Intractable vomiting as a presentation of adrenal insufficiency – a case report

Case report

A 45-year old female presented with a six-month history of recurrent nausea, vomiting, and generalized weakness. The vomiting was associated with each meal, occurring 1–2 h afterwards, and was associated with a significant weight loss c.10% of body weight over the previous six months. Before presenting to us, the patient had undergone an upper gastro-intestinal endoscopy twice, ultrasonography of the abdomen, oesophageal manometry, barium follow-through, and CT brain scan, all of which were unremarkable. She was treated with various antiemetics and prokinetics without improvement. She had a prior history of pulmonary tuberculosis two years previously, for which she was treated and declared cured.

At presentation, she was conscious, oriented, with signs of mild dehydration, a mild tachycardia (rate: 96/minute) and hypotension (94/72 mmHg). Physical examination revealed no abnormal findings. Blood investigations showed: haemoglobin = 123 g/L, total leucocyte count 9.5 × 10⁹ /L, platelet count 2,76 × 10⁹ /L, random blood glucose = 4.22 mmol/L, serum creatinine = 114.9 umol/L, serum sodium = 131 mmol/L, serum potassium = 4.2 mmol/L, serum chloride = 90 mmol/L. Liver function tests were within normal limits. In view of significant weight loss with hyponatraemia adrenal insufficiency was suspected; further investigations showed a morning serum cortisol level was 55.2 nmol/L (normal range: 138–690 nmol/L), and her adrenocorticotrophic hormone (ACTH) level was 112.74 pmol/L (normal range: 2.2–13.3 pmol/L). An abdominal CT scan showed atrophy and calcification of both adrenals, most likely due to prior tuberculosis. Therefore, Addison's disease was concluded. With oral prednisolone 40 mg/day with gradual tapering over the next four weeks to 10 mg/day and oral fludrocortisone 0.05 mg/day, her symptoms started improving within one week, and by the third week, she had completely recovered.

Discussion

The most common cause of primary adrenal insufficiency in rich countries is autoimmune disease, while tuberculosis and other infections remain an important cause in low and middle-income countries. ¹ Haematogenous spread of tuberculosis will initially lead to adrenal gland enlargement and later fibrosis and calcification. Treatment with anti-tuberculous drugs can restore adrenal function in tuberculosis-affected adrenals, but adrenal insufficiency may be evident years after treatment, ² depending on how much damage has been caused.

Most cases of adrenal insufficiency have a chronic presentation with an acute crisis occurring in a subset of patients, usually precipitated by stress. ¹ In a previous study, the most common manifestation was hyperpigmentation (76%), followed by gastrointestinal symptoms, with nausea and vomiting present in around 40% of the cases. ³ However, the diagnostic dilemma in our case was the absence of hyperpigmentation and a normal serum potassium, which may have been due to chronic vomiting.

A suspected case of adrenal insufficiency should undergo testing for early morning serum cortisol and ACTH levels, the former being low, and the latter high. In secondary adrenal insufficiency, serum cortisol levels are low with low to normal ACTH levels. The rapid adrenocorticotropin stimulation test is ideal for confirming the diagnosis. Following 250 μg of cosyntropin administration, a serum cortisol level >550 nmol/L rules out primary adrenal insufficiency. ⁴

To conclude, any patient with unexplained weight loss and gastrointestinal symptoms should be suspected and investigated for adrenal insufficiency after ruling out the common conditions, especially if a previous history of tuberculosis is established. Failure to detect the disease in time may result in considerable morbidity and mortality.