HYPERTHYROIDISM: LOOKING BEYOND PHYSICIAN'S PERSPECTIVE

Author(s):  
Meghna Prashant Nair ◽  
Shubhi Shubhangi Bhatnagar ◽  
Ansh Chaudhary ◽  
Bhupendra Chaudhary

Hyperthyroidism with its excess circulatory thyroid hormones commonly presents with systemic features like palpitation, weight loss and heat intolerance. This hyperadrenergic, hypermetabolic state with its peripheral and central nervous system affection produces protean neurological manifestations which are generally overlooked by internist. Features of neuropsychiatric nature, cognitive impairment, and dementia movement disorder like tremors or chorea may be presentation of undetected hyperthyroidism. Affliction for muscles presents with proximal myopathy with or without myalgia in 50-70% of long standing hyperthyroid state. Similarly thyrotoxic periodic paralysis due to low serum potassium in adult male is often misdiagnosed as Guillain-Barré syndrome, however replacement of potassium drastically reverse the condition. There is a strong association between autoimmune thyroiditis and ocular myesthenia which post difficulties in clinical diagnosis. Despite of so much variability in clinical presentation attainment of euthyroid state coupled with beta blocker in many situations is helpful to resolve most of the issues. Keywords: Hyperthyroidism, Grave's, Tremors, Myopathy, Periodic paralysis.

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.


2020 ◽  
Vol 77 (4) ◽  
pp. 440-444
Author(s):  
Petar Ristic ◽  
Tamara Dragovic ◽  
Sasa Kikovic ◽  
Dragana Ristic ◽  
Marija Zdravkovic ◽  
...  

Introduction. Hypokalemic thyrotoxic paralysis is a very rare form of periodic paralysis in Caucasian population. In this population, a more frequent form is familiar hypokalemic periodic paralysis with the same clinical presentation. It is flaccid paralysis of proximal muscles in extremities. Having in mind that clinical presentation of hyperthyroidism in these patients is milder than it could be expected with given values of thyroid hormones, differential diagnosis to other forms of hypokalemic paralysis is essential. Case report. We presented a case of a young male with hyperthyroidism and severe periodic flaccid paralysis particularly of leg muscles. Laboratory findings showed elevated thyroid hormones levels and hypokalemia during the attacks with normalized potassium levels between attacks. The patient had no relatives with the similar condition. Also, he never had anything like these attacks prior to development of hyperthyroidism. After differential diagnosis, other reasons for hypokalemic periodic paralysis were excluded. We intensified the hyperthyroidism treatment and resolved hypokalemic periodic paralysis attacks with potassium chloride (KCl) infusions. The patient was advised to start a definitive treatment of hyperthyroidism after stabilization of hormonal levels. Conclusion. Hypokalemic thyrotoxic paralysis is a rare and potentially dangerous condition which, if recognized, can be prevented by resolving hyperthyroxinemia and the use of nonselective ? blockers.


2012 ◽  
Vol 2012 ◽  
pp. 1-2
Author(s):  
Andrew Word ◽  
Kevin Davidson ◽  
Essam Elsayed

Thyrotoxic induced hypokalemic periodic paralysis is a rare disorder that had been described in middle-aged men, predominantly Asians and Hispanics. This case presented with generalized weakness and hypokalemia after changing prescription for levothyroxine and starting prednisone to treat upper respiratory infection in a previously asymptomatic middle-aged Hispanic male. In this paper, we will go over the clinical presentation, mechanisms, and treatment of thyrotoxic induced hypokalemic periodic paralysis. Our objectives are to identify the classic constellation of findings in thyrotoxic periodic paralysis and to recognize the importance of considering thyrotoxic periodic paralysis among patients with hypokalemia.


2019 ◽  
Author(s):  
Sing Yee Sim ◽  
Michael Pierides ◽  
Kishor Patel ◽  
Hamidreza Mani

Author(s):  
Ayca Inci ◽  
Ali Rıza Caliskan ◽  
Melahat Coban ◽  
Refik Olmaz ◽  
Suheyla Ayca Gulenay ◽  
...  

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