Endocrine Abstracts

A 36-year-old man was referred to the neurologists for leg weakness and pain, fatigue and lethargy for 2 years. Sarcoidosis was diagnosed 6 years previously, on the basis of uveitis, lower motor neurone facial palsy, hilar lymphadenopathy and transbronchial biopsy. Prednisolone had been discontinued 3 years prior to his current presentation.

His blood pressure was 99/71. Examination was otherwise unremarkable. His ACE was 109 U/l (10–70). His TSH was 1.29 mU/l., with a free T4 of 5.9 pmol/l. Cortisol was 56 nmol/l. Prolactin was 818 mU/l (75–375 mU/l). LH and FSH were undetectable. Testosterone was very low at 0.3 nmol/l. GH was 0.5 U/l. IGF-1 was 9 nmol/l (13–64). Other bloods, and an LP were unremarkable. MRI of brain and spine showed thickening and contrast enhancement around the pituitary infundibulum and hypothalamus.

Peak cortisol on SST was 450 nmol/l. He was commenced on hydrocortisone 10 mg, 5 mg, 5 mg, and thyroxine 50 mcg. He was given 1 g methylprednisolone daily for 3 days. He complained of polyuria and polydipsia. His serum osmolality was 302 mOsmol/kg. Concurrent urinary osmolality was 119 mOsmol/kg. A formal water deprivation test was performed.

The patient complained of symptoms of thirst during the test. His urine osmolality failed to concentrate to 700 mOsmol/l. Urine concentrated to 595 mOsmol/l after DDAVP. The test supported a diagnosis of partial cranial diabetes insipidus. 10 mcg intranasal DDAVP daily improved his symptoms.

Free water clearance in the kidney is dependent on a background level of cortisol. Neurosarcoid, by causing both ACTH and ADH deficiency is one of the few conditions where the ADH deficiency is masked by ACTH deficiency. Treatment of sarcoidosis with steroids therefore unmasks diabetes insipidus