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Rhabdomyolysis in hypokalaemic periodic paralysis: a clue to the mechanism that terminates the paralytic attack?

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Summary

The changes in serum levels of myoglobin (Mb) and creatine kinase (CK) during a spontaneous attack of hypokalaemic periodic paralysis were studied. During paralysis, serum Mb and CK were normal. A rise in plasma potassium, resulting in clinical recovery, was associated with a simultaneous rise in serum Mb, and followed by a rise in serum CK. It is postulated that hypokalaemia might cause muscle ischaemia, which would result in an accumulation of free fatty acids (FFA) within the muscle cells. High concentrations of FFA may induce molecular changes and increase the permeability of the sarcolemma. This might be the mechanism by which potassium is released from muscle cells into the circulation and muscle membrane excitability is restored.

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References

  1. Adams RJ, Cohen DW, Gupte S, Johnson JD, Wallick ET, Wang T, Schwartz A (1979) In vitro effects of palmityl carnitine on cardiac plasma membrane N+, K+—ATPase and sarcoplasmic reticulum Ca++-ATPase and CA transport. J Biol Chem 254:12404–12410

    Google Scholar 

  2. Brooke MH, Carroll JE, Davis JE, Hagberg JM (1979) The prolonged exercise test. Neurology 29:636–643

    Google Scholar 

  3. Buruma OJS, Schipperheyn JJ (1981) Periodic paralysis. In: Vinken PJ, Bruyn GW (eds) Handbook of clinical neurology, vol. 41. North Holland, Amsterdam, pp 147–174

    Google Scholar 

  4. Falholt K, Falholt W (1984) Metabolism in ischemic muscles before and after treatment with glucose-insulin-potassium infusion. Acta Med Scand [Suppl] 687:77–83

    Google Scholar 

  5. Florence JM, Fox PT, Planer J, Brooke MH (1985) Activity, creatine kinase, and myoglobin in Duchenne muscular dystrophy: a clue to etiology? Neurology 35:758–761

    Google Scholar 

  6. Hofmann WW, Adornato BT, Reich H (1983) The relationship on insulin receptors to hypokalemic periodic paralysis. Muscle Nerve 6:48–51

    Google Scholar 

  7. Horn GV, Drori JB, Schwartz FD (1970) Hypokalemic myopathy and elevation of serum enzymes. Arch Neurol 22:335–341

    Google Scholar 

  8. Johnsen T (1977) Trial of prophylactic effect of diazoxide in the treatment of familial periodic hypokalemia. Acta Neurol Scand 56:525–532

    Google Scholar 

  9. Johnsen T (1981) Familial periodic paralysis with hypokalaemia. Dan Med Bull 28:1–27

    Google Scholar 

  10. Knochel JP, Schlein EM (1972) On the mechanism of rhabdomyolysis in potassium depletion. J Clin Invest 51:1750–1758

    Google Scholar 

  11. Kurien VA, Oliver MF (1970) A metabolic cause for arrhythmias during acute myocardial hypoxia. Lancet II:813–815

    Google Scholar 

  12. Maclachlan TK (1932) Familial periodic paralysis. A description of six cases occurring in three generations of one family. Brain 55:47–76

    Google Scholar 

  13. Pennington RJT (1981) Biochemical aspects of muscle disease. In: Walton J (ed) Disorders of voluntary muscle. Churchill Livingstone, Edinburgh, pp 417–447

    Google Scholar 

  14. Van Beaumont W, Strand JC, Petrofsky JS, Hipskind SG, Greenleaf JE (1973) Changes in total plasma content of electrolytes and proteins with maximal exercise. J Appl Physiol 34:102–106

    Google Scholar 

  15. Zierler KL, Andres R (1951) Movement of potassium into skeletal muscle during spontaneous attack in family periodic paralysis. J Clin Invest 36:730–737

    Google Scholar 

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De Keyser, J., Smitz, J., Malfait, R. et al. Rhabdomyolysis in hypokalaemic periodic paralysis: a clue to the mechanism that terminates the paralytic attack?. J Neurol 234, 119–121 (1987). https://doi.org/10.1007/BF00314116

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  • DOI: https://doi.org/10.1007/BF00314116

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