scholarly journals DECREMENTAL RESPONSE ON PROLONGED EXERCISE TEST IN A PATIENT WITH THYROTOXIC PERIODIC PARALYSIS

2022 ◽  
Vol 8 (1) ◽  
pp. 64-67
Author(s):  
Piyush Ostwal ◽  
Maher Alshaheen

Paralysis of acute onset often presents a diagnostic challenge for the assessing physician because of a large number of differential diagnosis and overlap of clinical features among them. Thyrotoxic periodic paralysis is an uncommon cause of acute weakness. In addition to serological tests, electromyography findings during prolonged exercise test are very helpful in confirming the diagnosis. Only a few case reports of thyrotoxic periodic paralysis have been published from Middle East and none of them have described this specific electrophysiological data. A man in his 20s presented to us with acute onset weakness in both legs which was evaluated further and found to have hypokalemia. The work up for the etiology revealed thyrotoxic status and a final diagnosis of thyrotoxic periodic paralysis was established. The prolonged exercise test performed in this patient showed typical progressive decremental respsonse with nadir at 40 minutes after the exercise.

2011 ◽  
Vol 10 (4) ◽  
Author(s):  
Chris Roseveare ◽  

Once again, 12 months seem to have f lown by and we find ourselves at the end of this journal’s 10th Anniversary year. So what will 2012 have in store for us? Will financial chaos send us spiralling into the abyss or will the Olympics and Diamond Jubilee bring back the long-awaited ‘feel good factor’? Maybe the England football team will finally win a trophy, and surely we are due for some decent weather. I prefer to stay optimistic, and believe predictions of ‘barbeque summers’, rather than those of Nostradamus! One thing we can certainly look forward to in 2012 is a ‘silver’ anniversary for SAM – as well as the first to be held overseas, the spring meeting in Dublin will be the 25th held by the Society. I hope that many UK readers will be able to make the short trip across the Irish Sea to attend this special event. The year’s end also brings the cluster of festive bank holidays – 3 in England and 4 for those North of the border, each co-inciding with weekends. Some will take this opportunity to recharge the batteries before the onslaught of January; for others the challenge of 7 day working will be brought back into sharp focus. Many readers will be familiar with the aftermath of these long holiday weekends when it often feels like the whole hospital has ground to a halt. Higher weekend mortality has attracted some Press attention during the past year; this has added weight to those arguing for greater levels of consultant cover outside of traditional working hours. The paper from Dublin, published in this edition, suggests that higher illness severity might contribute to this weekend mortality. The model of medical service is a little different to that which operates in most UK hospitals, but the findings are still of interest. Does this diminish the need to expand consultant cover? Absolutely not, in my view – sicker patients require more senior care, not less; whether this will inf luence outcome for these patients is yet to be proven, but the principle remains clear. We should strive to provide the same level of care for patients, irrespective of the day on which they are admitted. Achieving this is a bigger challenge – particularly in the current financial climate – which will require close cooperation between SAM and the Royal Colleges. Acute physicians will need to continue on rotas working alongside ‘general’ physicians to achieve this as the numbers gradually expand. Mark Temple, recently appointed as Acute Care Fellow at the Royal College of Physicians of London and writing in this edition, has reiterated the RCPL’s line on this issue; a ‘toolkit’ is being produced in collaboration with SAM to provide practical solutions to this problem. On a lighter note, I hope readers will enjoy the series of clinical articles to be found in this issue. Case reports from both sides of the world document some unusual causes of ‘collapse’, a common reason for admission on the AMU, requiring a broad differential. Serotonin syndrome and thyrotoxic periodic paralysis may not be top of the list of causes, but these articles highlight the need to keep an open mind in such cases. Our problem-based review series continues, with paracetamol overdose and pleural effusions being the subjects on this occasion. Although forming part of the ‘trainee’ section, I am certain that the content will also provide a useful insight into these topics for our many ‘trained’ readers. Finally, I would like to take this opportunity to thank all those who have contributed to the journal over this ‘anniversary’ year – and the previous nine. I am particularly grateful for the efforts of the editorial board in helping to make this a ‘quarterly’ publication in 2011. The numbers of contributions continues to rise, as does the quality of submissions, no doubt fuelled by the recent listing of the journal in Medline. As a consequence we are still looking to expand our pool of expert referees, so please contact me at the email address on this page, indicating any specific areas of interest / expertise, if you are able to help. Wishing all readers a happy Christmas and New Year


Author(s):  
E Rasheed ◽  
J Seheult ◽  
J Gibney ◽  
G Boran

Thyrotoxic periodic paralysis is a rare complication of hyperthyroidism where increased influx of potassium into skeletal muscle cells leads to profound hypokalaemia and paralysis. Most cases arise sporadically in Asians; however, it is being increasingly reported in Caucasians. It is regarded as a channelopathy where a genetic and/or acquired defect in the sodium-potassium (Na/K-ATPase) pump renders it more sensitive to excess thyroid hormone in susceptible individuals. Because the clinical presentation is similar to familial hypokalaemic periodic paralysis, genes implicated in this autosomal-dominant condition became candidates for thyrotoxic periodic paralysis, particularly if they were known to have thyroid hormone-responsive elements. These include the voltage-gated calcium (CACNA1S) and sodium (SCN4A) channel genes, KCNJ18 which encodes the inwardly rectifying potassium channel Kir2.6, and subunits of the Na/K-ATPase genes. Although no single pathogenetic mutation has been identified in thyrotoxic periodic paralysis, several single-nucleotide polymorphisms in these genes have been associated with it. We describe a 27-year-old Caucasian Irish male who presented with acute onset limb paralysis and severe hypokalaemia. He was diagnosed as having thyrotoxic periodic paralysis secondary to Graves’ disease based on clinical presentation, biochemical findings and rapid response to intravenous potassium. Genetic analysis identified heterozygous variants in three candidate genes: KCNJ18 (c.576G>C), SCN4A (c.2341G>A) and CACNA1S (c.1817G>A). Since these variants are not disease causing and occur at high prevalences of 50%, 2–3% and 1%, respectively, in the normal population, they do not explain the clinical phenotype in our patient suggesting that acquired environmental triggers or as-yet unidentified gene mutations remain as leading pathogenetic co-factors in thyrotoxic periodic paralysis.


2009 ◽  
Vol 120 (2) ◽  
pp. e95
Author(s):  
S. Kim ◽  
H. Kim ◽  
S. Oh ◽  
J. Sung ◽  
Y. Hong ◽  
...  

2015 ◽  
Vol 24 (3) ◽  
pp. 264-267 ◽  
Author(s):  
Denise L. Shields

Thyrotoxic periodic paralysis is an acute endocrine emergency characterized by hyperthyroidism, profound muscle weakness and/or paralysis, and hypokalemia that is not due to potassium deficiency. Typically described in young males of Asian descent, it is becoming increasingly recognized outside of this demographic group and is believed to be an underrecognized cause of symptomatic hypokalemia. Thyrotoxic periodic paralysis usually manifests as acute onset of symmetrical distal extremity weakness and is treated with careful potassium replacement and nonselective β-blockers. In this case, a 43-year-old African American woman with thyrotoxic periodic paralysis had recurrent lower extremity myopathy and acute respiratory failure precipitated by noncompliance with treatment for Graves disease.


1992 ◽  
Vol 15 (10) ◽  
pp. 1069-1071 ◽  
Author(s):  
Carlayne E. Jackson ◽  
Richard J. Barohn

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