scholarly journals Hypokalemic thyrotoxic periodic paralysis in a young Serbian male

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.

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A966-A967
Author(s):  
Bishow Chandra Shrestha ◽  
Chheki Sherpa ◽  
Swarup sharma Rijal ◽  
Vasudev Magaji ◽  
Vinita Singh

Abstract Background: Thyrotoxic periodic paralysis (TPP) is a rare but serious thyroid emergency characterized by hypokalemia, acute onset flaccid paralysis & thyrotoxicosis. Typically, seen in an Asian male with untreated hyperthyroidism symptoms, who awakens at night or in the early morning with flaccid ascending paralysis. This is precipitated by exercise, alcohol or carbohydrate rich meal. TPP is widely reported & studied in Asian population. Its prevalence is about 2 % in Asian hyperthyroid patients. However, incidence is 0.1-0.2% in non-Asian hyperthyroid patients. Clinical Case: 33-year-old Caucasian male with celiac disease and no thyroid disease sought emergency care for complaints of sudden onset severe weakness in all extremities. He reported 20-pound unintentional weight loss, intermittent palpitations and low-grade fever. He noticed leg cramps with numbness and unable to move his extremities. At initial evaluation, he had acute flaccid paralysis and tachycardia. Initial laboratory studies showed potassium at 1.9 mmol/l, Magnesium at 1.8, suppressed TSH <0.005 uIU/ml with elevations in free T4 at 2.43 ng/dl and total T3 at 1.9 ng/ml. CT and MRI head were normal. Patient’s aldosterone level was normal. The patient’s paralysis and hypokalemia resolved after potassium replacement. Thyroid stimulating immunoglobulin was elevated and increased vascularity suggestive of Grave’s disease noted on thyroid Ultrasound. Methimazole and propranolol were initiated. His neurological workup was negative. After resolution of paralysis and hypokalemia he was discharged home. Since our patient presented with severe hypokalemia, flaccid paralysis and hyperthyroidism, that resolved promptly with potassium replacement, hence likely diagnosis of thyrotoxic periodic paralysis. Discussion: Thyrotoxic periodic paralysis is potentially reversible and mostly seen with Graves’ disease among Asian population. Early diagnosis & treatment prevents life threatening complications. Differential diagnosis of TPP includes familial periodic paralysis, Guillain-Barre Syndrome & acute intermittent porphyria. Diagnosis is based on family history, characteristic presentation, hyperthyroidism with low serum potassium level. Possible mechanism is increased sodium-potassium ATPase activity in the skeletal muscle membrane leading to intracellular shift of potassium causing hypokalemia and muscle inexcitability. Treatment includes potassium replacement, nonselective beta-blocker and definitive treatment of hyperthyroidism, to prevent further episodes.


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.


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.


2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Chatchon Kaewkrasaesin ◽  
Patinut Buranasupkajorn ◽  
Paisith Piriyawat ◽  
Sarat Sunthornyothin ◽  
Thiti Snabboon

Thyrotoxic periodic paralysis is an unusual neurological manifestation of thyrotoxicosis, and even rarer when it occurs in thyrotropin-secreting pituitary adenoma, only 6 cases having been previously reported. We describe a case of pituitary microadenoma with clinical syndromes of thyrotoxicosis complicated with hypokalemic periodic paralysis. Clinical manifestations and proposed management are discussed.


2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Sarawut Summachiwakij ◽  
Issac Sachmechi

Hyperthyroidism can result in several musculoskeletal conditions such as thyrotoxic periodic paralysis, thyrotoxic myopathy, and thyroid ophthalmopathy. Rhabdomyolysis has been rarely reported to be associated with hyperthyroidism. We describe a 33-year-old man who presented with bilateral thigh pain and dark brown urine after regular squatting. He had a past medical history of hyperthyroidism but stopped taking it 2 months prior to admission. He was found to have rhabdomyolysis, myoglobinuria, and thyrotoxicosis. Presence of thyroid-stimulating immunoglobulins (TSI) and high radioiodine uptake confirmed a diagnosis of Graves' disease. He received aggressive fluid resuscitation and sodium bicarbonate intravenously along with monitoring fluid and electrolyte. Methimazole was also resumed. The patient responded to treatment and rhabdomyolysis gradually resolved. Therefore, nonstrenuous exercise can potentially induce rhabdomyolysis in patients with hyperthyroidism. Although hyperthyroidism is not widely recognized as a cause of rhabdomyolysis, it should be considered in the differential diagnosis of rhabdomyolysis.


CJEM ◽  
2014 ◽  
Vol 16 (03) ◽  
pp. 247-251 ◽  
Author(s):  
Fu-Chiang Yeh ◽  
Wen-Fang Chiang ◽  
Chih-Chiang Wang ◽  
Shih-Hua Lin

ABSTRACT Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by β2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled β2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP.


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.


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