Yamada T, Nakanishi T, Uyama O, Iida T, Sugita M
Fifth Dept. of Internal Medicine, Hyogo College of Medicine.
Nihon Jinzo Gakkai Shi. 1991 Jun;33(6):581-6.
We described a patient with the milk-alkali syndrome induced by the ingestion of small amount of milk (200 ml/day) and ice cream (145 g/day) and the administration of small dose of absorbable alkali (magnesium oxide 2.0 g/day) for the treatment of chronic constipation. The present case shows not only triads, i.e., hypercalcemia (s-Ca 14.3 mg/dl), metabolic alkalosis (s-HCO3- 37.4 mEq/L), and renal insufficiency (s-Cre 2.3 mg/dl) but also hypernatremia (s-Na 161 mEq/L) and hypertonic dehydration after the frequent episodes of elevated body temperature. The milk-alkali syndrome has been defined as the hypercalcemia with a metabolic alkalosis from a high amount of calcium intake and long term administration of absorbable alkali in any form, usually as calcium carbonate for the treatment of peptic ulcer. As the present case could be distinguished from any other cases previously reported with regard to the amount of calcium (0.4 g/day) and alkali (36 mEq/day) intake and the clinical situations that induced the syndrome, we compared the present case with the previous reports, calculating the amount of calcium and alkali intake from milk and absorbable alkali. After the introduction of the H2 blockers for peptic ulceration, the most cases with milk-alkali syndrome had provoked by the smaller amount of calcium than previously reported, which were associated with the treatment of relatively large amount of alkali (50-150 mEq/day), suggesting the role of sustained metabolic alkalosis for the development. In the present case the metabolic alkalosis induced by hypertonic dehydration and enhanced by absorbable alkali intake also could cause an increase of renal tubular reabsorption of calcium and a decrease of ionized calcium which might produce increased secretion of parathyroid hormone followed by vitamin D3 activation and increased Ca absorption from the gut. The metabolic alkalosis might be essential to the development of the milk-alkali syndrome without a high calcium and absorbable alkali intake.
我们描述了一名患者,其因摄入少量牛奶(每天200毫升)和冰淇淋(每天145克)以及服用小剂量可吸收性碱(氧化镁,每天2.0克)以治疗慢性便秘而诱发了乳-碱综合征。该病例不仅表现出三联征,即高钙血症(血清钙14.3毫克/分升)、代谢性碱中毒(血清碳酸氢根37.4毫当量/升)和肾功能不全(血清肌酐2.3毫克/分升),还出现了高钠血症(血清钠161毫当量/升)以及在体温频繁升高后发生的高渗性脱水。乳-碱综合征被定义为因大量摄入钙以及长期服用任何形式的可吸收性碱(通常为碳酸钙用于治疗消化性溃疡)而导致的高钙血症伴代谢性碱中毒。由于该病例在钙摄入量(每天0.4克)和碱摄入量(每天36毫当量)以及诱发该综合征的临床情况方面与之前报道的任何病例都有所不同,我们将该病例与之前的报道进行了比较,计算了从牛奶和可吸收性碱中摄入的钙和碱的量。在引入用于消化性溃疡的H2阻滞剂后,大多数乳-碱综合征病例是由比之前报道的钙量更少所诱发的,这与相对大量碱(每天50 - 150毫当量)的治疗有关,提示持续的代谢性碱中毒在其发病中的作用。在本病例中,高渗性脱水诱发并因可吸收性碱摄入而加重的代谢性碱中毒,也可能导致肾小管对钙的重吸收增加以及离子钙减少,这可能会促使甲状旁腺激素分泌增加,随后维生素D3活化,肠道对钙的吸收增加。代谢性碱中毒可能在没有高钙和可吸收性碱摄入的情况下对乳-碱综合征的发生至关重要。