A 49 year old lady was investigated for palpitation and weight loss of 12 kg over 6 months. She was diagnosed thyrotoxic (TSH- not detectable; free thyroxine-66.4; normal: 1222 pmol/L and triiodothyronine-8.6; normal: 1.33.1 nmol/L) and commenced on 40 mg of carbimazole. Ultrasound of thyroid showed multinodular goitre. Her systolic BP was low (100/70 mm Hg) and she felt tired. Her morning cortisol was 104 (normal; 220700 nmol/L). A short synacthen test showed a base line cortisol of 76 (low) with levels of 849 and 986 nmol/L at 30 and 60 mins respectively following 250 ug of synacthen injection (normal response). Base line ACTH was 6 ng/ml (normal 555). Gonadotrophins and prolactin were normal. MRI of pituitary was normal. The patient was diagnosed with isolated ACTH deficiency. He was treated with hydrocortisone 20 mg (morning) and 10 mg(evening). Gradually carbimazole was reduced to 15 mg od and hydrocortisone 10 mg (morning) and 5 mg (evening). In 1 year the patient gained 16.7 kg. She underwent radioactive iodine treatment and subsequently required levothyroxine.
A day cortisol profile was normal with morning level 337 nmol/L. Following omission of morning hydrocortisone, a SST undertaken showed cortisol levels of 297 (base line) and 722 and 884 nmol/L 30 and 60 mins respectively after injection. Hydrocortisone dose was reduced and eventually stopped. Seven months later the patients morning cortisol was 734 nmol/L and was biochemically euthyroid while on levothyroxine 150 mcg od and no hydrocortisone.
The initial low base line plasma cortisol with adequate response to short synacthen could be due to reasons that ACTH can over stimulate partially atrophied adrenals and produce a deceivingly adequate cortisol response and also normal adrenal response to synacthen occurs in less than 6 weeks of ACTH deficiency. The patients morning cortisol normalised as she became biochemically euthyroid.