
Male infertility contributes to approximately half of all cases of couple infertility worldwide, yet its diagnostic cornerstone, conventional semen analysis anchored in World Health Organization (WHO) criteria, suffers from inter-observer variability that can reach 30–40
Emergency contraception (EC) is most effective when used within appropriate biological timing, yet many women make decisions based on perceived or estimated ovulation rather than objectively confirmed ovulation. Evidence directly examining women’s decision-making after ovulation remains limited. To synthesize evidence on women’s fertility awareness, understanding of ovulation timing, mechanisms and timing of EC methods, and the social and healthcare factors influencing decisions about EC when intercourse is perceived or estimated to have occurred around or after ovulation. A structured narrative review was conducted using PubMed, PubMed Central, Europe PMC, Scopus, and Embase, supplemented by major reproductive-health journals, World Health Organization guidance, professional society resources, and the International Consortium for Emergency Contraception literature database. Evidence published through February 2026 was identified using predefined eligibility criteria and synthesized thematically. Sources were interpreted according to whether ovulation was biologically confirmed, clinically estimated, or participant-perceived/app-predicted. Formal risk-of-bias assessment and statistical pooling were not performed. Clinical evidence indicates that levonorgestrel and ulipristal acetate primarily prevent pregnancy before ovulation, whereas the copper intrauterine device remains the best-established intrauterine EC option when ovulation may have occurred. The 52-mg levonorgestrel-releasing intrauterine device is supported by randomized evidence within the studied insertion window. Across diverse populations, fertility awareness was frequently limited, with many women inaccurately identifying the fertile window or relying on calendar calculations and mobile applications. Knowledge gaps, stigma, partner influence, healthcare access, and counseling quality further shaped EC-related decisions. EC decisions around perceived or estimated ovulation reflect biological timing, fertility awareness, pregnancy-risk perception, and access-related factors. Direct evidence on decision-making after objectively confirmed ovulation remains limited, highlighting the need for improved counseling and research integrating objective ovulation assessment with women’s actual EC decisions.
Abstract In May 2026, a global consensus of 56 academic, clinical, and patient organisations formally renamed Polycystic Ovary Syndrome (PCOS) to Polyendocrine Metabolic Ovarian Syndrome (PMOS), following a 14-year international process and more than 14,000 survey responses (1). This narrative review examines the rationale for renaming, the consensus process, and the diagnostic, clinical, therapeutic, and implementation implications for Indian reproductive medicine. PMOS is used throughout this review to refer to the current nomenclature; PCOS is reserved for historical terms, original diagnostic criteria, and quoted nomenclature. PubMed/MEDLINE, Scopus, and Embase were searched for literature on PCOS/PMOS nomenclature, epidemiology, diagnosis, phenotyping, management, mental health, and Indian/South Asian clinical characteristics. A narrative rather than systematic review was chosen given the recency of the nomenclature change and the aim of providing a broad, contextual clinical overview; PRISMA-based study selection and meta-analysis were not performed. Contemporary Indian/South Asian literature from 2015 to 2026 was prioritised, while foundational studies were included without date restriction. The 2023 International Evidence-based Guideline and the 2026 nomenclature consensus were used as primary normative sources. Globally, PMOS affects an estimated 6 to 21% of women of reproductive age depending on diagnostic criteria and population studied (2). The nationwide Indian study by Ganie et al. reported a weighted prevalence of 19.6% by Rotterdam criteria, with phenotype C predominating at 40.8% (3). The PMOS transition may improve recognition of the disorder’s systemic metabolic and psychological dimensions, but it should not be used to justify testing or treatment beyond current evidence. We distinguish guideline-supported care from emerging or experimental approaches and discuss Indian-specific feasibility, affordability, and evidence gaps.
CAH (Congenital Adrenal Hyperplasia) is a group of hereditary disorders of steroidogenesis, most commonly caused by 21-hydroxylase deficiency. The disease leads to abnormal cortisol and/or aldosterone synthesis, as well as excessive androgen production. The clinical manifestations are varied and depend on the type and severity of the enzyme deficiency. An impairment of the adrenal cortex hormone biosynthesis pathway underlies CAH. The enzyme deficiency causes an increase in ACTH (Adrenocorticotropic Hormone) level, leading to compensatory adrenal hypertrophy and overproduction of androgen precursors. This results in masculinisation of the genitalia in girls, precocious virilisation in boys and water and electrolyte disturbances. Endocrine disorders and steroid treatment may exert an adverse effect on the fertility of CAH patients. Impaired ovulation is observed in women and reduced quality of semen in men, often due to the presence of TARTs (Testicular Adrenal Rest Tumours). However, with appropriately managed treatment, it is possible to preserve or restore reproductive function. Substitution of glucocorticoids (hydrocortisone) and mineralocorticoids remains the mainstay of treatment. Prenatal treatment with dexamethasone remains controversial and is only available under certain conditions. New therapeutic directions includes continuous subcutaneous infusion of hydrocortisone, modifies-release preparations of hydrocortisone, selective ACTH receptor modulators, androgen synthesis inhibitors (e.g. abiraterone), gene therapies and drugs modifying the activity of steroidogenesis enzymes.