Cases reported "Magnesium Deficiency"

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1/164. magnesium deficiency in children with urolithiasis.

    In a group of 57 children with urolithiasis hypomagnesaemia was found in 15 cases (26.3%). All children but one with abnormally low serum magnesium levels had recurrent or bilateral nephrolithiasis or nephrocalcinosis. prevalence of hyperoxaluria and hypercalciuria, marked severity of the clinical features, abnormality of Ca metabolism and its responsiveness to MgO treatment were demonstrable in Mg deficiency. ( info)

2/164. Regulatory hyperparathyroidism: the role of C-cell hyperplasia.

    Four cases with clinical and biochemical evidence of hyperparathyroidism are reported. The syndrome was due to DHT-intoxication of iatrogenic origin in the first case to histologically confirmed C-cell hyperplasia of the thyroid in the three others. The collective term "regulatory hyperparathyroidism" is porposed for the syndromes which, in distinction to secondary parathyroidisms, have a pathogenesis other than a negative calcium balance. Management of the syndrome is discussed with particular emphasis on the removal of the TCT-producing hyperplasia or adenoma, and the restoration of the electrolyte balance. ( info)

3/164. Primary hypomagnesemia caused by isolated magnesium malabsorption: atypical case in adult.

    Isolated magnesium malabsorption is a rare disorder, which bas been described in no more than 30 patients worldwide. patients with this disorder typically present with convulsion and diarrhea in early infancy. Hypomagnesemia and hypocalcemia were found in a 35-year-old man with muscle cramps, who bad been diagnosed as primary hypoparathyroidism. Oral magnesium therapy corrected the low serum calcium, magnesium and parathyroid hormone levels. We report an atypical case of isolated magnesium malabsorption in an adult. ( info)

4/164. Aminoglycoside-associated hypomagnesaemia in children with cystic fibrosis.

    Hypomagnesaemia in children with cystic fibrosis (CF) is under-recognized. We report a child with CF who developed significant hypomagnesaemia following intravenous (i.v.) treatment with aminoglycosides for exacerbations of pseudomonas aeruginosa infection. Three additional cases have also been observed. Investigations in two patients have revealed excessive renal loss of magnesium. It is postulated that renal tubular damage secondary to the cumulative effects of repeated courses of aminoglycosides resulted in hypomagnesaemia, and we suggest screening for this problem by monitoring serum magnesium regularly in all patients with CF receiving multiple courses of aminoglycosides. ( info)

5/164. External hydrocephalus in primary hypomagnesaemia: a new finding.

    This paper reports a new finding in two siblings with primary hypomagnesaemia as a result of renal magnesium wasting, namely, rapidly increasing head size. External hydrocephalus and brain shrinkage in primary hypomagnesaemia seen on computed tomography of the brain with reversibility after magnesium treatment has not been reported previously. ( info)

6/164. Primary infantile hypomagnesaemia: outcome after 21 years and treatment with continuous nocturnal nasogastric magnesium infusion.

    Primary infantile hypomagnesaemia is an infrequent cause of neonatal hypocalcaemic seizures but one that responds well to magnesium supplementation. We describe a 22-year-old male, first reported at 4 months of age, who is currently free of neurological deficit but has suffered from intermittent hypomagnesaemic tetany and chronic diarrhoea due to large oral magnesium supplements. Hypothesizing that modest hypercalcaemia might prevent the tetany, we conducted a trial of 5 microg/day 1,25(OH)2D3 over 5 days. Despite the resultant increase in calcium, he developed tetany with the reduction of magnesium intake and decline of serum magnesium from 0.63 to 0.39 mmol/l (normal >0.65 mmol/l). After 1,25(OH)2D3 was stopped and the parenteral magnesium injections suspended, 33% of his usual oral supplement was given instead by continuous nasogastric infusion and serum magnesium rose to 0.60 mmol/l. This regimen was better tolerated because of decreased gastrointestinal side-effects and freedom from parenteral injections. We observed that 1,25(OH)2D3 supplements do not promote magnesium retention nor does the resultant hypercalcaemia prevent hypomagnesaemic tetany. CONCLUSION: Continuous nocturnal nasogastric infusion may be considered in lieu of parenteral therapy in primary infantile hypomagnesaemia. ( info)

7/164. Refractory cardiac arrhythmia due to hypomagnesmia.

    A case of ventricular bigeminy possibly due to magnesium deficiency is reported. Magnesium sulphate was successfully used for its management. Differential diagnosis of idiopathic cardiac arrhythmias should always include hypomagnesemia as one of the causes and magnesium should be replaced for its proper management. ( info)

8/164. cisplatin ototoxicity, increased DPOAE amplitudes, and magnesium deficiency. Distortion product otoacoustic emissions.

    Outer hair cell (OHC) metabolism is blocked by cisplatin. Concurrent changes in the renal handling of magnesium occur because of the damage cisplatin causes to the renal proximal tubule cells within the thick ascending loop of henle. Although there is no evidence of cisplatin within the OHCs, there are significant levels of intracellular calcium, the antagonist to magnesium at the cell membrane. The OHC motile response is dependent on intracellular calcium. When the calcium current is suppressed by an antagonist, the extracellular OHC microphonic potential decreases. magnesium deficiency is known to produce hyperexcitability within the central nervous system, including fatal audiogenic seizures. In addition, increases in the amplitude of the auditory brainstem response wave V occur with aminoglycoside therapy and magnesium deficiency. This paper illustrates the amplitude growth of distortion product otoacoustic emissions in two patients treated with cisplatin and explores the possible underlying reasons why this may be related to magnesium metabolism. ( info)

9/164. syndrome of hypokalemic metabolic alkalosis and hypomagnesemia associated with gentamicin therapy: case reports.

    Nephrotoxicity, as evidenced by renal insufficiency is a well-known consequence of gentamicin therapy. We report two patients with gentamicin-induced syndrome of hypokalemic metabolic alkalosis and hypomagnesemia. Both had complete recovery of renal tubular function after cessation of antibiotic therapy. These cases emphasize the need to routinely monitor patients receiving gentamicin therapy for electrolyte abnormalities to avoid potential morbidity. ( info)

10/164. Magnesium deficit after renal transplantation with secondary posttransplantation hypocalcemia and hypophosphatemia.

    Hypomagnesemia, hypocalcemia and hypophosphatemia after renal transplantation in an 18-year-old patient is described. serum magnesium decreased in consequence of increased renal transplant function with high urinary magnesium excretion. At the time of serum magnesium depletion, pretransplantation hypocalcemia persisted and severe hypophosphatemia developed. magnesium oxide treatment was followed by the increment not only in serum magnesium but also in serum calcium and phosphate to normal level. Causal relationship between magnesium deficit and impaired renal transplant tubular reabsorption of magnesium and between magnesium deficit and serum calcium and phosphate depletion in the patient is suggested. ( info)
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