Sustained Metabolic Alkalosis Associated with Development of the Milk-Alkali Syndrome

Takeshi Nakanishi, MD, 5th Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya 663 (Japan) Dear Sir, The milk-alkali syndrome (MAS) has been described as hypercalcemia and metabolic alkalosis from the treatment for peptic ulcer with a high calcium and absorbable alkali intake in any form, usually as calcium carbonate. After the introduction of H2 Mockers has altered the basis of treatment of peptic ulcer, MAS may still occur with the ingestion of a smaller amount of calcium and alkali [1-3]. The pathogenesis of MAS has not been fully understood. The evidence below suggests that the sustained alkalosis might be related to MAS. (a) Patients with accelerated acid excretion or suppressed alkali excretion, i.e., duodenal ulcer or renal complication, are more inclined to develop MAS and to a much greater degree [4]. (b) Increased tubular reab-sorption of calcium is maintained in chronic metabolic alkalosis [5, 6]. We saw a patient with MAS suggesting that only sustained metabolic alkalosis could develop MAS. This 74-year-old man had a history of cerebral infarction (middle cerebral artery region), and improved activity during the course of rehabilitation. The patient had been prescribed magnesium oxide (2 g/day = 35.5 mEq alkali) for chronic constipation and ingested milk (200 ml = 0.22 g calcium) and ice cream (145 g = 0.19 g calcium) every day for 4 months. He had several episodes of aspiration pneumonia and elevated body temperature and was treated with minocyc-line and ofloxacine. When the patient began to feel severe nausea and anorexia, hypercalcemia (serum Ca 14.3 mg/dl), hypernatremia (serum Na 161 mEq/1), metabolic alkalosis (HCOi 37.4 mEq/1), and renal insufficiency (serum creatinine 2.34 mg/dl) were observed. A predisposition to hypercalcemia could not be shown by any known factors. On cessation of therapy and correction of dehydration, the serum Ca rapidly returned to normal within 1 week. TRP on diagnosing this disorder was 50.5%, which suggested hyperparathyroid-ism, and returned to a 90% normal range when serum Ca was restored to its normal range. Although the present case showed triads of MAS, hypercalcemia, metabolic alkalosis, and renal insufficiency, it could be distinguished from any other case previously reported with regard to the small amount of calcium (0.4 g/day) and alkali (35.5 mEq/ day) intake and the two clinical situations outlined below. The patient did not have the complication of peptic