Endocrine Abstracts

: A 78-year-old male with a background of renal cell carcinoma and bilateral adrenal metastasis presented with leg cramps and lethargy. He was on Prednisolone 10 mg od for immune therapy induced pneumonitis. Prior to commencing Prednisolone, he was on Dexamethasone 2 mg for 4 months for weight loss, nausea and vomiting. He underwent a Short Synacthen Test (SST) as his serum Na was low at 119 mmol/L (134–146). His SST showed a flat response with baseline and 30 minutes cortisol levels were low at 24 and 25 nmol/L respectively. He was diagnosed with secondary adrenal insufficiency (SAI). He was restarted on Dexamethasone before discharge as he felt better on Dexamethasone. 6 weeks later, he was readmitted with left pyelonephritis, tiredness, lethargy and weakness. His Na was low at 125, K 5.3 mmol/L (3.4–5.2), urea 8.7 mmol/L (3.4–8.0), creatinine 104 umol/L (60–126). His Na dropped further to 116. Paired serum and urine osmolalities were 247 and 384 mosm/kg respectively. His urine Na was high at 53 mmol/l. He was diagnosed with SIADH and was fluid restricted. The endocrine team advised to check renin and aldosterone. He started to experience postural hypotension and was commenced on Fludrocortisone before testing for renin and aldosterone. Na improved to 126 and K 4.69. The endocrine team advised to withhold Fludrocortisone for 24 hours before checking renin and aldosterone levels. Unfortunately, Fludrocortisone was not restarted after renin and aldosterone levels were taken. He was commenced on Tolvaptan 7.5 mg on alternate days initially and then daily as his Na continued to drop to 121. Patient was reviewed by psychologists as he continued to complain of tiredness and lethargy and was advised relaxation exercises. Renin results were not available due to technical issues. He continued to be hyponatraemic, extremely tired and intermittently hypotensive. Finally, the renin result was available and was high at 373 mIU/L (4.2–59.7) indicating Primary Adrenal Insufficiency (PAI). He was immediately commenced on IV Hydrocortisone and oral Fludrocortisone. He clinically improved and his Na normalised to 136, K 3.8. He was discharged home on oral Hydrocortisone and Fludrocortisone.

Conclusions: We describe a case of PAI incorrectly diagnosed as SAI and SIADH which resulted in inappropriate treatment and prolonged hospital stay. Our case highlights the difficulties and delays in recognising the signs and symptoms of PAI in patients who are on exogenous glucocorticoids. Prompt diagnosis and treatment may prevent severe adrenal crisis.