Thyrotoxic Periodic Paralysis Research Articles

Thyrotoxicosis and thyrotoxic periodic paralysis in hong kong: a population-based cohort study

Thyrotoxicosis and thyrotoxic periodic paralysis in hong kong: a population-based cohort study

Thyrotoxic Periodic Paralysis after Surgery: A Case Report and Literature Review

Thyrotoxic periodic paralysis (TPP) is a rare but potentially life-threatening muscle disease in a thyrotoxic patient. Due to the lack of knowledge, the diagnosis is easily missed. Diagnosis of TPP is made by documentation of hypokalemia and hyperthyroidism in acute generalized muscle weakness. Hypokalemia is caused by an intracellular shift of potassium because of an increased Na-K-ATPase pump activity and the inhibition of the inward rectifying potassium (Kir) channels. The initial treatment aims to treat potentially life-threatening cardiac arrhythmias caused by severe hypokalemia. This can be done with potassium substitution and nonselective beta-blockers, being aware of the potential of rebound hyperkaliemia. Definitive treatment consists of avoiding triggers and correcting the hyperthyroid state with antithyroid drugs, radioactive iodine, or thyroidectomy. Once patients are, permanently euthyroid complete remission of the paralytic attacks usually occurs. We present a case of a 37-year-old male with diffuse muscle weakness after surgery. A new diagnosis of thyrotoxic periodic paralysis was made in the emergency department. This review summarizes the epidemiology, clinical manifestations, pathogenesis, diagnostics, and treatment of TPP.

SAT449 Clinical Characteristics Of Patients With Thyrotoxic Periodic Paralysis; An Experience From A Tertiary Care Hospital

Abstract Disclosure: T. Park: None. I. Goak: None. H. Jin: None. K. Lee: None. Y. Kim: None. Backgrounds: Thyrotoxic periodic paralysis (TPP) is a life-threatening complication characterized recurrent episodes of hypokalemia and muscle weakness in the setting of thyrotoxicosis. The present study aimed to describe clinical manifestation and outcome of patients admitted for TPP in emergency department (ED). Methods: This retrospective study analyzed 42 patients with TPP who were admitted ED from January 2000 through December 2020 in a single tertiary referral hospital. Their clinical characteristics were reviewed retrospectively. Results: 42 patients with TPP were identified. The mean age of the patients was 35.0±12.4 years; all were males. The month in which the most patients occurred paralysis symptoms was February (16.7%), followed by October (14.3%). 5 patients had a history of severe exertion, 7 patients had ingested a heavy carbohydrate meal, one patient had an infection, 5 patients had ingested alcohol, but more than half of the patients (57.1%) were without a precipitating cause. TPP was the first presentation of thyrotoxicosis in 85.7% of patients. The most common cause of thyrotoxicosis in TPP patients was Graves' disease (88.1%). At the time of admission, the mean potassium level was 2.77±0.93 mmol/L (reference, 3.5-5.5), mean ionized calcium level was 1.17±0.15 mmol/L (1.13-1.32), mean Free T4 level was 43.36±16.92 pmol/L (11.5-22.7). About half of the patients (47.6%) suffered at least one further attack of TPP. 28 patients (66.7%) diagnosed with Graves’ disease had anti-thyroid drugs alone and 5 patients (11.9%) with thyrotoxic relapses eventually underwent radioactive iodine therapy. None of the patients underwent surgery. Conclusions: TPP can be the presenting feature of previously undiagnosed thyrotoxicosis and should be considered in the differential diagnosis in patients presenting with acute onset of motor paralysis. At the time of the TPP attack, a detailed interview and inquiry with a thorough physical examination usually provide clues to the diagnosis. Presentation: Saturday, June 17, 2023

