Some of the steroids in the mother's bloodstream are transferred to the baby. Occasionally this can be sufficient to switch off the baby's own production of steroids. The baby's steroid production will return, but rarely the baby may require steroid treatment until this happens. It is important to look out for signs of steroid deficiency in the baby in the first 2-3 days of life, which includes measurements of blood sugar and blood pressure. It is therefore important that the baby stays in the hospital for monitoring for 2-3 days after birth.
■ EFFECTS OF MATERNAL STEROID t
There are very few data available on the effects of maternal steroid therapy r i in humans. In animals maternal steroid therapy increases fetal resorp- a.*
d tion, decreases fetal size and viability, and increases the incidence of cleft ^
palate. In humans, a review (in 1960) of 272 pregnancies reported 1 abor- S
tion, 8 stillbirths, 15 premature deliveries, 4 cleft palates (on steroids before t the 14th week), and 1 neonatal adrenocortical failure of 3 days duration. §
A separate small study of six neonates exposed to prolonged maternal prednisolone, compared with eight neonates who were not, showed no difference in basal or adrenocorticotrophin hormone (ACTH) stimulated cortisol levels.
Although pregnancy is rare in maternal Cushing's syndrome due to ovu-latory disturbance, it does occur, with adrenal adenoma being more common than pituitary-dependent adrenal hyperplasia. ACTH-independent, pregnancy-induced Cushing's syndrome has also been described. A review of 65 pregnancies in 58 patients with Cushing's syndrome reported maternal pregnancy complications of hypertension (64.5%), pre-eclampsia (9.3%), glucose intolerance (32.3%), congestive cardiac failure (10.8%), and 3 deaths (7.7%). There were 2 miscarriages, 5 stillbirths, 5 neonatal deaths, and 42 preterm deliveries (20-28 weeks); 17 out of 65 had a birth weight < 10th cen-tile, but data were not available for all the cases. This series also reported two cases of Addisonian crisis in neonates soon after birth, decreased fetal adrenal size in a stillbirth at 32 weeks (narrowing and cystic degeneration of the fetal zone), and 1 cleft palate. Pregnancy-dependent Cushing's syndrome has also been reported to cause neonatal adrenal insufficiency.
Antenatal steroids used in the management of preterm labour cause transient suppression of fetal heart rate variability, and fetal biophysical activity. Repeated courses reduce birth weight and head circumference. In mice, repeated courses reduced lung growth. Permanent changes in the hippocampus have been reported in primates, and increased blood pressure and reduced glucose tolerance in rodent offspring. In humans, lower cord blood cortisol levels have been reported after antenatal steroids and lower plasma cortisol at 2 h of age, however no difference in baseline (days 2, 4, 6) or ACTH-stimulated cortisol levels, or difference in blood cortisol level days 1 and 3, or difference in ACTH or cortisol response to corticotrophin-releasing hormone (CRH) on days 7 and 14. Reduced pulse amplitude in cortisol secretion on the first day of life has been demonstrated in infants exposed to antenatal steroids, but no differenCe in number or duration of Cortisol t r seCretory bursts. In summary, antenatal steroids given for preterm labour l s do Cause subtle Changes in CirCulating Cortisol, although these are probably
5 not of CliniCal signifiCanCe.
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The first trimester is very important for the mother and the baby. For most women it is common to find out about their pregnancy after they have missed their menstrual cycle. Since, not all women note their menstrual cycle and dates of intercourse, it may cause slight confusion about the exact date of conception. That is why most women find out that they are pregnant only after one month of pregnancy.