Burnett and associates,1 in 1949, reported six cases presenting the following features: (1) hypercalcemia without hypercalciuria or hypophosphatemia, (2) calcinosis manifested especially by ocular lesions resembling band keratitis, and (3) renal insufficiency with azotemia, following the prolonged intake of milk and absorbable alkalis, usually for treatment of active peptic ulcer. This clinical entity has become known as the "milk-alkali syndrome." Since Burnett's initial description there have been sporadic reports of cases,* some of which have stressed complications such as metastatic calcification, nephrocalcinosis, and renal calculi. The early signs and symptoms produced by this syndrome are such as to be easily overlooked. It is the purpose of this paper to present the clinical and laboratory findings in eight cases of milk-alkali syndrome seen at the Mayo Clinic since 1949, in order to emphasize the hazards and relative clinical importance of this condition.
Medical literature is replete with references to untoward
SCHOLZ DA, KEATING FR. Milk-Alkali Syndrome: Review of Eight Cases. AMA Arch Intern Med. 1955;95(3):460–468. doi:10.1001/archinte.1955.00250090098012
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