Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 25 P98

Clinical biochemistry

Disappearing adrenal insufficiency

Earn H Gan1, Andy James2 & Simon H S Pearce1,2

1Institute of Human Genetics, Newcastle University, Newcastle upon Tyne, UK; 2Endocrine Unit, Royal Victoria Infirmary, Newcastle upon Tyne, UK.

After adrenal insufficiency is confirmed by synacthen testing, lifelong steroid replacement is expected. We report a case of apparent reversal of adrenal insufficiency. Case details: a 66-year-old man was referred for oral pigmentation, and a random cortisol level of 184 nmol/l. He reported a 2-year history of tiredness, nocturia, dry mouth and reduced libido. There was no dizziness, salt-craving, or weight loss. He denied taking any form of steroid or over-the-counter drugs. Examination showed punctate oral pigmentation and a pigmented patch on his finger, without generalised pigmentation. His blood pressure was 118/72 mmHg with a postural drop of 10 mmHg. He had a raised HbA1c (7.6%) and mild hyponatraemia (134 mmol/l). A 250 μg synacthen test showed a basal cortisol of 288 nmol/l; 30 min at 182 nmol/l and 60 min at 143 nmol/l. Hydrocortisone (20+10 mg daily) was instigated with the diagnosis of probable Addison’s disease. However, his ACTH level came back at 25 ng/l (5–55 ng/l); plasma renin and aldosterone levels were normal. Basal measurements of other anterior pituitary hormones and paired plasma/urine osmolality were normal. Adrenal autoantibody test was negative.

He was well taking hydrocortisone for 6 months but his HbA1c worsened to 10%. The original diagnosis of adrenal failure was re-considered. Serum DHEAS levels were normal, and there were detectable cortisol and aldosterone precursors in the urine. The hydrocortisone dose was weaned and repeat short synacthen testing demonstrated a basal cortisol of 258 nmol/l; peak 672 nmol/l. The diagnosis of adrenal insufficiency was revoked. This case illustrates the need to make a clear aetiological diagnosis of adrenal insufficiency. The abnormal initial synacthen test result could have been due to either unwitting exogenous steroid administration, transient isolated ACTH deficiency or failure to administer the ACTH1–34 during the synacthen test. The normal serum DHEAS and the urine steroid profile were helpful clues to the safety of a staged withdrawal of hydrocortisone.

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