Fetal neonatal proinflammatory cytokine response-relation to perinatal brain and lung damage [Fetal ve neonatal proenflamatuar sitokin yaniti - perinatal beyin ve akciger zedelenmesi ile ilişkisi]

Perinatal infections are known to lead to preterm rupture of membranes and preterm labor. The role of proinflammatory cytokines has recently been understood in these pathologies. It has also been suggested that periventricular leucomalacia and intraventricular hemorrhage, both of which are frequently seen in preterm infants, are related to perinatal cytokine response, most prominently to IL-1, IL-6, IL-8 and TNF and fetal inflammmatory response may lead to brain damage and cerebral palsy in preterm infants. Even further spastic cerebral palsy in term infants is shown to be related to cytokine damage, and bacterial lipopolysaccharides sensitize the immature brain to hypoxic-ischemic insult. Lower scores in biophysical profile and depression and clinical asphyxia at birth may be the clinical symptoms of fetal inflammatory response. These patients are shown to have increased neonatal morbidity due to organ damage caused by increased cytokine response. Cytokines are also accused of in utero programming of the immature lung to increased postnatal inflammatory response and bronchopulmonary dysplasia in preterm infants. Prevention of perinatal infection and inflammation has crucial importance not only to prevent preterm delivery but also persistent brain and lung damage