scholarly journals Does thyrotoxic periodic paralysis have a genetic predisposition? A case report

2018 ◽  
Vol 55 (6) ◽  
pp. 713-716 ◽  
Author(s):  
E Rasheed ◽  
J Seheult ◽  
J Gibney ◽  
G Boran
Keyword(s):  
Thyroid Hormone ◽  
Clinical Presentation ◽  
Normal Population ◽  
Rare Complication ◽  
Gene Mutations ◽  
Periodic Paralysis ◽  
Acute Onset ◽  
Nucleotide Polymorphisms ◽  
Thyrotoxic Periodic Paralysis ◽  
Inwardly Rectifying Potassium Channel

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.

A Case of Thyrotoxic Periodic Paralysis With Respiratory Failure in an African American Woman

2015 ◽  
Vol 24 (3) ◽  
pp. 264-267 ◽  
Author(s):  
Denise L. Shields
Keyword(s):  
African American ◽  
Respiratory Failure ◽  
African American Woman ◽  
American Woman ◽  
Periodic Paralysis ◽  
Acute Onset ◽  
Thyrotoxic Periodic Paralysis ◽  
Young Males ◽  
Demographic Group ◽  
Potassium Replacement

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.

scholarly journals Thyrotoxic Periodic Paralysis with Hypokalemia in an Adult Male from Nepal: A Case Report

2019 ◽  
Vol 57 (220) ◽  
Author(s):  
Sabina Khadka ◽  
Indu K.C. ◽  
Rabindra Jang Rayamajhi ◽  
Pravakar Dawadi ◽  
Pravash Budhathoki
Keyword(s):  
Rare Complication ◽  
Sudden Onset ◽  
Thyroid Stimulating Hormone ◽  
Periodic Paralysis ◽  
High Serum ◽  
Thyrotoxic Periodic Paralysis ◽  
Potential Harm ◽  
Chief Complaints ◽  
High Index Of Suspicion ◽  
Thyrotoxic Hypokalemic Periodic Paralysis

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.

HYPERTHYROIDISM: LOOKING BEYOND PHYSICIAN'S PERSPECTIVE

2020 ◽  
Vol 4 (12) ◽  
Author(s):  
Meghna Prashant Nair ◽  
Shubhi Shubhangi Bhatnagar ◽  
Ansh Chaudhary ◽  
Bhupendra Chaudhary
Keyword(s):  
Central Nervous System ◽  
Clinical Presentation ◽  
Strong Association ◽  
Periodic Paralysis ◽  
Neurological Manifestations ◽  
Thyrotoxic Periodic Paralysis ◽  
Hypermetabolic State ◽  
Physician’S Perspective ◽  
Low Serum ◽  
Proximal Myopathy

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.

Thyrotoxic periodic paralysis: a rare complication of hyperthyroidism for 21-year-old male.

2018 ◽  
Author(s):  
Modesta Petraviciute ◽  
Gintare Naskauskiene ◽  
Vigantas Dunauskas ◽  
Zydrune Visockiene
Keyword(s):  
Rare Complication ◽  
Periodic Paralysis ◽  
Thyrotoxic Periodic Paralysis

scholarly journals THYROTOXIC PERIODIC PARALYSIS A RARE COMPLICATION OF HYPERTHYROIDISM

CHEST Journal ◽  
2020 ◽  
Vol 158 (4) ◽  
pp. A925
Author(s):  
Moeez Qureshi ◽  
Dharam Patel ◽  
Purnadeo Persaud
Keyword(s):  
Rare Complication ◽  
Periodic Paralysis ◽  
Thyrotoxic Periodic Paralysis

scholarly journals A Case of Recurrent Paralysis and Low Potassium: Is It the Thyroid?

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A909-A909
Author(s):  
Justin Do ◽  
Hoveda Mufti
Keyword(s):  
Radioactive Iodine ◽  
Rare Complication ◽  
Periodic Paralysis ◽  
Definitive Treatment ◽  
Free T4 ◽  
Thyrotoxic Periodic Paralysis ◽  
Sodium Potassium ◽  
Potassium Atpase ◽  
Hispanic Male ◽  
Hyperthyroid Patients

