Journal of Obstetrics and Gynaecology Research最新文献

In Japan, approximately 20% of women in their twenties are underweight (BMI < 18.5 kg/m²), representing one of the highest prevalences among developed nations. Underweight and undernutrition are associated with decreased bone mass, menstrual abnormalities, impaired glucose tolerance, sarcopenia-like changes, and systemic symptoms including depression and fatigue, significantly impacting health from young adulthood through the life course. This situation is influenced by complex factors including the societal internalization of thinness ideals, social media and mass media influences, the off-label use of GLP-1 receptor agonists, and socioeconomic factors such as poverty. However, while current healthcare and screening systems have advanced in addressing obesity, systematic approaches to underweight remain inadequately developed. Based on discussions by an expert working group established by the Japan Society for the Study of Obesity in collaboration with multiple related academic societies, this paper proposes a novel disease concept: Female Underweight/Undernutrition Syndrome (FUS). FUS encompasses the diverse physical and psychological health disorders arising from underweight or undernutrition, aiming to establish clear diagnostic criteria and frameworks for early detection and preventive intervention. Comprehensive measures are required, including stigma prevention, collaboration with educational and industrial sectors, integration into health screening systems, and addressing underlying social determinants. Through the proposal of FUS, we anticipate progress toward comprehensive interventions addressing the societal challenges surrounding women's health and body image.

Pregnancy complicated by severe osteogenesis imperfecta (OI) is rare, and chronic abruption-oligohydramnios sequence (CAOS) is an uncommon obstetric disorder characterized by persistent bleeding and oligohydramnios without membrane rupture. To our knowledge, this is the first report describing the coexistence of type III OI and CAOS. A 24-year-old woman with OI developed recurrent bleeding early in pregnancy. Genetic testing revealed a novel COL1A1 splice-site variant (c.1876-2A>C). Ultrasonography showed a circumferential subchorionic hematoma and progressive fluid loss, leading to CAOS diagnosis at 19 weeks. Despite amnioinfusion, the amniotic cavity collapsed, and pregnancy was terminated via cesarean section at 20 weeks. Placental pathology showed hemosiderin and fibrin deposition. In this case, both functional and structural factors possibly associated with type I collagen abnormalities may have contributed to CAOS development. Although causality cannot be proven, persistent bleeding in severe OI may warrant greater caution for progression to CAOS.

Placental insufficiency is a central pathological condition underlying fetal growth restriction and is strongly associated with adverse outcomes during the neonatal period. Although epidemiological and clinical studies have consistently linked compromised placental function to neonatal respiratory, neurological, gastrointestinal, and infectious morbidity, the mechanisms through which placental insufficiency translates into organ-specific neonatal vulnerability remain unclear. Increasing evidence from human observations and experimental animal models indicates that placental insufficiency disrupts coordinated fetal development through alterations in perfusion, vascular patterning, cellular differentiation, barrier maturation, and immune responsiveness, rather than through uniform growth failure. This review summarizes current progress in the understanding of organ-specific mechanisms by which placental insufficiency shapes neonatal vulnerability, with a focus on the lung, brain, intestine, and immune system. We further discuss how these developmental perturbations interact with postnatal environmental exposures and highlight future perspectives for identifying at-risk infants and developing targeted strategies to mitigate adverse neonatal outcomes.