Abstract
Hypercalcemia is a relatively common clinical problem in both outpatient and inpatient settings. Primary pathophysiology is the entry of calcium that exceeds its excretion into urine or deposition in bone into circulation. Among a wide array of causes of hypercalcemia, hyperparathyroidism and malignancy are the most common, accounting for greater than 90 percent of cases. Concordantly, there has been a resurgence of milk-alkali syndrome associated with the ingestion of large amounts of calcium and absorbable alkali, making it the third leading cause of hypercalcemia (Beall and Scofield, 1995 and Picolos et al., 2005). This paper centers on a case of over-the-counter calcium and alkali ingestion for acid reflux leading to milk alkali with concordant use of thiazide diuretic for hypertension.
Highlights
Sippy, almost 100 years ago, developed a calcium-laden milk and antacid regimen for the treatment of peptic ulcer disease [1]
In the milk-alkali syndrome, hypercalcemia develops because the input of calcium exceeds the output
Factors that can increase calcium input include increased dietary calcium intake, ingestion of supplemental calcium, enhanced intestinal absorption of calcium usually resulting from stimulation by vitamin D that is present in some calcium supplements, and other dietary factors
Summary
Almost 100 years ago, developed a calcium-laden milk and antacid regimen for the treatment of peptic ulcer disease [1]. Cope in 1936 first recognized hypercalcemia as a major feature of this toxicity [4] He showed a rapid resolution of alkalosis and hypercalcemia after cessation of treatment, but the recovery of renal function was much slower. Punsar and Somer in 1963 classified milk-alkali syndrome into three different types: acute, subacute (Cope’s syndrome), and chronic (Burnett’s syndrome) toxicity [6]. In contrast to the acute form, there was less rapid improvement in symptoms and the recovery of renal function was slower. Presentation of Burnett’s syndrome included complains of pruritus, diffuse musculoskeletal symptoms, nephrocalcinosis, and band keratopathy with large soft tissue calcium deposits [5, 8].
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