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Published on: March 5, 2022
Polyendocrine Metabolic Ovarian Syndrome (PMOS; Formerly Polycystic Ovary Syndrome/PCOS) and Susceptibility to
Ali Samareh1,2,3, Mohammad Samare-Najaf4, Mehrangiz Ghafari5
1Student Research Committee, Afzalipour Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.
Abstract:
Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a common endocrine-metabolic disorder characterized by hyperandrogenism, insulin resistance, ovulatory dysfunction, and chronic low-grade inflammation. Recent studies suggest that PMOS may also be associated with altered immune regulation and changes in the gut and vaginal microbiomes. This review summarizes current evidence on the possible relationship between PMOS and susceptibility to microbial infections, with emphasis on mechanisms, clinical management, and reproductive consequences. A narrative review of mechanistic, clinical, epidemiological, and microbiome studies was conducted to evaluate how PMOS-related endocrine, metabolic, inflammatory, and microbial changes may influence infection risk and reproductive outcomes. Available evidence suggests that women with PMOS may be more vulnerable to selected infection-related conditions, especially vaginal dysbiosis, bacterial vaginosis, and vulvovaginal candidiasis. Proposed mechanisms include insulin resistance, hyperandrogenism, chronic inflammation, altered immune cell activity, impaired mucosal defense, and reduced Lactobacillus dominance. Evidence for urinary tract infections, systemic bacterial infections, and viral infections is less consistent and is often affected by confounding factors such as obesity and metabolic disease. PMOS may involve altered immune and microbiome regulation rather than generalized immunosuppression. Clinical care should focus on established PMOS management, metabolic optimization, risk-based infection evaluation, and treatment of confirmed infections. Microbiome-targeted therapies remain investigational until supported by stronger PMOS-specific evidence.
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