Polyendocrine Metabolic Ovarian Syndrome: Pathophysiology, Phenotypic Heterogeneity, and Clinical Implications

Polyendocrine metabolic ovarian syndrome (PMOS), formerly polycystic ovary syndrome (PCOS), is a common and heterogeneous endocrine-metabolic disorder with reproductive, metabolic, dermatological and psychological manifestations. The 2026 global consensus terminology was introduced to address limitations of the former name, which implied pathological ovarian cysts and insufficiently reflected the multisystem nature of the condition. This narrative review synthesizes selected evidence on the epidemiology, diagnostic heterogeneity, pathophysiology, long-term consequences and management of PMOS. Current evidence supports a network model in which neuroendocrine dysregulation, ovarian androgen excess, insulin resistance, adipose tissue dysfunction, inflammation, genetic susceptibility and environmental influences interact to produce variable clinical phenotypes. Diagnostic expression differs across age, adiposity and phenotype, and neither obesity, insulin resistance nor polycystic ovarian morphology is universally present. Clinical consequences extend beyond menstrual dysfunction and infertility to pregnancy complications, dysglycemia, cardiovascular risk factors, endometrial pathology and psychological morbidity. Management should therefore be individualized according to dominant symptoms, reproductive goals and metabolic risk, with lifestyle support, hormonal therapies, metformin, anti-obesity pharmacotherapy and fertility treatment used selectively. Important evidence gaps remain regarding long-term cardiovascular outcomes, endometrial risk, reproductive safety of emerging metabolic therapies and biologically meaningful subtype classification. The PMOS nomenclature provides a broader framework for integrated, phenotype-aware and life-course-oriented care while preserving continuity with the established PCOS evidence base.