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Analysis reveals the connection between beta hCG and Ki67 biomarkers and placental function in stillbirths, indicating potential diagnostic avenues.
Fetal death rate and Perinatal Mortality rate are important indicators of a country's Health care system. Stillbirth is more common in the third trimester constituting 72.4% cases and peaks at 27-30 weeks of gestation. Placental pathology is more frequently associated with stillbirth with 44.8% -60% 1. Despite advances in prenatal care causes of many still births remain elusive. Accurate assessment of the cause is required for future stillbirth prevention 2,3. Associated placental pathology and dysregulated syncytiotrophoblast (STB) formation disrupts the integrity of the placental exchange surface, reducing the ability of the fetus to compensate for subacute events in late pregnancy, which lead to fetal growth restriction and intrauterine foetal demise 4. Beta hCG and Ki67 are hence studied in context of idiopathic still births to understand how these biomarkers relate to placental function in idiopathic still births and provide new avenues for early diagnosis and prevention. Conclusion: Decreased expression of Beta hCG and Ki67 may be linked to impaired placental development and function and hence contribute to idopathic still births.
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Padmavathy et al. (2025) studied this question.
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