Cases reported "Magnesium Deficiency"

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1/76. 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.
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2/76. 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.
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3/76. 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.
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4/76. role of cofactors in the treatment of malnutrition as examplified by magnesium.

    In the absence of appropriate amounts of metabolically important cofactors such as magnesium, replenishment of malnourished patients with protein and carbohydrate will exaggerate the underlying abnormality even though the primary deficiency is corrected. The malnourished patients cannot utilize the food substances provided unless they have within their cells commensurate amounts of all the necessary cofactors required for the metabolism of the food supplied. This therapeutic problem in malnutrition is illustrated by three different examples of clinical deterioration when caloric and vitamin replenishment have been undertaken in the face of magnesium deificiency.
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5/76. Latent tetany and anxiety, marginal magnesium deficit, and normocalcemia.

    The identification of marginal magnesium deficit, such as we have detected in a patient with anxiety, depression, and psychomatic complaints, is a difficult diagnostic problem. electromyography of a limb, rendered acutely ischemic either just before or after hyperventilation, can elicit latent tetany in this condition, as well as in calcium deficiency. We have demonstrated iterative electrical activity in our patient, whose magnesium deficit is attributable to renal wasting of magnesium. We have elicited similar patterns in several other patients, who had marginally low serum magnesium and who also exhibited weakness, anxiety, and psychosomatic disorders. This preliminary report suggests the need for further consideration of the possibility that chronic magnesium-deficit may contribute to the syndrome of latent tetany, psychosomatic complaints, and weakness.
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6/76. magnesium deficiency during lactation as a precipitant of ventricular tachyarrhythmias.

    A young ICD recipient with a history of syncope and idiopathic polymorphic ventricular tachycardia/ventricular fibrillation presented after an ICD discharge. She had delivered her first child 8 days prior to the event and she had been lactating. Numerous short runs of polymorphic ventricular tachycardia/ventricular fibrillation resolved with aggressive replacement of magnesium and elimination of breast-feeding.
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7/76. Hypomagnesemia with increased metabolism of parathyroid hormone and reduced responsiveness to calcitropic hormones.

    A patient with severe hypomagnesemia due to chronic alcoholism is presented who repeatedly exhibited marked hypocalcemia with a dissociation between radioimmunoassay findings for mid region of parathyroid hormone (PTH-M) and immunoradiometric assay findings of serum intact PTH (PTH-intact). serum PTH-M was moderately elevated whereas serum PTH-intact was in a low normal range every time when her serum magnesium (Mg) concentration was markedly reduced. There was also a marked reduction in serum osteocalcin concentration. Supplementation of Mg resulted in a sharp increase in serum PTH level with a rapid disappearance of the dissociation between the two immunoassays of PTH. Shortly after serum PTH and 1,25(OH)2D levels reached their peak, serum osteocalcin started to increase, and was elevated into a supranormal level with normalization of serum Ca concentration. Mg is thought to act as a mimic/antagonist of calcium (Ca), and high extracellular Ca is shown to cause an inhibition of secretion with a stimulation of degradation of PTH. Thus, these observations are consistent with the hypothesis that Mg deficiency causes an increase in the metabolism of PTH and a reduction in the secretion of bioactive intact PTH by increasing the sensitivity of parathyroid cells to Ca. In addition, the fact that hypocalcemia disappeared concomitant with a marked increase of serum osteocalcin from undetectable levels suggest that refractoriness of bone to calcitropic hormones is present which plays a significant role in the development of hypocalcemia under hypomagnesemia, and that serum osteocalcin can be a good marker for the assessment of the responsiveness of bone to calcitropic hormones in these patients.
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8/76. Gitelman's syndrome with exercise-induced ventricular tachycardia.

    A 62-year-old female with palpitations was admitted to hospital where she recorded 12,299 monofocal ventricular premature contractions (VPCs) in 24 h and nonsustained ventricular tachycardia (VT) on exertion. She had hypokalemia with renal potassium wasting, a chloride-resistant metabolic alkalosis, elevated plasma renin, elevated plasma aldosterone (relative to the serum K concentration), hypomagnesemia with renal magnesium wasting, decreased urine calcium excretion, and normal blood pressure. The hypokalemia and hypomagnesemia were thought to have precipitated the VT. The coronary angiogram showed normal coronary arteries; however, the left ventriculogram revealed akinesis of the posterolateral wall. Because the VT could not be induced by programmed electrical stimulation either before or during intravenous administration of isoproterenol, the VPC with the same QRS morphology as the VT became the target of radiofrequency catheter ablation (RF-CA). Intracardiac mapping showed that the earliest activation site was situated in the asynergic area of the left ventricle (LV) and radiofrequency catheter ablation directed at the LV asynergy area completely eliminated the VPCs without any complications. During the follow-up period (6 months), she was free from palpitation and VT was not clinically documented.
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ranking = 0.48026889023563
keywords = potassium
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9/76. Depressive state and paresthesia dramatically improved by intravenous MgSO4 in Gitelman's syndrome.

    A 69-year-old woman was referred to our department for evaluation of hypokalemia, which had been treated by oral potassium for more than ten years. She complained of headache, knee joint pain, sleeplessness and paresthesia in extremities and, most prominently, depression. Laboratory data suggested Gitelman's syndrome, which is caused by mutations in the gene encoding the thiazide-sensitive Na-Cl cotransporter. Direct sequencing of the gene in this patient revealed homozygous mutation R964Q in exon 25. Intravenous supplement of MgSO4 dramatically improved both the depression and the paresthesia, suggesting that hypomagnesemia played a role in the clinical manifestations.
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ranking = 0.48026889023563
keywords = potassium
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10/76. Electrocardiographic manifestations: electrolyte abnormalities.

    Because myocyte depolarization and repolarization depend on intra- and extracellular shifts in ion gradients, abnormal serum electrolyte levels can have profound effects on cardiac conduction and the electrocardiogram (EKG). Changes in extracellular potassium, calcium, and magnesium levels can change myocyte membrane potential gradients and alter the cardiac action potential. These changes can result in incidental findings on the 12-lead EKG or precipitate potentially life-threatening dysrhythmias. We will review the major electrocardiographic findings associated with abnormalities of the major cationic contributors to cardiac conduction-potassium, calcium and magnesium.
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ranking = 0.96053778047127
keywords = potassium
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