Peer-reviewed article
Narrative Review on Therapies That Influence Inflammatory Responses During Extremely Premature Perinatal Respiratory Transition.
Hallman M ·
Summary
Written by AI, not yet AICS's view · claude-haiku-4-5-20251001This review examines medical treatments that affect inflammation during premature birth and the early breathing transition in extremely premature infants born before 28 weeks. It discusses how inflammatory signals trigger premature delivery and how various therapies including anti-inflammatory agents and glucocorticoids affect outcomes. The review notes that while survival rates have improved, serious complications affecting the lungs, body and brain remain common despite these advances. The authors call for better optimized treatments and continued multidisciplinary research to improve both survival and long-term health for this extremely vulnerable population.
Key points
- Spontaneous extremely premature delivery is induced by inflammatory signals, either from infection (chorioamnionitis) or as a result of premature birth itself triggering lung development
- Non-steroidal anti-inflammatory agents are effective in prolonging pregnancy but are toxic to very premature newborns
- Antenatal glucocorticoids advance fetal lung maturity but glucocorticoid excess interferes with growth and neurodevelopment, requiring optimized dosing
- Despite advances extending survival to 22-24 weeks, acute and chronic pulmonary, somatic and neurosensory diseases have barely decreased
- Inhibitors of inflammatory receptors and augmentation of anti-inflammatory defences show promise in animal studies for preventing inflammation-induced preterm delivery
Limitations
This is a narrative review that synthesizes existing literature rather than presenting original research or systematic evidence synthesis. It does not quantify the evidence base or provide systematic comparison of different therapeutic approaches.
Abstract
Aims and methods Advances in neonatal care have extended borderline survival to 22-24 post-conceptional weeks. Present review discusses approaches for prolonging short pregnancies and prevention of serious morbidities in extremely premature infants born before 28 weeks of pregnancy. Results Spontaneous extremely premature delivery and foetal alveolar differentiation are induced by inflammatory signals. They either coexist in chorioamnionitis or first premature birth triggers functional differentiation of immature pulmonary alveoli. Infections, other acquired or genetic factors predispose to extremely premature births. Non-steroidal anti-inflammatory agents are effective in tocolysis. However, they are toxic to very premature newborns. In recent animal studies, inhibitors of inflammatory receptors or augmentation of deficient intrauterine anti-inflammatory defences have prevented inflammation-induced preterm deliveries. Antenatal glucocorticoid advances foetal maturity, but glucocorticoid excess interferes with growth and neurodevelopment. Optimizing indications and dosage of glucocorticoid is needed. Despite increasing survival, acute and chronic pulmonary, somatic and particularly neurosensory diseases have barely decreased. Practices of ventilation and multiple other therapies need to be refined for this extremely high-risk population. Conclusion Aiming to medical treatments that safely prolong extremely premature pregnancies and promote the management and safety of extremely premature infants would increase the healthy life years. These goals require persistent multidisciplinary research.