Endocrine Abstracts

A 76-year-old lady with a background of Crohn’s disease (ileostomy in 1991) was referred to endocrinology in March 2022. Her 9-am cortisol level was <50 nmol/l, with a sodium of 130 mmol/l. These were done as she reported tiredness, lethargy and dizziness since November 2021. She had also lost 7 lb of weight. No evidence of hyperpigmentation. She had then been empirically started on hydrocortisone (10 mg-morning, 5 mg-afternoon and 5 mg-evening) pending evaluation of her pituitary function. It was initially believed that the chronic use of steroids in the past (for her Crohn’s) may have caused the adrenal insufficiency. Anterior pituitary profile done at 9-am showed a random GH of 0.9 µg/l, IGF-1 of 18.7 nmol/l, TSH of 2.1 mIU/l, FT4 of 8.6 pmol/l, normal prolactin, FSH of 0.3 IU/l, LH <0.3 IU/l, cortisol <50 nmol/l, and ACTH <5 ng/l, with a normal MRI pituitary. Based on these tests, she was labelled as idiopathic hypopituitarism, and the hydrocortisone was continued (the dose subsequently altered to 5 mg TDS following a cortisol day curve). Levothyroxine was added. In the clinic, reconciliation of her medications revealed her to be on codeine since 2003 and loperamide (structurally similar to opioids) since 1998-both prescribed to control her stoma output. Since many years, she had been on 120 mg/day of codeine (equating to a daily dose of 12 mg of morphine), and 16 mg/day of loperamide. She was asymptomatic, with her only issues being stoma-related. ≥16 mg/day of loperamide has been shown to suppress ACTH. Opioids suppress the release of the GnRH and CRH. In the absence of a structural pituitary abnormality, it was postulated that the hypopituitarism was secondary to chronic usage of loperamide, exacerbated by chronic codeine use.