Abstract Introduction: Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that is characterized by episodes of hypokalemia and acute weakness. Although hyperthyroidism is more common in females, over 95% of cases of TPP have been observed in males, especially in Asian males with an incidence of 2% among hyperthyroid patients. In non-Asian populations, the incidence in hyperthyroid patients is estimated to be around 0.1 to 0.2% [1]. We describe a case of TPP seen in a Hispanic male. Case Report: A 36-year-old Hispanic male with no past medical history presents with weakness in all extremities and difficulty breathing after consuming a carbohydrate heavy meal the night prior. He reports a recent, similar episode evaluated in another ER, which resolved after given potassium supplementation. He denied any vomiting, diarrhea, polyuria, diaphoresis, use of insulin or other medications, or any family history of paralysis. His labs were significant for hypokalemia of 1.9, TSH of &lt;0.005 (0.358-3.740), free T4 of 2.22 (0.76-1.46), and total T3 of 2.7 (0.60-1.81). Thyroid stimulating immunoglobulin was 0.12 (0.0-0.55). His symptoms improved and potassium levels normalized following the administration of potassium chloride. He was discharged on propranolol and advised to follow up for further workup of his hyperthyroidism with radioactive iodine uptake scan. Discussion: Thyrotoxic periodic paralysis is a potentially life-threatening condition associated with cardiac arrhythmias and respiratory failure. Hyperthyroidism increases response to β-adrenergic stimulation, which increases activity of the sodium-potassium ATPase and causes hyperpolarization of skeletal muscle [2]. Hyperthyroid patients are prone to episodes of paralysis due to their increased susceptibility to the hypokalemic action of insulin, which activates the sodium-potassium ATPase pump, and epinephrine, which stimulates β-adrenoreceptors. Management of an acute attack of TPP includes potassium administration. In cases where paralysis and hypokalemia are not reversed, intravenous propranolol has been shown to resolve the attack by blocking the β-adrenergic receptors. Definitive treatment of TPP includes managing the hyperthyroid state with medical therapy, radioactive iodine therapy, or surgery. Until the euthyroid state is reached, a β-blocker can prevent episodes of acute paralysis. Avoidance of carbohydrate heavy meals, exercise, and stress are recommended as these factors can potentially exacerbate hypokalemia. In patient with acute paralysis, it is important to consider the diagnosis of TPP as this condition can be prevented once euthyroidism is achieved. Diagnosis and management will lead to prevention of morbidity and mortality associated with the hypokalemia. References: 1.Vijayakumar A, et al. J Thyroid Res. 2014;2014:649502. 2.Layzer RB. Annals of Neurology. 1982;11(6):547–552.

scholarly journals THYROTOXIC PERIODIC PARALYSIS IN A COMPETITIVE BODYBUILDER WITH THYROTOXICOSIS FACTITIA

2020 ◽  
Vol 6 (5) ◽  
pp. e252-e256
Author(s):  
Amy J. Patel ◽  
Stephanie Tejera ◽  
Stanislaw P. Klek ◽  
Gary D. Rothberger
Keyword(s):  
Thyroid Hormone ◽  
Muscle Weakness ◽  
Potassium Level ◽  
Periodic Paralysis ◽  
Free Thyroxine ◽  
Thyroid Peroxidase ◽  
Fluid Restriction ◽  
Thyrotoxic Periodic Paralysis ◽  
Thyroxine Level ◽  
Free Thyroxine Level

Objective: We report a case of thyrotoxic periodic paralysis (TPP) in a bodybuilder who developed paralysis secondary to thyrotoxicosis factitia after taking a supplement containing thyroid hormone. Interestingly, the patient had no intrinsic thyroid disease. Prompt recognition of thyrotoxicosis is critical to avoid progression of paralysis and subsequent complications. Methods: We discuss a 27-year-old body builder who presented after a 3-day bodybuilding competition with sudden upper and lower extremity paralysis. He admitted to taking anabolic steroids, a supplement containing an unknown amount of thyroid hormone for 2 weeks, and furosemide 40 mg twice daily with near-complete fluid restriction for 3 days. Results: Laboratory results showed a thyroid-stimulating hormone (TSH) level of <0.010 μIU/mL (normal, 0.3 to 5.8 μIU/mL), normal total triiodothyronine level, elevated free thyroxine level of 3.6 ng/dL (normal, 0.8 to 1.9 ng/dL), and potassium level of 1.9 mEq/L (normal, 3.7 to 5.2 mEq/L). Thyroid peroxidase antibody, thyroid-stimulating immunoglobulin, and thyroglobulin antibody levels were normal. Thyroid uptake was 1% (normal, 8 to 25%) after administration of I-123 and thyroglobulin level was 9 ng/mL (normal, 1.4 to 29.2 ng/mL). The patient was treated with normal saline infusion, magnesium supplementation and a total of 230 mEq of potassium within 12 hours of hospitalization. Muscle weakness resolved within this time period and potassium level normalized. By the third day of hospitalization free thyroxine level also normalized and TSH improved to 0.1 mIU/L. Conclusion: TPP is a rare complication of thyrotoxicosis that should be considered in bodybuilders who are presenting with acute muscle weakness.

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
Keyword(s):  
Exercise Test ◽  
Prolonged Exercise ◽  
Case Reports ◽  
Final Diagnosis ◽  
Periodic Paralysis ◽  
Acute Onset ◽  
Diagnostic Challenge ◽  
Serological Tests ◽  
Thyrotoxic Periodic Paralysis ◽  
Work Up

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.

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