Fukumoto S, Matsumoto T, Tanaka Y, Harada S, Ogata E
Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.
J Clin Endocrinol Metab. 1987 Dec;65(6):1301-4. doi: 10.1210/jcem-65-6-1301.
We studied a patient with severe hypomagnesemia due to small bowel resection who had marked renal magnesium (Mg) loss in response to iv Mg infusion. She had an undetectable serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] level before treatment. Although Mg infusion increased her serum Mg levels and enhanced renal PTH action, as evidenced by an elevation in nephrogenous cAMP, the serum 1,25-(OH)2D level remained low. After the administration of 1 alpha-hydroxyvitamin D3, her serum 1,25-(OH)2D level increased, and fractional excretion of Mg decreased. With the elevation in serum 1,25-(OH)2D, serum Mg levels could be maintained without Mg infusion, although they were still subnormal. These results are consistent with the assumption that patients with the short bowel syndrome and Mg deficiency have reduced renal tubular Mg reabsorption which causes renal Mg loss, and that impaired tubular Mg reabsorption is due at least in part to deficient renal action of 1,25-(OH)2D. Because depressed serum 1,25-(OH)2D levels cannot be corrected rapidly by Mg infusion, administration of 1 alpha-hydroxyvitamin D3 or 1,25-(OH)2D3 appears to be the treatment of choice for Mg deficiency in patients with short bowel syndrome.
