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Changes in amniotic fluid optical density at 450 millimicron in Rh-sensitized patients after maternal hydrocortisone
In anticipation of elective premature delivery (32 to 34 weeks of gestation), five Rh-sensitized pregnant women were given hydrocortisone succinate for enhancement of fetal lung maturation. Serial amniocenteses were performed and an abrupt drop in the optical density at 450 millimicron (OD450) was observed in all cases immediately after administration of the steroid. Two infants in whom the OD450 remained low were followed safely to term. The others were delivered prematurely. All infants were Rh-sensitized and required one or more exchange transfusions, and all survived. It is tempting to speculate that glucocorticoids alter the antigen-antibody affinity and inhibit splenic macrophage sequestration, thus reducing erythrocyte destruction. Maternal steroid administration may prove to be therapeutic in the management of Rh-sensitization, but until its mechanisms are further delineated, extreme caution must be used in the interpretation of OD450 changes.
In anticipation of elective premature delivery (32 to 34 weeks of gestation), five Rh-sensitized pregnant women were given hydrocortisone succinate for enhancement of fetal lung maturation. Serial amniocenteses were performed and an abrupt drop in the optical density at 450 millimicron (OD450) was observed in all cases immediately after administration of the steroid. Two infants in whom the OD450 remained low were followed safely to term. The others were delivered prematurely. All infants were Rh-sensitized and required one or more exchange transfusions, and all survived. It is tempting to speculate that glucocorticoids alter the antigen-antibody affinity and inhibit splenic macrophage sequestration, thus reducing erythrocyte destruction. Maternal steroid administration may prove to be therapeutic in the management of Rh-sensitization, but until its mechanisms are further delineated, extreme caution must be used in the interpretation of OD450 changes.