ULTRASOUND TREATMENT AS INTERVENTION IN INTRAUTERINE HYPERPARATHYROIDISM

Abstract

Hypocalcemia during pregnancy reduced the normal foetal growth, skeletal mineralization and serum calcium concentration. Untreated maternal hyperparathyroidism associated hypocalcemia predisposed the foetal to intrauterine hyperparathyroidism resulting in adverse effect to skeletal mineralization. In vivo study has discovered that prenatal ultrasound exposure has the ability to reduce the foetal PTH level. Ten-month-old nulliparous New Zealand White (NZW) does were assigned  to three different groups; Control (C), healthy NZW does and free from ultrasound exposure; hypoparathyroidism (HyPT), negative control groups having hypocalcemia condition established through external parathyroidectomy surgery and free from  prenatal abdominal ultrasound exposure; treatment (T),  experimental groups  having hypocalcemia condition and receiving prenatal abdominal ultrasound exposure during pregnancy as intervention to hypoparathyroidism. In the treatment group, rabbits were exposed for 30, 60 and 90 minutes to parathyroid ultrasound on the 1st, 2nd and 3^rd gestational stage accordingly. Following birth, foetal serum calcium (SCa), body weight (BW), crown-to-rump length (CRL), total body length (TBL), bi-parietal diameter (BPD) and femur length (FL) of the foetal were measured. Maternal hypocalcemia during pregnancy gave birth to litters with small to gestational age (SGA) and the reduction of  BW, CRL, TBL, BPD, FL and SCa were also noted. Meanwhile, the outcome of ultrasound exposure given during the middle of 2^nd gestational stage resulted in significant increase in progeny mean average BW, CRL, TBL, BPD FL and SCa compared to the HyPT group. Prenatal abdominal ultrasound helps to control the level of foetal parathyroid hormone and while still in the womb limits the postnatal complication.