THU228 Thyrotoxic Periodic Paralysis In Three Adolescent Males

Abstract Disclosure: E. Ra: None. J. Austin: None. Thyrotoxic periodic paralysis (TPP) is a rare but potentially fatal complication of hyperthyroidism associated with Graves disease. Paralysis is due to hypokalemia caused by overactivation of the sodium potassium adenosine triphosphatase (Na+/K+ ATPase). TPP is usually seen in males between 20 - 40 years of age who are of Asian descent. We report 3 Hispanic American adolescent males, as young as 13 years old, who presented with TPP without an existing diagnosis of Graves disease. All three presented with leg weakness and were found to be hypokalemic and ultimately diagnosed with hyperthyroidism. Each patient was supplemented with potassium, either intravenously or orally, with their symptoms resolving within 24 hours. Although TPP is most prevalent in Asian adult males, theorized to be due to an underlying genetic preposition related to a variant of the KCNJ18 gene, there are increasing reports of non - Asian adolescents presenting in TPP. Therefore, pediatric care providers should consider TPP in their differential if a patient presents with weakness and hypokalemia, even without a pre-existing diagnose of hyperthyroidism. Presentation: Thursday, June 15, 2023

SAT507 New Onset Graves’ Thyrotoxicosis Complicated by Hypokalemic Periodic Paralysis: A Late Sequela of COVID- 19 Infection

Abstract Disclosure: E. Askar: None. H. Basharat: None. L. Lotfi: None. Y. Jamal: None. Background: Thyrotoxic periodic paralysis (TPP)is a rare endocrine emergency identified by hypokalemia and ascending symmetrical paralysis of extremities. If left untreated, it can lead to cardiopulmonary collapse. There are cases in the literature highlighting that Covid-19 infection or Covid vaccination can cause hypokalemic periodic paralysis with or without thyroid dysfunction. To our knowledge, four cases of Covid induced TPP and three cases of TPP after Covid vaccination have been reported in the literature. In all cases, the patients developed TPP soon after (within two months) Covid-19 infection or vaccination. However, we describe a case of a young, healthy euthyroid male who developed TPP as an initial manifestation of new-onset Graves' disease after five months of Covid infection. Even though Covid-19 infection has been known to cause thyroid dysfunction, especially subacute thyroiditis, there have only been a few case reports of Covid induced Graves' disease presenting as TPP at initial diagnosis. Clinical Case: A 37-year-old Asian male with no past medical history presented to the emergency department with lower extremity paralysis, palpitations, tremors and diaphoresis one day prior to presentation. He was diagnosed with mild COVID 19 infection, five months prior to presentation. Since then, he has been having intermittent palpitations but did not have any other symptoms. Vital signs on admission revealed heart rate of 100 beats/min, respiratory rate of 16 breaths/min, blood pressure of 131/66 mmHg, temperature of 97.5°F and oxygen saturation of 98% on room air. Physical examination was significant for an anxious young male with tender enlarged thyroid gland. There was positive thyroid bruit. Pemberton sign was negative. Muscle strength of 1/5 in bilateral lower extremities with brisk deep tendon reflexes and tremors in both hands were noticed. Laboratory studies showed white blood cell count of 13.07 (3.80-10.50 x 109/L), serum potassium of 1.4 mmol/L (3.5-5.3) and thyroid stimulating hormone of <0.01 mIU/L (0.358-3.74), free thyroxine of 5.5 ng/dl (0.9-1.8), total Triiodothyronine of 438 ng/dl (80-200) and positive thyroid stimulating immunoglobin of 4.22 IU/l (0.00-0.55) confirming Graves' disease as a diagnosis causing thyrotoxicosis with periodic paralysis. Patient did not have any history of thyroid disease with no available previous thyroid function tests. Patient was admitted to intensive care unit. Judicious repletion of potassium was done and he was started on propranolol 40 mg daily and methimazole 30 mg daily that lead to resolution of his paralysis and hyperthyroid symptoms. Conclusion: Here we report a case of new onset Graves' disease with TTP after COVID 19 increasing the likelihood that Covid 19 is a direct cause of new onset autoimmune thyroid illness. More studies are required to identify the mechanism and to confirm if the relationship is causal. Presentation Date: Saturday, June 17, 2023

