Background &aim
To highlight cortisol deficiency as a rare cause of hyperemesis gravidarum.
Method
Case report and literature review.
Results
A 29-old-woman presented at 8 weeks’ gestation with a 2-week history of nausea/vomiting unresponsive to anti-emetics, following 12 months of fatigue and postural
presyncope. Three days earlier she had commenced thyroxine for primary hypothyroidism (free thyroxine 9.5pmol/L, TSH 12 mIU/L with positive thyroid antibodies). Pulse was 80/min and blood pressure 90/60 mmHg. Serum sodium was119mmol/L, potassium 4.0mmol/L, serum cortisol <50nmol/L, ACTH 339ng/L (5-50), Hb 86g/L (110-140).Hydrocortisone initiated with resolution of nausea and vomiting, thyroxine was withheld. Following fluid resuscitation supine aldosterone was 14pmol/L (30-400*) mass renin 27.9mU/L (2-29*). In retrospect,
she reported increased pigmentation but denied salt craving. 21-hydroxylase antibodies were negative. One-week later TSH was 2.3 mIU/L and Hb 111g/L off thyroxine.
Seven previous case reports describe new diagnosis of cortisol deficiency presenting with hyperemesis gravidarum - five with Addison disease, and 2 ACTH deficiency. 1-7 Five of the seven patients had significant hyponatraemia, and three anaemia. Four of the individuals with Addison disease had hypothyroidism.
Thyroxine therapy may precipitate adrenal crisis in undiagnosed/inadequately replaced cortisol deficiency. 8, 9 TSH elevation and cytopenias may resolve with glucocorticoid therapy in untreated cortisol deficiency. 10-12
Conclusion
Cortisol deficiency warrants exclusion in treatment-refractory hyperemesis gravidarum, associated with hyponatraemia, or with other autoimmune endocrinopathies. Thyroxine therapy should be withheld if there is any suspicion of cortisol deficiency, as treatment may precipitate adrenal crisis, and TSH elevation may be reversible with glucocorticoid therapy alone.