The milk-alkali syndrome.

Abstract

Although alkalosis and renal compromise may occur from the use of antacids and milk, severe disease with features corresponding to those which Burnettet al. described could be found in only 33 cases through 1963. Many more cases of transient changes have been reported, sometimes under the eponym of “Burnett's syndrome.” Generally, there was a long history of excessive intake of milk and absorbable alkali, mostly sodium bicarbonate. The most common manifestations were anorexia, dry mouth, dizziness, pruritus, polyuria, or other manifestations of renal insufficiency. Azotemia and hypercalcemia were present; the serum phosphorus was normal or elevated, and the alkaline phosphatase was normal. Previous renal disease was present in about one-third of the cases. Urinary calcium excretion was normal. Band keratopathy, nephrocalcinosis, or other metastatic calcification was usually present. The pathogenesis is obscure. The amount of calcium appeared to be greater than normal. A long history of high milk intake was present in 29 of 32 patients and absorbable alkali (mostly sodium bicarbonate) in all 33 of the patients with Burnett's syndrome. Pre-existing renal disease was present in about one-third of the patients. Other metabolic abnormalities such as potassium depletion may contribute to the renal impairment. The major condition to be considered in differential diagnosis is primary hyperparathyroidism. Improvement on a diet low in calcium and absorbable alkali may be useful in patients without irreversible renal disease. Surgical exploration and examination of the parathyroid tissue may be necessary in some instances. Treatment consists principally of a low calcium diet, a high fluid intake and discontinuance of absorbable alkali.