Abstract
Postnatal exposure to ST has been associated with HCM in the newborn, in a dose-related fashion. Such an effect has not been described in infants born to mothers who received antenatal ST. We report three newborns delivered whose mothers received Betamethasone (Be) prenatally for prevention of hyaline membrane disease and who developed various degrees of HCM. Infant A, gestational age (GA) 36 weeks (wks) and birth weight (BW) 3640 grams (gms); infant B, GA 29 wks, BW 1400 gms, and infant C, GA 34 wks., BW 1870 gms. Maternal intake of Be was 12 mg per dose twice weekly for a total of 16 doses for infant A, 8 and 5 doses for infants B and C respectively. There was no maternal evidence of diabetes except in infant A whose mother had a normal fasting blood sugar and glucose tolerance test (GTT) at 23 weeks but developed an abnormal GTT after 8 weeks of Be with a normal HbA 1C level. There was no family history of HCM, no history of maternal intake of medications and no significant hypertension in all three newborns. Echocardiography (echo) in these infants was done because of cardiac murmurs noted on physical exam. It revealed significant increase as compared to controls in: left ventricular free wall thickness in end-systole and end-diastole and systolic (S) and diastolic (D) interventricular septal thickness for all infants. There was significant decrease in S and D LV dimensions in the 3 newborns as compared to norms. These HCM changes were most prominent in infant A and more prominent in infant B than in infant C. There was characteristic echo appearance of mild LV and RV intracavitory obstruction (IO) in infant A and mild RV IO in infant B, and none in infant C. Follow up echo revealed complete resolution of the HCM changes in infant A five months later, and decrease from moderate-severe to mild in infant B three months later. No IO was noted on follow up in both infants A and B. All infants had a benign outcome.Conclusion : We report 3 newborns with transient HCM with antenatal maternal Be intake. We suggest that antenatal maternal ST intake may cause changes of HCM in the newborn. These changes appear to be dose-related and are mostly reversible. A prospective controlled study to evaluate these observations is warranted.
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