scholarly journals A Case of Thyrotoxic Periodic Paralysis

2013 ◽  
Vol 12 (3) ◽  
pp. 320-321
Author(s):  
George Sarin Zacharia ◽  
Rajakumari PK

Hypokalemic periodic paralysis is an uncommon manifestation of thyrotoxicosis and the condition is most commonly reported in young Asian men. Patient often presents with acute onset symmetrical flaccid muscle paralysis and proximal limb muscles may be more severely involved compared to distal muscles. Thyroid swelling as well as features of thyrotoxicosis may not be overt. A very high index of suspicion is often required for the diagnosis of thyrotoxic periodic paralysis. Treatment of throtoxicosis prevents further episodes of paralysis. We report a case of thyrotoxic periodic paralysis in a young male.Bangladesh Journal of Medical Science Vol. 12 No. 03 July ’13 Page 320-321 DOI: http://dx.doi.org/10.3329/bjms.v12i3.12719 

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.


2021 ◽  
Vol 8 (8) ◽  
pp. 1229
Author(s):  
Pranav Ravi Kulkarni ◽  
Jagadeesan M. ◽  
Mariraj I. ◽  
Prasanna Karthik S.

Thyrotoxic periodic paralysis (TPP) is a rare etiology for muscle paralysis. It is frequently seen in Asian men. Apart from paralysis, most of them are asymptomatic and are devoid of other clinical features of hyperthyroidism. Due to the rarity of this condition, it is often missed and hence fatal. The metabolic derangement seen in TPP is hypokalemia and is thought to be the pathogenesis of the muscle paralysis. Although in rare clinical encounters, patients with TPP may present with normokalemia. The disorder usually presents in the 3rd decade. The cause for mortality in patients with TPP may be due to respiratory muscle paralysis leading to compromise of the respiratory function or refractory arrhythmias due to hypokalemia. Here we report a rare case of TPP with normokalemia. 


Author(s):  
Ajith Dungdung ◽  
Vishwanath Malkappa Jalawadi ◽  
Upendra Prasad Yadav

Background: Hypokalemic periodic paralysis (HPP) is a rare autosomal dominant channelopathy characterised by muscle weakness or paralysis when there is a fall of potassium level in the blood. In individuals with mutation, attack begins during adolescents and most commonly occurs after sleep on awakening, rest after strenuous exercise, high carbohydrate diet and meal with high sodium content. This study was conducted to analyse the age of incidence and prevalence of HPP with various clinical presentations, diagnosis and its effective treatment.Methods: A retrospective analysis of 50 patients of Hypokalemic periodic paralysis was analysed in tertiary care centre “Rajendra institute of medical science” Ranchi, Jharkhand, India, with reference to its clinical presentation, age of incidence and prevalence with laboratory parameters and treatment outcomes.Results: Incidence of attack is more common in men between 26-35 years of age. Sudden onset of flaccid quadriparesis was the most common presentation with history of high carbohydrate diet on the background of strenuous work during summer season. Around 60% had similar history of attacks in the past and most of the patients had serum potassium levels between 2.1-3.0mEq/L. Electrocardiography (ECG) abnormalities associated with hypokalemia had been observed in 90% of patients, and also significant clinical, biochemical changes have been observed as well.Conclusions: Early diagnosis not only helps in definitive management with potassium replacement, but also prevents patient going for life threatening respiratory failure.  Patients recover completely without any clinical sequelae. Therefore, it is imperative for physicians, particularly those working in acute care settings, to be aware of this condition. Further management depends on the cause, frequency of attacks, severity of symptoms and the duration of the illness.


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.


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.


2019 ◽  
Vol 57 (220) ◽  
Author(s):  
Sabina Khadka ◽  
Indu K.C. ◽  
Rabindra Jang Rayamajhi ◽  
Pravakar Dawadi ◽  
Pravash Budhathoki

Thyrotoxic periodic paralysis is rare complication of hyperthyroidism characterized by the sudden onset of hypokalemia and muscle paralysis. It is typically present in young Asian males. There are very few literatures regarding the occurrence of thyrotoxic hypokalemic periodic paralysis in Nepal. We reported a case of a 35-year-old male presented with the chief complaints of weakness of all four limbs of 1 day duration. He was diagnosed as a case of hyperthyroidism in the past, received treatment for 6 months and left medications on his own 6 months ago. Evaluation during admission revealed severe hypokalemia with serum potassium level 1.3mEq/l and high serum Triiodothyronine (>20.00µg/L) and low serum Thyroid Stimulating Hormone (<0.01µg/L). Potassium supplements resolved muscle weakness and the patient was restarted with anti-thyroid drugs. Hence, hypokalemic paralysis is a reversible cause of paralysis and high index of suspicion as well as timely interventions are required to prevent potential harm.


2019 ◽  
Vol 12 (10) ◽  
pp. e231241 ◽  
Author(s):  
Farah Gul Khan ◽  
Sidra Namran

Bilateral symmetrical weakness of acute onset is not very uncommon and the differential varies widely from life-threatening neurological illnesses to metabolic and electrolyte derangements. We report the case of a young female with severe muscle weakness, respiratory distress and hypokalemia who required immediate intubation on arrival to emergency department. During hospital course, even after normalisation of serum potassium and some improvement in limb weakness, patient failed multiple attempts of extubation because of type II respiratory failure. Subsequently, acetyl cholinesterase antibodies were checked which came out positive, and diagnosis of myasthenia gravis and hypokalemic periodic paralysis was made. She was successfully extubated after intravenous pulse steroids, pyridostigmine and plasmapheresis. Patient was finally discharged home on oral steroids, pyridostigmine and azathioprine. In a patient presenting with hypokalemic weakness, the suspicion of a second disorder should be very high if weakness fails to resolve following correction of hypokalemia.


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