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Milk-alkali syndrome is characterised by hypercalcaemia, alkalosis and renal failure. It results from excessive ingestion of calcium and absorbable antacids such as milk or calcium carbonate. The frequency of this syndrome has decreased since the availability of H2 receptor antagonists (and then proton pump inhibitors) for the treatment of peptic ulcer disease.
There seems a genetic factor in the development of this syndrome because many patients are treated with calcium carbonate without developing the syndrome.
There is a cycle of mild hypercalcaemia which leads to bicarbonate retention which turn in causes alkalosis and subsequent renal calcium retention. This sequence of events results in severe hypercalcaemia. This cycle perpetuates hypercalcaemia and alkalosis as long as calcium and absorbable alkali are ingested.
Features of this syndrome include weakness, myalgia, irritability and apathy. Impairment of renal function, hypercalcaemia and alkalosis all reverse rapidly upon stopping the intake of calcium and alkali.