Problems in the Differentiation of the Milk-Alkali (Burnett’s) Syndrome and Hyperparathyroidism, Illustrated by Two Case Reports
THE milk-alkali (Burnett’s) syndrome and hyperparathyroidism under certain circumstances may be practically indistinguishable clinically.1 Those special circumstances are illustrated in the two case histories that will be presented following a brief comparison of the characteristics, causes, and courses of the two diseases.
Burnett’s syndrome is characterized by hypercalcemia without hypercalciuria (Table). It does not cause skeletal damage. The etiologic factor is the excessive intake of milk and absorbable alkali. The condition eventually results in renal failure, but just before renal failure, hypocalciuria becomes evident in an alkaline urine.
Hyperparathyroidism is characterized by hypercalcemia with high urinary calcium excretion, which eventually results in renal failure. However, when renal failure occurs as a late complication of the disease, the low serum phosphorus and the hypercalciuria may disappear, and as in Burnett’s syndrome, hypercalcemia without hypercalciuria exists (Table). In about one third of the patients having hyperparathyroidism there is skeletal damage, and pathognomonic roentgenographic findings are osteitis fibrosa cystica and absence of the dental lamina dura. The etiologic factor generally is a tumor of one or more parathyroid glands, which when aberrant may be situated somewhere in the mediastinum.
Case 1. A 63-year-old farmer was first seen on April 26, 1954. His presenting complaint was that of daily “heartburn” of many years’ duration. His appetite had become poor and he had lost 5 pounds in weight during the previous month. He had muscular weakness, constipation, moderate thirst, and nocturia.
Findings on physical examination were not unusual. However, a KUB roentgenogram disclosed. . .