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Thyrotoxic periodic paralysis in western countries
  1. R Sinharay
  1. Tameside General Hospital, Fountain Street, Ashton-Under-Lyne, Lancashire OL6 9RW, UK; ranjitsinharay{at}hotmail.com

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    I read with interest the case report by Dixon and Jones on thyrotoxic periodic paralysis (TPP) in a white woman.1 TPP is, indeed, extremely rare in women and also in the white population. However, TPP is an extremely common presentation with hypokalaemia in Orientals.2 It is imperative that any person of Oriental origin presenting with hypokalaemic weakness has their thyroid status checked2; doctors are quite likely to face this situation in the west because of increased immigration.

    Attacks of TPP are very common in the early hours of the night,3 but unfortunately there was no mention of the time of occurrence in the case reported.1

    The authors confirmed that their patient did not require β-blockers, yet this is standard practice in this condition as potassium replacement in this sort of hypokalaemia can cause rebound hyperkalaemia.4 I agree that the signs and symptoms of thyrotoxicosis in TPP may be subtle in the west, but this is in contradiction to the Asian experience.4

    It is, indeed, puzzling as to why there is a male predominance in TPP with hypokalaemia, while Graves’ disease is more common in females. It is, however, more puzzling as to why there is a racial difference in this condition. I agree with the authors that there may be a difference in the HLA subtypes. HLA subtypes in different ethnic groups with TPP have been widely studied. HLA DRw8 makes the Japanese more susceptible to TPP,1 and yet the same HLA subtype in the white population make them susceptible to Graves’ disease, but without periodic paralysis.5 This phenomenon contradicts the authors’ view that there may be a difference in the HLA subtypes and whether one would develop TPP or not, with the background of Graves’ disease. Within the same HLA subtype, a genetic mutation in the control of sodium-potassium ATPase activity or some other environmental factor may be the explanation.

    I certainly cannot agree with the view that once these patients are euthyroid that they are not at increased risk of hypokalaemic paralysis. Control of Graves’ disease with antithyroid drugs is very variable. Altogether 70% may relapse during the course of treatment, and therefore are at risk of developing TPP. Therefore, it has been suggested that I131 ablation in TPP may need to be carried out, irrespective of age at presentation, because of the dangers of severe hypokalaemia. However, the caveat is that even in this group of ablated patients there is a risk of paralytic episodes, even with thyroxine replacement, which invariably this group will require in the longer term.

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    Authors’ reply

    We welcome the comments made by Sinharay. They certainly highlight some of the controversies surrounding this condition that we raised in the case presented. We certainly agree that all patients presenting with hypokalaemic paralysis should have their thyroid status checked as, especially in white patients, signs and symptoms of thyrotoxicosis may be subtle and therefore we hightlighted this is the summary points.

    This patient did in fact present in the evening. We were not involved in the patient’s initial management, but we find it hard to criticise the initial treatment by on-call doctors to use oral and intravenous potassium supplements as the diagnose of thyrotoxicosis had not been made (and was not suspected) and thyroid function tests (TFTs) are not available out-of-hours. Serum potassium levels were closely monitored. The results from TFTs were only received two days later when the patient was normokalaemic and off potassium supplements. We do agree that there is a risk of hyperkalaemia by using this potassium supplements and therefore highlighted this in our discussion.

    We welcome Sinharay’s comments on the puzzling male predominance of TPP in a condition that has a female preponderance and that any explanations at present are speculative.

    Sinharay disagrees with our comment that when patients are euthyroid they are not at risk of hypokalaemic paralysis. This is contrary to previous experience.1,2 However, we do agree that patients are at risk of hypokalaemic paralysis if thyrotoxicosis reoccurs. As there is a risk of relapse of hypokalaemic paralysis with recurrence of thyrotoxicosis we agree that there is a case to be made for early definitive treatment.

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