Hypertension is one of the most serious side effects of glucocorticoid therapy. We retrospectively investigated the frequency of hypertension during treatment of adrenal crisis and analyzed the factors associated with its development. Patients who were admitted for primary hypoadrenalism due to diagnosed or suspected adrenal crisis were included. In the analysis, the subjects were divided into two groups: the hypertensive group (group H) and non-hypertensive group (group Non-H). The primary endpoint was the difference in the hourly therapeutic hydrocortisone (HDC) dosage between the two groups. The hourly therapeutic HDC dose in the two groups was defined as the hourly HDC dose from the start of HDC infusion until the development of hypertension in group H or until the last blood pressure measurement in group Non-H. Nine of 19 crises led to hypertension. There was no significant difference in the therapeutic HDC dosage between the groups (p = 0.108). In conclusion, hypertension developed in some patients during treatment for adrenal crisis. There was no significant difference in the therapeutic HDC dosage between groups H and Non-H.

Glucocorticoid (GC)-induced diabetes mellitus (DM) is theoretically unlikely to occur in patients with adrenal insufficiency if adequate physiological replacement doses of GC are given. Herein we report a patient with holoprosencephaly who developed GC-induced DM due to frequent and prolonged administration of high-dose GC for suspected adrenal crisis (AC). GC treatment should be started whenever AC cannot be ruled out. However, the initial and subsequent doses should be adjusted to the severity of AC and to the pace of clinical recovery with treatment, respectively.

A 35-year-old primiparous woman was diagnosed with Turner syndrome at the age of 12 yr due to short stature. Her karyotype showed a mosaic pattern [45, X(19)/46, XX(11)]. She had been followed up by the pediatric service. GH was not prescribed because, although she was of relatively short stature, her growth trajectory was reasonable. She was started on estrogen replacement therapy at 15 yr of age and switched to Kaufmann therapy after 1 yr. After transitioning her care to the gynecology service at 20 yr of age, she was screened for complications and Kaufmann therapy was continued. No abnormalities were detected in the pre-pregnancy screening. She conceived by in vitro fertilization and embryo transplantation with oocyte donation. No severe complications occurred during gestation, and she gave birth to a female neonate vaginally at 41 wk and 6 d of gestation. The neonate’s birthweight was 3166 g, and her Apgar scores were 8 and 9 at 1 and 5 min, respectively. No severe complications occurred during the postpartum period. Comprehensive medical treatment and appropriate transition from pediatric to adult services may improve the pregnancy outcomes of women with Turner syndrome.