SAT478 A Rare Case of Thyrotoxic Periodic Paralysis in a Patient with Concomitant Methimazole-Induced Agranulocytosis

Abstract Disclosure: K.S. Wei: None. S.M. Cannon: None. T.E. Angell: None. Introduction: Thyrotoxic state may precipitate sudden-onset unilateral or bilateral extremity weakness brought on by transient hypokalemia requiring specific management. Clinical Case: A 48-year-old woman presented to our hospital with fevers, sore throat, and sudden-onset bilateral leg weakness. Ten weeks prior, she was started on methimazole 20mg daily for a new diagnosis of Graves’ disease. Two days prior to presentation, she had consumed a carbohydrate-heavy meal and that night experienced acute-onset lower extremity weakness rendering her unable to walk. She also had been experiencing sore throat, odynophagia, and intermittent fevers. On admission, the patient was found to be febrile, tachycardic, and in shock with WBC <0.5 (ref: 4.5-10 K/cumm), potassium 2.6 (3.5-5.1 mmol/L), lactate 4.1 (0.5-2.2 mmol/L), TSH <0.01 (0.27-4.2 uIU/mL), fT4 4.04 (0.93-1.7 ng/dL) and was admitted to the ICU for neutropenic fever and septic shock. Computed tomography (CT) imaging of the thorax showed right lung consolidation suggesting pneumonia. Magnetic resonance imaging of the spine and CT head did not demonstrate an etiology for her weakness. She was diagnosed with thyrotoxic periodic paralysis (TPP) and treated with potassium. For severe hyperthyroidism with methimazole contraindication, she received broad spectrum antibiotics, lithium 300mg orally every 8 hours, and propranolol 10-20mg every 8 hours. Given minimal improvement in both weakness and hypokalemia after 48 hours of therapy, she was also diagnosed with refeeding syndrome and potassium repletion was intensified. The patient’s shock resolved, with slow improvement of lower extremity weakness over a two-week period and resolution of agranulocytosis and fevers. Conclusion: This rare presentation offers several distinct points regarding the patient’s care. Firstly, TPP is a rare hyperthyroidism-related hypokalemia that can cause weakening of the extremities due to a rapid intracellular shift of potassium (1) and is an important syndrome to consider on the differential for any thyrotoxic patient presenting with sudden-onset weakness. Secondly, gentle potassium repletion is recommended to prevent rebound hyperkalemia. However, our patient had both total body loss of potassium from refeeding syndrome and intracellular shift from TPP, requiring more aggressive potassium repletion to treat her paralysis than is typical for TPP alone. In settings where weakness and hypokalemia do not improve with beta blockade and gentle potassium repletion, it is important to investigate other causes of hypokalemia and consider concurrent overlapping diagnoses. Lastly, patients with methimazole-induced agranulocytosis may require alternative treatments, such as lithium to control hyperthyroidism. 1) Lin, Shih-Hua. Thyrotoxic Periodic Paralysis. Mayo Clin Proc. 2005;80(1):99-105. Presentation Date: Saturday, June 17, 2023

FRI550 Case Of Thyrotoxic Periodic Paralysis In African American Man With Cannabis Use

