On the back of sheep experiments showing that uterine
hypoxia induces a rapid and sustained elevation of fetal
activin A levels, we undertook two prospective studies to explore whether this novel observation could be exploited clinically. The first was a prospective labour ward study investigating whether umbilical arterial
activin A levels at delivery correlated with either neonatal hypoxic ischaemic
encephalopathy or pH. Unfortunately, we were unable to demonstrate a link with either, but found that levels were significantly depressed among those who had an emergency
Caesarean section, suggesting a possible role in active labour. Second, we investigated the link between
activin A and
intrauterine growth restriction (IUGR), a condition of fetoplacental
hypoxia, by measuring levels in women presenting for antenatal ultrasound biometry with clinical suspicion of a small baby. We found that, compared to pregnancies with a baby that was small for gestational age (SGA) but otherwise healthy, levels were 2.4 and 8 times higher, respectively, in pregnancies complicated by IUGR, and those complicated by both IUGR and
preeclampsia. However, a single blood sample of
activin A was unable to distinguish between IUGR and SGA pregnancies with sufficient sensitivity to be clinically useful. Our studies were unable to demonstrate clinical utility for the experimental observation linking
activin A and
hypoxia.