Milk-Alkali Syndrome

Milk-alkali syndrome is characterized by a triad of elevated calcium levels, metabolic alkalosis, and acute kidney injury that commonly occurs due to the combined intake of large amounts of calcium and absorbable alkali. The syndrome can have an acute onset with the rapid development of hypercalcemia and, if left untreated, may cause acute renal failure and metastatic calcification. The milk-alkali syndrome was first recognized in the early 20th century when Bertram Sippy introduced a treatment regimen for peptic ulcer disease. The 'Sippy regimen' consisted of multiple daily doses of milk and cream combined with an absorbable alkali such as magnesium oxide, sodium bicarbonate, or bismuth subcarbonate to protect the gastric ulcer from further erosion by gastric acid. The results were highly favorable, and it soon became a popular therapy. Soon after, various toxic effects were reported, including hypercalcemia and metabolic alkalosis, and some cases of acute kidney injury were also reported. With the advent of newer drugs for treating peptic ulcer disease, such as histamine type-2 receptor blockers, in the 1980s, the syndrome virtually vanished from the world.

Recently, however, more cases of milk-alkali syndrome have been reported. This is likely due to the common use of over-the-counter calcium preparations for preventing and treating osteoporosis in women who are postmenopausal. Calcium carbonate is also frequently prescribed to patients with chronic kidney disease to prevent secondary hyperparathyroidism. Various scholars have also suggested changing the syndrome's name to calcium-alkali syndrome due to the changing etiopathology. Milk-alkali syndrome now accounts for more than 10% of the cases of hypercalcemia and is the third most common cause of hypercalcemia in hospitalized patients (after hyperparathyroidism and hypercalcemia of malignancy).