Milk-alkali syndrome (MAS) as a complication of the treatment of hypoparathyroidism — a case study

Abstract

Milk-alkali syndrome (MAS) is a severe and life-threatening complication of the treatment of hypoparathyroidism characterised by renal failure, metabolic alkalosis, and hypercalcaemia. The clinical course often begins abruptly and without prodromal symptoms. Although it is closely related to the doses of calcium carbonate and active Vitamin D preparations, its occurrence does not depend on the duration of hypoparathyroidism treatment. Among other factors triggering MAS are drugs influencing the glomerular filtration rate (angiotensin receptor blockers, sartans, aldosterone receptor antagonists, thiazide diuretics), lack of adequate control measures during hypoparathyroidism treatment, changes in calcium carbonate supplementation, dehydration, a diet rich in pH-basic foods (i.e. vegetarian diet), and pregnancy. A higher calcium carbonate dose is directly associated with an increased risk of milk-alkali syndrome. In cases of high calcium demand it is necessary to control renal function and monitor the level of serum calcium frequently, aiming for the lower end of the reference range. If MAS is confirmed or there are alarming neurological symptoms suggestive of hypercalcaemia, immediate hospitalisation is required. Treatment of MAS involves discontinuing calcium and Vitamin D supplementation and administering an intravenous infusion of normal saline solution to eliminate volume deficiencies and achieve forced diuresis while maintaining proper fluid balance. As soon as there is improvement in the clinical condition, it is necessary to begin treatment of comorbidities increasing the risk of renal failure or alkalosis (i.e. vomiting, diarrhoea).