Abstract Disclosure: H. Al Jumaili: None. A. Mahaldar: None. S. Campbell: None. A. Gosmanova: None. Introduction: Recent changes in cannabis use (CU) laws led to growing interest in its use for recreational and therapeutic purposes. may have serious health problems such as hypokalemia, paralysis and rhabdomyolysis. Thyrotoxic Periodic Paralysis (TPP) is a rare and life-threatening complication of the thyrotoxicosis characterized by acute reversable painless muscle weakness or paralysis and hypokalemia due to massive intracellular shift of potassium. This condition is mainly seen males of Asian descent. Case: A 31-year-old African American man with Graves’ disease admitted to the hospital for upper and lower extremities weakness after Thanksgiving Day. He woke up with sudden inability to move any of his extremities with. He had high carbohydrate meal, on the evening. Patient reported having similar periodic episodes of paralysis, usually worse in the lower extremities for the last 2 years. This episode lasted longer than usual. On exam, he had enlarged thyroid gland and tachycardia. motor weakness, worse on lower extremities, hyporeflexia and intact sensation. Potassium was 1.8 mmol/l, magnesium 1.5 mg/dl, TSH <0.01 mIU/ml, FT4 4.3 ng/dl, FT3 18.3 ng/dl, anti-thyroid antibodies were elevated at 18 IU/L, and urine screen was positive for cannabinoid. Potassium was replaced, he was given propranolol and continued on methimazole. Patient's paralysis had improved in all four limbs, with serum potassium of 4.1 mmol/L. Discussion: TPP is a rarely seen condition in US but is known in an eastern Asian population, and in US the incidence rate was reported to be around 0.1 to 0.2%. American Indian are thought to be the higher risk. Underlying mechanism is imbalance in potassium homeostasis due to increased cellular Na-K ATPase pump activity with shift of potassium to the intracellular space. There are many theories regarding the cause of exaggerated intracellular potassium influx in TPP. Na-K ATPase activity is directly stimulated by thyroid hormone and insulin response to carbohydrate ingestion which promotes potassium uptake into muscle correlating with clinical observation that paralysis seen after a high carbohydrate meal. KCNJ18 gene mutations which alter the function of an inwardly rectifying potassium channel named Kir2.6 have been detected in some patients. In our patient, additional factor such as cannabis use potentiated intracellular potassium shift and hypokalemia. Recent evidence suggests that the CB1 receptor is expressed not only in the brain, but also found in lungs, heart, and skeletal muscle. Stimulation of (CB1) and activation of G protein-coupled inwardly rectifying potassium (GIRK) channels through intra-cellular signal cascades promotes hypokalemia and paralysis. Conclusion: This case raises awareness of TPP in non-Asian population and highlights the importance to consider cannabis as additional trigger for hypokalemia and paralysis. Presentation: Friday, June 16, 2023

FRI507 Thyrotoxic Periodic Paralysis: A Rare Occurrence Of Exogenous Thyroid Replacement

Abstract Disclosure: J. Case: None. D. Suravajjala: None. V. Eranki: None. Thyrotoxic periodic paralysis (TPP) occurs suddenly through excess thyroxine in tandem with insulin spurring an intracellular shift of potassium via increased activity of Na+/K+ ATPase pump leading to depletion of extracellular potassium with subsequent destabilization of cellular membranes and ensuing paralysis presenting with proximal muscle weakness of the legs. Common triggers involve vigorous exercise, infection, carbohydrate-rich meals, thyroiditis and graves' disease. Patients may be treated with IV potassium, non-selective beta blockers and treating the underlying cause. Exogenous thyroid hormone replacement causing iatrogenic hyperthyroidism as a cause of TPP is very rare. We present one such case below. A 61-year-old male with a history of primary hypothyroidism on thyroid replacement, atrial fibrillation, diabetes mellitus and hypertension, was admitted in September 2019 for lower extremity weakness at which time he was found with hypokalemia; he symptomatically improved following potassium replacement. He had a similar hospitalization in October, 2022 at which time he was found to have weakness alongside hypokalemia and hypomagnesemia, both of which were replaced with symptomatic improvement. He presented as an outpatient for follow up with likely etiology being TPP. Upon further review he had been taking both LT4 (Synthroid) 75mcg daily and T4/T3(Armour) 60mg daily; of note his TSH had been suppressed since 2019, three years prior to presentation. He was unsure why he had been on combination therapy. At our initial visit his labs were: TSH <0.005mIU/mL, free T4 1.38 ng/dL and T3 199 ng/dL. He was advised to stop all thyroid hormone replacement and experienced symptomatic improvement with normalization of potassium and magnesium. Repeat TFTs are pending for appropriate replacement dosing. Recognition of TPP and distinguishing from other etiologies of lower extremity weakness as well as other forms of periodic paralysis would aid in early resolution of an easily treatable, yet severe, condition given the implications of prolonged hypokalemia; earlier recognition of TPP in this patient as a sign of thyrotoxicosis may have prevented later hospitalizations and reduced risk of development of atrial fibrillation. This case also demonstrates the need for adequate monitoring and dosing of thyroid hormone supplement as well as potential complexities and risks of combination therapy in preventing an exogenously induced thyrotoxic state. Presentation: Friday, June 16, 2023

