OBJECTIVES: To report three cases of primary hypomagnesemia (PH) with secondary hypocalcemia in symptomatic infants, born to consanguineous parents, and to present Mg metabolic studies. METHODS: Classic metabolic balances of Mg were performed during three consecutive days, using carmin as fecal marker, with and without Mg supplementation. RESULTS: The patients (one male) presented, between 15 and 28 days old, with convulsions and persistent hypocalcemias, which could not be controlled with anticonvulsivants and/or intravenous calcium gluconate. After diagnostic was established the above symptoms and hypomagnesemia were controlled with Mg supplementation. Without supplements, mean daily balances were negative or below daily needs, showing final magnesemias lesser than 0.7 mEq/L and hypocalcemias about 3 mEq/L. The renal conservation test performed for six days after Mg repletion showed at the beginning of the study normal magnesemias (1.4 to 1.5 mEq/L) decreasing to 0.7 or 0.8 mEq/L in the first 24 hours, indicating absence of response from the body stores. Mg total renal excretion was smaller than 1 mEq, during six consecutive days, indicating adequate renal Mg reabsorption. Intestinal absorption of Mg varied from 6 to 15% of intake. With Mg supplementation, daily balances were positive, correcting progressively the serum Ca and Mg. The intestinal absorption was greater than 22% of intake in this situation.In pacient LPCJ, urinary excretion was 35% of the administered dosis, confirming Mg depletion. CONCLUSIONS: Besides confirming specific intestinal malabsorption of Mg, adequate renal conservation and an homeostatic extracellular defect of Mg were observed, probably caused by an incapacity of mobilization of Mg from tissue reserves.
OBJECTIVES: To report three cases of primary hypomagnesemia (PH) with secondary hypocalcemia in symptomatic infants, born to consanguineous parents, and to present Mg metabolic studies. METHODS: Classic metabolic balances of Mg were performed during three consecutive days, using carmin as fecal marker, with and without Mg supplementation. RESULTS: The patients (one male) presented, between 15 and 28 days old, with convulsions and persistent hypocalcemias, which could not be controlled with anticonvulsivants and/or intravenous calcium gluconate. After diagnostic was established the above symptoms and hypomagnesemia were controlled with Mg supplementation. Without supplements, mean daily balances were negative or below daily needs, showing final magnesemias lesser than 0.7 mEq/L and hypocalcemias about 3 mEq/L. The renal conservation test performed for six days after Mg repletion showed at the beginning of the study normal magnesemias (1.4 to 1.5 mEq/L) decreasing to 0.7 or 0.8 mEq/L in the first 24 hours, indicating absence of response from the body stores. Mg total renal excretion was smaller than 1 mEq, during six consecutive days, indicating adequate renal Mg reabsorption. Intestinal absorption of Mg varied from 6 to 15% of intake. With Mg supplementation, daily balances were positive, correcting progressively the serum Ca and Mg. The intestinal absorption was greater than 22% of intake in this situation.In pacient LPCJ, urinary excretion was 35% of the administered dosis, confirming Mg depletion. CONCLUSIONS: Besides confirming specific intestinal malabsorption of Mg, adequate renal conservation and an homeostatic extracellular defect of Mg were observed, probably caused by an incapacity of mobilization of Mg from tissue reserves.