INTRAUTERINE GROWTH-RETARDATION - THE ROLE OF INSULIN-LIKE GROWTH-FACTORS IN THE REGULATION OF FETAL GROWTH

Fetal growth retardation and preterm delivery remain the most importan t risk factors contributing to perinatal mortality and morbidity. Furt hermore, as shown in recent follow-up studies, IUGR children often suf fer from retarded somatic and psychomotor development, i.e. poor speec h development, deficient audio-visual perception, poor fine- and coars e-motor skills and abnormal social behaviour, as well as slow growth. The incidence of IUGR ranges from 3-10% in industrial countries, depen ding on definition of the term. Symmetric and asymmetric IUGR can be d ifferentiated by evaluation of etiological factors and the time of ons et of IUGR. Detection of IUGR requires meticulous prenatal care and ob servation, including early determination of gestational age by ultraso und examination, and close monitoring of fetal growth throughout pregn ancy. Doppler ultrasound investigation of the fetal circulation is an important means of monitoring the growth-retarded fetus. There is stil l no screening method for IUGR. Fetal growth in utero is determined by several factors. The question of how it is regulated has been intensi vely researched. It is now well established that insulin-like growth f actors (IGFs) and their binding proteins (IGFBPs) as well as growth ho rmone (GH) and human placental lactogen (HPL) play an important role i n the regulation of fetal growth in utero. IGFs and IGFBPs are detecta ble in fetal, maternal and placental tissues from early pregnancy onwa rds. Levels of IGF-I and IGF-II in the fetal circulation increase duri ng pregnancy, and, at term, levels of IGF-I are directly related to bi rthweight. The main binding proteins for IGFs in the human fetus are I GFBP-1 and IGFBP-2. Fetal levels of circulating ICF-I are reduced in c ases of IUGR, while fetal levels of IGFBP-1 and IGFBP-2 are increased. Maternal levels of IGFBP-1 are elevated in IUGR. Recent studies have attempted to elucidate feedback mechanisms underlying IUGR at the mole cular-biological level. Our long-term aim is to find a way to treat IU GR in utero. In view of the early- and late morbidity of children affe cted by this condition, this remains an urgent task.