understood.
- Closing excerpt
- These findings reveal androgen-induced ferroptosis as a key mechanism in placental dysfunction and highlight a potential application of metformin for treatment of early pregnancy loss associated with PCOS.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (191 words)
Polycystic ovary syndrome (PCOS) patients with hyperandrogenemia exhibit an increased risk of early pregnancy loss; however, the underlying mechanisms remain poorly understood. Ferroptosis, an iron-dependent form of cell death driven by phospholipid peroxidation, has been implicated in various diseases. This study identifies significant iron homeostasis disorders and ferroptosis in PCOS patients with hyperandrogenemia, which is mediated by androgen-induced reduction of ferritin heavy chain 1 (FTH1) protein levels in trophoblasts. Specifically, androgens upregulate FTH1 mRNA and protein synthesis by binding to androgen response elements on the FTH1 promoter via the androgen receptor (AR). Simultaneously, elevated androgen levels enhance chaperone-mediated autophagy (CMA) through upregulating LAMP2A (lysosomal-associated membrane protein 2), thereby promoting FTH1 protein degradation. When androgen levels are excessive or AR is overactivated, this CMA-driven degradation exceeds FTH1 protein synthesis, leading to a reduction in FTH1 level. Furthermore, metformin was found to compete with androgens for AR binding, thereby stabilizing FTH1 and protecting trophoblasts from ferroptosis. In PCOS-model mice, metformin significantly reduced early embryonic absorption. These findings reveal androgen-induced ferroptosis as a key mechanism in placental dysfunction and highlight a potential application of metformin for treatment of early pregnancy loss associated with PCOS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41400098 · DOI · PMC12948281
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report [5]
- Research article The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited [6]
- Research article Polycystic ovary syndrome [7]
- Research article Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies [8]
- Research article Polycystic ovarian syndrome: Correlation between hyperandrogenism, insulin resistance and obesity [9]
- Research article Polycystic ovary syndrome [10]
References
- Zhao H, Zhang J, Cheng X, Nie X, He B. Insulin resistance in polycystic ovary syndrome across various tissues: an updated review of pathogenesis, evaluation, and treatment. . 2023. PMID 36631836 · DOI · PMC9832677
- O'Reilly MW, Kempegowda P, Jenkinson C, Taylor AE, Quanson JL, Storbeck KH, et al.. 11-Oxygenated C19 Steroids Are the Predominant Androgens in Polycystic Ovary Syndrome. . 2017. PMID 27901631 · DOI · PMC5460696
- Armanini D, Boscaro M, Bordin L, Sabbadin C. Controversies in the Pathogenesis, Diagnosis and Treatment of PCOS: Focus on Insulin Resistance, Inflammation, and Hyperandrogenism. . 2022. PMID 35456928 · DOI · PMC9030414
- Zhou H, Yang W, Liu N, Liu Q, Jin J, Zhao C, et al.. Hyperandrogenemia Induces Trophoblast Ferroptosis and Early Pregnancy Loss in Patients With PCOS via CMA-Dependent FTH1 Degradation. . 2026. PMID 41400098 · DOI · PMC12948281
- Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, et al.. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril. 2009. PMID 18950759 · DOI
- Rosenfield RL, Ehrmann DA. The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited. Endocr Rev. 2016. PMID 27459230 · DOI · PMC5045492
- Joham AE, Norman RJ, Stener-Victorin E, Legro RS, Franks S, Moran LJ, et al.. Polycystic ovary syndrome. Lancet Diabetes Endocrinol. 2022. PMID 35934017 · DOI
- Sanchez-Garrido MA, Tena-Sempere M. Metabolic dysfunction in polycystic ovary syndrome: Pathogenic role of androgen excess and potential therapeutic strategies. Mol Metab. 2020. PMID 32244180 · DOI · PMC7115104
- Zeng X, Xie YJ, Liu YT, Long SL, Mo ZC. Polycystic ovarian syndrome: Correlation between hyperandrogenism, insulin resistance and obesity. Clin Chim Acta. 2020. PMID 31733195 · DOI
- Stener-Victorin E, Teede H, Norman RJ, Legro R, Goodarzi MO, Dokras A, et al.. Polycystic ovary syndrome. Nat Rev Dis Primers. 2024. PMID 38637590 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.