PCOS Linked to Higher Risk for Cardiometabolic Diseases

TOPLINE:

Women with polycystic ovary syndrome (PCOS) face an increased risk for type 2 diabetes (T2D), metabolic dysfunction–associated steatotic liver disease (MASLD), and cardiovascular disease (CVD), although these risks vary depending on PCOS phenotype.

METHODOLOGY:

• PCOS features intrinsic insulin resistance, regardless of body weight, potentially due to increased liver fat deposition, which may exacerbate adverse clinical outcomes.
• To understand the association between PCOS and the risk for cardiometabolic diseases, cancer, and dementia, researchers conducted a prospective study including 1008 women with PCOS and 5017 age- and body mass index–matched control participants without PCOS using data from the UK Biobank.
• Liver, cardiac, and brain health were assessed using multiorgan MRI, and the impact of PCOS phenotypes (hyperandrogenic and normoandrogenic) on disease risk was evaluated.
• The primary outcomes were the prevalence and incidence of metabolic diseases (T2D, MASLD, and obstructive sleep apnea), all-cause CVD and CVD components, hormone-dependent cancers, and dementia.

TAKEAWAY:

• Incidence rates of T2D (adjusted hazard ratio [aHR], 1.47) and all-cause CVD (aHR, 1.76) were higher in women with PCOS than in control participants.
• Compared with control participants, women with PCOS had a higher prevalence of hepatic steatosis (P = .02) and greater hepatic fibroinflammation (P ≤ .01).
• PCOS was significantly associated with the incidence of all-cause CVD in normoandrogenic PCOS (aHR, 1.90) but not in hyperandrogenic PCOS. However, hyperandrogenic PCOS was associated with greater liver fat content and hepatic fibroinflammation than normoandrogenic PCOS (P < .01).
• The incidence of cancer or dementia was not significantly different among women with PCOS and control participants.

IN PRACTICE:

“More careful characterization of PCOS phenotype, specifically addressing clinical and biochemical androgen status, with tailored surveillance based on the phenotype-specific differential risk is needed,” the authors wrote.

SOURCE:

The study was led by Alex E. Henney, MBChB, MRes, Department of Cardiovascular and Metabolic Medicine, University of Liverpool, Liverpool, England. It was published online in The Journal of Clinical Endocrinology & Metabolism.

LIMITATIONS:

Some control participants might have undiagnosed PCOS due to the lack of transvaginal ultrasound imaging data. The study participants were primarily peri- or postmenopausal, and their hormonal profiles may have changed over time, potentially leading to diagnostic misclassification. Residual confounding and reporting bias may have occurred due to the reliance on electronic health records by the UK Biobank.

DISCLOSURES:

No funding sources were disclosed for the study. Some authors reported receiving funding, grants, or honoraria/honoraria for lectures from or having other ties with various pharmaceutical companies and other sources.

This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.