Roentgen manifestations of milk drinker's syndrome.

Abstract

The roentgen finding of calcinosis in the presence of a history of prolonged and excessive milk consumption (usually for peptic ulcer) and renal insufficiency should indicate the diagnosis of milk drinker's syndrome. It is our purpose in this paper to present the clinical syndrome, demonstrate its roentgen manifestations, and discuss its pathological physiology. Historical In 1949, Burnett et al. (3) described a syndrome following prolonged intake of excessive quantities of milk and alkali. The essential components were hypercalcemia without hypercalcuria or hypophosphatemia, calcinosis manifested by band keratitis, renal insufficiency with azotemia and mild alkalosis, and improve-ment on a diet low in milk and absorbable alkali. The cases resembled hyperparathyroidism with renal insufficiency but were differentiated from the latter by normal urinary calcium, normal or elevated serum phosphorus, absence of skeletal demineralization, and lowering of serum calcium on a low calcium diet. On theoretical grounds the authors thought that a combination of elevated serum calcium and normal or slightly elevated phosphorus would predispose to metastatic calcinosis. The calcinosis was uniformly present as band keratitis, but in only one instance as widespread subcutaneous calcifications. Elimination of milk from the diet resulted in significant lowering of serum calcium and phosphorus. Roentgen Findings The characteristic roentgen appearance of metastatic calcinosis is one of calcific deposits in the subcutaneous tissues, usually in proximity to joints. The masses are amorphous; they vary in size from nodules to bulky tumors, and are unaccompanied by change in osseous structure. Ancillary findings include widespread calcifications in blood vessels, falx cerebri, kidneys, and lungs. Pathological Physiology Albright (1) stated that in primary hyperparathyroidism elevated serum and urinary calcium predispose to the formation of calcium phosphate and oxalate stones. Later, nephrocalcinosis causes renal failure and phosphorus retention. At this stage, kidney damage is no longer reversible. Secondary hyperparathyroidism following chronic renal disease occurs when phosphorus retention causes a lowering of serum calcium which, in turn, stimulates the parathyroid glands. Rebound elevation of calcium results, and in time metastatic calcinosis occurs. Wermer et al. (7) postulated the role of the kidney to be the same regardless of the parathyroid function. They concluded that the prerequisite for calcinosis is saturation of the circulating blood with calcium and phosphorus. Renal calcinosis occurs when the two cations are precipitated in the postglomerular paren-chyma. Later the disease progresses to metastatic calcinosis, occurring in normal tissue in contradistinction to the dystrophic tissues calcified in scleroderma.