Hindawi Publishing Corporation Case Reports in Medicine Volume 2011, Article ID 729862, 4 pages doi:10.1155/2011/729862 Case Report Milk Alkali and Hydrochlorothiazide: A Case Report Babar Parvez, Chinenye Emuwa, Marquetta L. Faulkner, and John J. Murray Department of Internal Medicine, Meharry Medical College, 1818 Albion Street, Nashville, TN 37208, USA Correspondence should be addressed to Chinenye Emuwa, chinemuwa@yahoo.com Received 9 November 2010; Revised 12 February 2011; Accepted 28 March 2011 Academic Editor: Robert A. Kozol Copyright © 2011 Babar Parvez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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. 1. Introduction Sippy, almost 100 years ago, developed a calcium-laden milk and antacid regimen for the treatment of peptic ulcer disease [1]. The rationale was to neutralize the hyperacidity that was deemed responsible for peptic ulcer disease. The Sippy regimen until the 1970s was used for the treatment of peptic ulcer disease, a disorder that was predominant in middle- aged men, when nonantacid treatment was ﬁrst introduced [1, 2]. Sippy’s original recommendation consisted of the hourly administration of milk and cream together with what became known as the Sippy powders, which were 10 grains (1 grain = 65 mg) each of heavily calcinated magnesia and sodium bicarbonate, alternating with a powder that contained 10 grains of bismuth subcarbonate and 20 to 30 grains of sodium bicarbonate [1]. Hardt and Rivers in 1923 gave a detailed description of the toxicity that was associated with the antacid and milk regimen [3]. The symptoms consisted of nausea, vomiting, headache, dizziness, musculoskeletal pains, and weakness followed by prostration. There was an associated elevation of blood urea nitrogen (BUN) and serum creatinine, alkalosis, and albuminuria. Cope in 1936 ﬁrst recognized hypercal- cemia as a major feature of this toxicity [4]. He also showed a rapid resolution of alkalosis and hypercalcemia after cessation of treatment, but the recovery of renal function was much slower. Fundamentally, the diﬀerentiation of milk- alkali syndrome from primary hyperparathyroidism was evident due to the absence of hypophosphatemia and the resolution of the hypercalcemia once treatment with antacids was stopped. Burnett et al. in 1949 described a chronic variant of the milk-alkali syndrome in which renal failure was persistent and soft tissue calciﬁcations were extensive [5]. Punsar and Somer in 1963 classiﬁed milk-alkali syn- drome into three diﬀerent types: acute, subacute (Cope’s syndrome), and chronic (Burnett’s syndrome) toxicity [6]. Shortly thereafter, McMillan and Freeman formulated a comprehensive table and compared clinical presentation, biochemical ﬁndings, and resolution of the three diﬀerent types of the milk-alkali syndrome [7]. The subacute form (Cope’s syndrome) was seen during therapy with calcium and alkali that had been used intermittently for years. In contrast to the acute form, there was less rapid improvement in symptoms and the recovery of renal function was slower. The chronic form (Burnett’s syndrome) occurred after a long history of ingestion of large amounts of calcium and alkali. Presentation of Burnett’s syndrome included complains of pruritus, diﬀuse musculoskeletal symptoms, nephrocalcinosis, and band keratopathy with large soft tissue calcium deposits [5, 8]. Although symptoms usually improved with the discontinuation of calcium antacids, the resolution of hypercalcemia was slow, especially in patients