Of 1,366 consecutive southern Chinese patients with thyrotoxicosis (1,188 females and 178 males) 25 (1.8%) gave a history of attacks of periodic paralysis, and of these 23 (13%) were males and 2 (0.17% were females. Since it proved possible to induce attacks of paralysis in 2 of the 13 male patients without a history of such, there was additionally a group of potential paralytics. It is concluded that the incidence among the Chinese is approximately the same as that reported among the Japanese, yet, strangely, there is a lack of reports of its occurrence. The clinical, biochemical, and electrocardiographic findings during spontaneous and induced attacks are described. In view of the frequency of occurrence of arrhythmias during both forms of attacks it is concluded that attempts to induce attacks should be made only under continuous cardiac monitoring. There are similarities between thyrotoxic periodic paralysis and the familial form. In both there is a preponderance in males, the factors which induce attacks are the same, and if the manifestations of thyrotoxicosis are excluded the clinical pictures during attacks are identical. The biochemical changes are similar. There is retention of water and sodium without alteration in serum sodium concentration. There is invariably a fall in serum potassium concentration, associated with a proportional reduction in the potassium excreted in the urine. There is no evidence of excessive potassium loss in the stools. The response of attacks of paralysis to treatment is similar, and salts of potassium and aldosterone antagonists are effective in a proportion of patients in preventing the induction of attacks. However, neither of the two forms can be explained solely by a fall in serum potassium concentration. On the other hand, thyrotoxic periodic paralysis differed from the familial form in certain important particulars. In none was there a family history. The age at onset was later and corresponded with the age incidence of thyrotoxicosis. The great majority of attacks occurred in the hot season. Furthermore, the attacks of paralysis occurred only during the period of thyrotoxicosis, and, in the euthyroid state, could no longer be induced even when hypokalaemia was produced by priming with 9-a-fluorohydrocortisone. The occurrence of attacks of paralysis was not related to the duration or the severity of the thyrotoxicosis, and by no available evidence could distinction be made between those with and those without paralysis. This, together with the high incidence among mongoloids, suggests that the basic defect may be genetically determined. But the evidence presented indicates that the 'defect manifests itself only when challenged by thyrotoxicosis. © 1967, British Medical Journal Publishing Group. All rights reserved.
CITATION STYLE
Mcfadzean, A. J. S., & Yeung, R. (1967). Periodic Paralysis Complicating Thyrotoxicosis in Chinese. British Medical Journal, 1(5538), 451–455. https://doi.org/10.1136/bmj.1.5538.451
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