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Hypokalaemic paralysis
  1. A S KASHYAP
  1. Department of Medicine
  2. Department of Hospital Administration
  3. Armed Forces Medical College, Pune 411040, India
    1. SUREKHA KASHYAP
    1. Department of Medicine
    2. Department of Hospital Administration
    3. Armed Forces Medical College, Pune 411040, India
      1. SUSHIL K AHLAWAT
      1. 89-50 56th Ave, #2J, Elmhurst, NY11373, USA

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        Sir,Ahlawat et al,1 in their excellent review, fail to mention the presence of hypophosphataemia and mild hypomagnesaemia in thyrotoxic periodic paralysis (TPP). In a retrospective review of 24 episodes of TPP in 19 patients, Manoukian et al,2 found hypokalaemia in all patients. In addition, a mild to moderate hypophosphataemia (serum phosphorus 0.36–0.77 mmol/l; normal levels 1.0–1.4 mmol/l), was noted in 12 of 15 episodes when serum phosphorus was measured within 1.5 h of hospital admission or while the potassium level was still low. Neutra-phos was administered in only four episodes; nevertheless, serum phosphorus returned to normal, or was slightly elevated after paralysis was resolved in all episodes evaluated. Hypophosphataemia during paralysis in patients with TPP has been previously reported3 and may contribute to muscle weakness along with hypokaelemia. Phosphorus is a major intracellular anion, and its influx into and efflux from the cell most probably occurs in conjunction with potassium transport. Hypophosphataemia and hypokalaemia are well known causes of rhabdomyolysis, and the mild elevation of creatine kinase concentration seen by Manoukian et al 2 in 12 of 18 episodes may be related to the low serum phosphorus and potassium levels.

        Mild hypomagnesaemia was noted2 in all 19 patients during paralysis, with an increase of 0.1 mmol/l or more after resolution of paralysis. This has also been observed by other workers.4Endogenous catecholamines may contribute to hypomagnesaemia during stress without depleting total body stores of magnesium by causing an intracellular shift in magnesium. Yeo et al 5 found that four of 10 patients with TPP had an increase in skeletal muscle magnesium content during paralysis.

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        This letter was shown to the authors who responded as follows:

        Sir,In response to the comments of Dr Kashyapet al on our article,1-1 I would like to point out that although hypophosphataemia and hypomagnesaemia have been reported in patients with thyrotoxic periodic paralysis (TPP), this reporting has been inconsistent. On the other hand, hypokalaemia is considered to be the most consistent electrolyte abnormality in TPP and a hallmark of the syndrome, along with hyperthyroidism. The retrospective review by Manoukianet al 1-2 is the only study in which hypophosphataemia and hypomagnesaemia were seen in a large number of cases. This was a hospital-based study and out of 30 patients seen, only 19 could be included because metabolic data were not available for the remaining patients. There are only a few other case reports which mention these electrolyte abnormalities (hypophosphataemia, hypomagnesaemia) in TPP.1-3-1-5 Because of inconsistent observations and the lack of prospective data, their therapeutic implication remains unclear.

        References

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