no tumours on CT imaging of the chest, abdomen and pelvis, and an undetectable PTH-related peptide level. He had no clinical or radiological evidence on CT or gallium scan of sarcoidosis or lymphadenopathy. Also, his 1,25(OH)2 Vitamin D level was not elevated, making sarcoidosis and other granulomatous conditions unlikely to be the underlying cause of hypercalcaemia. Further assessment of this PTH-independent hypercalcaemia effectively excluded the differential diagnoses of hyperthyroidism, Vitamin D intoxication, Vitamin A intoxication, rhabdomyolysis, milk-alkali syndrome, immobility and acromegaly. His morning serum cortisol was found to be markedly low at 46 nmol/l (RR 200–600 nmol/l) in the context of a normal sleep–wake cycle. His hospital file was carefully reviewed and he was confirmed to have not received any exogenous glucocorticoids during his hospital admission, including during the period of critical illness in the ICU. There were no previous cortisol results for comparison, as there had been no clinical need for testing earlier in his admission. The hypocortisolaemia was promptly further investigated.