Management of panhypopituitarism during pregnancy: A case re
A 30-year-old woman with panhypopituitarism due to aplasia of the anterior pituitary and an ectopic posterior pituitary (EPP) achieved pregnancy after the first attempt at induction of ovulation. On cycle day 2, stimulation with human menopausal gonadotropin (hMG; 150 IU/day) started and lasted 11 days. After this stimulation period, three follicles were observed and human chorionic gonadotropin (hCG; 250 g) was administered to induce ovulation. Preconception counseling and investigations took place in advance of ovulation induction. A vaginal ultrasound scan showed inactive ovaries and a small uterus. Preconception laboratory test results were all within normal ranges. Investigations of the partner revealed no abnormalities.

Immediately upon pregnancy diagnosis, growth hormone, DHEA, and estradiol/dydrogesterone administration were stopped and vaginal progesterone (200 mg, three times a day) was administered throughout the first trimester. During pregnancy, the dose of levothyroxine was gradually increased to 200 g/day based on FT4 levels, which were determined every four to six weeks, thereby maintaining FT4 levels in the upper half of the normal range. The dosage of hydrocortisone and desmopressin remained unaltered. The first and second trimesters were uneventful. During the third trimester, she developed gestational diabetes, which was diagnosed using the one-step 75 g oral glucose tolerance test. She had normal fasting plasma glucose but abnormal plasma glucose after two hours. However, no pharmacological intervention was required. An adrenal crisis at 31 weeks of gestation was successfully treated with 30 mg hydrocortisone.

At 38 weeks of gestation, she was physically exhausted and therefore admitted for induction of labor. Intracervical insertion of a Foley catheter and misoprostol for cervical ripening resulted in no more than 3 cm of cervical dilatation. A cesarean section was performed on maternal request. During the cesarean section, a steroid replacement protocol was followed (two intravenous boluses of 50 mg and 100 mg hydrocortisone respectively, followed by a continuous infusion of 200 mg hydrocortisone over 24 hours). The procedure was complicated by a hemorrhage of 1000 ml caused by a surgical uterine bleed. In order to prevent further hemorrhage, an intravenous bolus of 5 IU oxytocin and a continuous infusion of 10 IU oxytocin over four hours were administered.

A boy weighing 3515 g was delivered in good condition. One day after the cesarean section, the continuous infusion of hydrocortisone was lowered to 100 mg over 24 hours. Thereafter, the continuous infusion of hydrocortisone was switched to oral administration (30 mg, three times a day) and the dosage was gradually lowered to 20 mg/day. Directly after the cesarean section, the dose of levothyroxine was lowered to 175 mg/day and the pre-pregnancy dosages of DHEA and growth hormone were restarted. Three days postpartum she experienced engorgement, but lactation was not initiated. She and her son were discharged from the hospital five days postpartum. The puerperium showed no abnormalities for either mother or child.