Endocrine Abstracts

A 35 year old lady presented with a one week history of back pain, myalgia, fatigue, epigastric pain, and persistent vomiting. She reported a four week history of reduced appetite and 4 kg weight loss. She had recently recovered from an uncomplicated COVID-19 infection. Past medical history included a previous eating disorder (anorexia and bulimia), and subsequent chronic gastritis. Drug history included Omeprazole 20 mg daily, Laxido 2 sachets daily and antacids (Rennies 4-8 tablets daily for the last 15 years). Physical examination revealed generalised abdominal and mild bilateral flank tenderness and no peripheral lymphadenopathy. Significant investigation findings included an adjusted Calcium 4.19 mmol/l (previously normal) [ref. 2.2-2.6], K+ 2.9 mmo/l [ref. 3.5-5.3], Creatinine 535 umol/l (baseline 80 umol/l) [ref. 55-110]. The urine dip was negative for hCG, blood and nitrites. ECG on admission showed a shortened QTc and bradycardia. A renal tract ultrasound was unremarkable and a Chest X-Ray did not suggest a granulomatous or neoplastic disease. Further investigations revealed a suppressed PTH (1.1 pmol/l) [ref. 1.6-7.2], with normal 25(OH)D (86.8 nmol/l) [ref. 50-150] and metabolic alkalosis (pH 7.47 [ref. 7.35-7.45], Bicarbonate 45 mmo/l [ref. 22-29]). Serum electrophoresis and serum ACE were normal. There was a low suspicion for PTHrP driven-hypercalcaemia due to a malignancy given the short duration of symptoms and examination findings. The patient was successfully managed for acute hypercalcaemia and pre-renal acute kidney injury, with aggressive intravenous fluid resuscitation. The severe hypercalcaemia was attributed to Milk-Alkali syndrome secondary to excessive prolonged calcium carbonate use and the calcium carbonate (Rennie) tablets were stopped. Adjusted calcium (2.41 mmol/l) and creatinine (86 umol/l/) promptly normalized and remained so on follow up. This interesting case acts as a reminder of the non-specific presentation of hypercalcaemia, highlights the importance of a detailed enquiry about over-the-counter medications when taking a drug history, and demonstrates an infrequent cause of PTH-independent hypercalcaemia. Milk-Alkali syndrome should be considered as a potential cause of hypercalcaemia, when sinister differentials for non-PTH driven hypercalcaemia have been excluded, and in the presence of the triad of hypercalcaemia, metabolic alkalosis and acute kidney injury, associated with the ingestion of large amounts of calcium and absorbable alkali. In this case, it is possible that concurrent chronic laxative use contributed to the electrolyte disturbances and metabolic alkalosis, and along with the recent COVID-19 infection could have precipitated the onset of Milk-Alkali syndrome.