The
milk-alkali syndrome became rare with the advent of modern
ulcer therapy with nonabsorbable
antacids, histamine2 blockers, and
sucralfate. An increased frequency of this syndrome seems likely with the growing popularity of the use of
calcium carbonate as an
antacid or as
calcium supplementation to prevent
osteoporosis. We treated five patients who had six episodes of the
milk-alkali syndrome; four of these cases were diagnosed between 1990 and 1992. All patients were ingesting massive quantities of
calcium and absorbable
alkali and were unaware of the toxic effects of these compounds. All patients presented with the triad of
hypercalcemia, metabolic
alkalosis, and
renal failure. All metabolic abnormalities were corrected, and renal function improved with appropriate supportive measures and cessation of
calcium and
alkali ingestion. In two patients, the
renal failure was so severe that dialysis was necessary. In four patients, either the serum
amino-terminal parathyroid hormone or
1,25-dihydroxycholecalciferol levels were appropriately decreased in response to
hypercalcemia. The serum
carboxy-terminal parathyroid hormone levels were increased because of
renal failure. Since both physicians and patients are often unaware of the
calcium and
alkali content of many nonprescription medicines, the diagnosis of the
milk-alkali syndrome, a reversible cause of
renal failure, can be missed if a detailed history of such intake is not elicited. Measurement of the serum
amino-terminal parathyroid hormone and
1,25-dihydroxycholecalciferol levels may help differentiate
milk-alkali syndrome from
primary hyperparathyroidism.