CORD PLASMA ERYTHROPOIETIN IN RELATION TO FETAL GROWTH RETARDATION

Abstract

From the first trimester the fetus can produce erythropoietin (EP). The only known stimulus for EP is hypoxia. Cord EP is elevated in pregnancies complicated by preeclampsia. Our aim was to assess if cord plasma EP is increased in fetal growth retardation (IUGR, <-2SD) of unknown cause (no maternal or fetal etiologic risk factor), or if it is a specific feature associated with preeclampsia. We measured cord plasma EP by RIA in 74 infants bom after preeclampsia of pregnancy, (geometric mean; range 98; 18-7900 mU/l, p<0.001 compared with controls), in 23 singleton infants with IUGR (56;12-805, NS), in 13 pairs of twins (33; 11-185, NS), and in 57 (20 preterm and 37 term) control infants (40; 13-486). EP did not correlate with gestational age in control infants, nor in any other study group. EP correlated weakly with the SD score of the birth weight (r=-0.284, p=0.014) in the preeclampsia group, but not in IUGR. The EP levels were similar in first and second born twin, no difference was seen in discordant twins. EP correlated with umbilical arterial pH in preeclampsia group (r=-0.31, p=0.007), but not in IUGR or twin group. We conclude that cord EP level is unrelated to gestational age, its correlation in preeclampsia with the degree of growth retardation suggests a relationship between this and hypoxia. However, EP is unrelated to the severity of IUGR of unknown cause, suggesting that most of these cases are unrelated to lack of oxygen.