Cardioskeletal mitochondria1 myopathy associated with chronic magnesium deficiency

Riggs, Jack E.; Klingberg, William G.; Flink, Edmund B.; Schochet, Sydney S.; Balian, Axel; Jenkins, Jesse J.

doi:10.1212/wnl.42.1.128

Cited by 33 publications

(13 citation statements)

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“…Our patient also had high CK and LDH levels. Studies have demonstrated that chronic hypocalcemia or hypomagnesemia may cause muscle degeneration (10,11). …”

Section: Discussionmentioning

confidence: 99%

Pseudohypoparathyroidism Presenting with Ventricular Arrhythmia: A Case Report

Işıkay¹,

Akdemir²,

Yılmaz³

2012

jcrpe

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Pseudohypoparathyroidism (PHP) is a rare disorder characterized by varying degrees of unresponsiveness to parathyroid hormone. Patients usually present with hypocalcemia-induced seizures or tetany, whereas no case of hypocalcemia-induced cardiac arrhythmia in PHP has been described to date. In this paper, we report the case of a male adolescent with PHP type 1a who presented with hypocalcemia-induced ventricular extrasystoles (bigeminy, trigeminy) and mild corrected QT interval prolongation. The patient had brachydactyly and his second fingers and toes were longer than the others, a finding consistent with PHP. Laboratory tests detected hypomagnesemia, as well as elevated levels of creatine kinase and lactate dehydrogenase. Ventricular arrhythmia and abnormal laboratory tests improved with calcium supplementation and vitamin D treatment. The findings in this patient suggest that hypomagnesemia may make patients with PHP more susceptible to hypocalcemia and may thus prompt a state of hypocalcemia-induced arrhythmia or other cardiac complications. Key words: Pseudohypoparathyroidism, arrhythmia, child Conflict of interest:None declared.

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“…Our patient also had high CK and LDH levels. Studies have demonstrated that chronic hypocalcemia or hypomagnesemia may cause muscle degeneration (10,11). …”

Section: Discussionmentioning

confidence: 99%

Pseudohypoparathyroidism Presenting with Ventricular Arrhythmia: A Case Report

Işıkay¹,

Akdemir²,

Yılmaz³

2012

jcrpe

View full text Add to dashboard Cite

show abstract

“…However, creatine kinase was found in very high levels due to myopathy despite the presence of hypomagnesemia in the present case. On the other hand, it has been reported that a patient in whom myopathy, both skeletal and cardiac, associated with high levels of serum creatine kinase, was the late manifestation of chronic hypomagnesemia due to renal tubular loss [22]. Since magnesium is necessary for the activation of several mitochondrial enzymes, hypomagnesemia may produce mitochondrial myopathy [22,23].…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, it has been reported that a patient in whom myopathy, both skeletal and cardiac, associated with high levels of serum creatine kinase, was the late manifestation of chronic hypomagnesemia due to renal tubular loss [22]. Since magnesium is necessary for the activation of several mitochondrial enzymes, hypomagnesemia may produce mitochondrial myopathy [22,23]. Although we were unable to make clear the major cause of the myopathy, it may be predominantly due to glycogenosis type II concomitant with chronic hypomagnesemia in the present case.…”

Section: Discussionmentioning

confidence: 99%

Renal Magnesium Wasting, Hypomagnesemic Hypocalcemia, Hypocalciuria and Osteopenia in a Patient with Glycogenosis Type II

Öktenli

2000

Am J Nephrol

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We describe a patient with late-onset glycogenosis type II with renal magnesium wasting, hypomagnesemic hypocalcemia, hypocalciuria and osteopenia. He was admitted to our hospital for evaluation of lower limb weakness and mild deterioration of liver function. Serum magnesium and calcium were low with low-to-normal levels of PTH in the patient. Echocardiogram revealed marked concentric hypertrophy of the left ventricle. An X-ray film of his spine showed a thoracic (Th12) vertebral compression fracture. Bone mineral density of the lumbar spine L2-L4 showed a reduced value. Kidney, liver and muscle biopsies were performed. These were found to have histologic features consistent with glycogenosis type II. In addition, accumulation of PAS-positive material in the cytoplasmic vacuoles of the tubular epithelium was present only in the distal tubules. An oral magnesium supplement was useful in helping to correct the hypomagnesemia, despite the presence of renal magnesium wasting in our patient. Magnesium supplement was also sufficient to maintain normal serum calcium concentrations. However, the hypocalciuria persisted in our patient despite correction of hypomagnesemia. In conclusion, the consistent association between the glycogen accumulation in distal tubules, renal magnesium wasting, hypomagnesemic hypocalcemia and hypocalciuria, in the absence of other identifiable reasons, suggests a cause-and-result relationship. Also, the combination of renal magnesium wasting, hypomagnesemia and hypocalciuria is a picture similar to that of Gitelman's syndrome in our patient. The glycogen accumulation in distal tubules may cause renal magnesium wasting and hypocalciuria through tubular injury. Therefore, we may speculate that the present case has glycogenosis type II-associated Gitelman's-like syndrome.

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“…There have also been occasional reports of an association between hypomagnesaemia of congenital or drug‐induced origin and ‘mitochondrial myopathy’ diagnosed on the basis of limb weakness and muscle biopsies showing ragged red fibres (Klingberg et al. , 1983; Riggs et al. , 1992; Larner et al.…”

Section: Introductionmentioning

confidence: 91%

Isolated familial hypomagnesaemia with novel neurological features: causal link or chance concurrence?

Larner

Williamson

Ward

et al. 2001

Euro J of Neurology

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We report a patient with isolated familial hypomagnesaemia with hypocalciuria, a rare congenital disorder of magnesium metabolism. During adolescence the patient developed neurological and ophthalmological features not hitherto reported in this condition, including seizures, myoclonus, and retinal pigmentary degeneration. These suggested the phenotype of mitochondrial disease, which has been occasionally reported in association with hypomagnesaemia, but subsequent investigations of mitochondrial function were normal. The pathogenesis of this unusual neurological and ophthalmological syndrome therefore remains uncertain.

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Cardioskeletal mitochondria1 myopathy associated with chronic magnesium deficiency

Cited by 33 publications

References 0 publications

Pseudohypoparathyroidism Presenting with Ventricular Arrhythmia: A Case Report

Pseudohypoparathyroidism Presenting with Ventricular Arrhythmia: A Case Report

Renal Magnesium Wasting, Hypomagnesemic Hypocalcemia, Hypocalciuria and Osteopenia in a Patient with Glycogenosis Type II

Isolated familial hypomagnesaemia with novel neurological features: causal link or chance concurrence?

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