E-Poster Presentation ESA-SRB-ANZBMS 2021

Milk alkali syndrome in a young woman with Gastro-oesophageal reflux after Laparoscopic gastric banding (#380)

Kate Flentje 1 , Reetu Gogna 1 , A/Prof Roland McCallum 1 2
  1. Department of Diabetes and Endocrinology, Royal Hobart Hospital, Hobart, Tasmania, Australia
  2. School of Medicine, University of Tasmania, Hobart, Tasmania, Australia

Introduction:

Milk alkali syndrome (MAS) consists of a triad of hypercalcemia, metabolic alkalosis, and acute renal failure due to ingestion of large amounts of calcium and absorbable alkali often in the form of over-the-counter antacid medications. Although MAS had become a rare presentation since the introduction of H2 antagonists and proton-pump inhibitors (PPIs) it has made a resurgence in recent years with increased use of calcium supplements for osteoporosis prevention.

 

Case Report:

A 35-year-old female presented to the emergency department with severe lethargy, nausea, thirst, and constipation for a few weeks. Initial bloods showed ionised calcium 1.84mmol/L [1.15-1.33], creatinine 334 µmol/L [45-85], bicarbonate 44mmol/L [20-32], parathyroid hormone (PTH) 3.5pmol/L [1.6-9.0] and vitamin D 56nmol/L [>49]. Medical history was significant for previous cholecystectomy, laparoscopic gastric banding (LAGB) and gastroesophageal reflux disease. She was taking no prescribed medications. Calcium levels normalised with intravenous fluids, but then rebounded again requiring readmission and further intravenous fluids plus 5mg zoledronic acid once eGFR >50 ml/min/1.73m2. Cinacalcet was commenced and dose titrated to 30mg BD. Nuclear sestamibi and ultrasound did not reveal a parathyroid adenoma. Further work up including CT chest-abdomen-pelvis, ACE level and serum protein electrophoresis were unremarkable. During a third admission to hospital with recurrent hypercalcaemia, it became evident she was also taking at least 6 chewable Quick-eze® tablets (containing 750mg calcium carbonate per tablet) per day secondary to difficulty swallowing PPI tablets after her LAGB. This raised the possibility of MAS as the cause of her recurrent hypercalcaemia. On cessation of these tablets and changeover to pantoprazole for acid suppression, calcium levels normalised within 48 hours and cinacalcet was able to be ceased.

 

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Conclusion:

Medical practitioners need to be aware of the potential adverse effects of ingesting excessive amounts of calcium carbonate and its role as a potential cause of hypercalcaemia.