FRI512 Thyrotoxic Periodic Paralysis With Extreme Hypokalemia Precipitated By Acute Alcohol Intoxication In A Patient With Graves’ Disease

Abstract Disclosure: J. Batra: None. A.R. Ankireddypalli: None. J. Kaur: None. Introduction: Thyrotoxic periodic paralysis (TPP) is a muscle and electrolyte disorder, mostly seen in the setting of hyperthyroidism. It is characterized by reversible painless muscle weakness and hypokalemia. Prevalence is highest in East Asian populations, approximately 2%, and 0.1-0.2% in other populations. Males are much more likely to be affected. Common provoking factors include exercise, fasting, and changes in diet. Clinical case: A 29-year-old male of East Asian ethnicity presented to the hospital with the complaint of multiple bouts of inability to lift his extremities for 1 day. He also complained of generalized weakness. He did not have any changes in his mental status and was fully oriented at the time of the presentation. No breathing difficulty was reported. He had been drinking the night before with his friends and drank 1 L of vodka. His past medical history was significant for hyperthyroidism secondary to Graves’ disease, which was diagnosed a year ago. He had been prescribed methimazole but had not been adherent to the medication. The basic metabolic panel revealed undetectable serum potassium of <1.5 (3.4 to 5.3 mmol/L). The rest of the electrolytes and renal function were unremarkable. TSH was suppressed at <0.01 (0.3 to 4.20 uIU/L) and free T4 levels were significantly elevated at 7.77 (0.9 to 1.70 ng/dL). The thyrotropin receptor antibody was 33 (0.00 to 1.75 IU/L). EKG showed sinus tachycardia with nonspecific T-wave abnormalities. Thyroid ultrasound showed diffusely heterogenous parenchyma with diffusely increased blood flow throughout the thyroid on doppler. Echocardiogram showed a normal ejection fraction of 55-60% with mild concentric left ventricular wall thickening consistent with left ventricular hypertrophy. He was initially treated with intravenous potassium replacement and high doses of propylthiouracil, hydrocortisone, and propranolol, leading to the resolution of his symptoms. He was discharged on methimazole and propranolol therapies. Learning points: • Patients with Graves’ disease are routinely counseled against tobacco use to avoid worsening of orbitopathy. Hyperthyroid patients should also be counseled regarding avoidance or moderation of alcohol intake to avoid this rare but potentially life-threatening complication of thyrotoxic periodic paralysis. • The incidence of TPP is significantly higher in the East Asian populations, especially among males (8.7-13%). Counseling regarding provoking factors, the importance of adherence to medications, and the maintenance of euthyroidism to avoid TPP is essential. Presentation: Friday, June 16, 2023

Thyrotoxic periodic paralysis: report of two cases

Thyrotoxic periodic paralysis: report of two cases

A rare complication of a relatively common disease: periodic paralysis caused by thyrotoxicosis

Thyrotoxic periodic paralysis is a sporadic form of hypo-kalemic periodic paralysis and it is most commonly presents as sudden onset weakness in the proximal muscles. It is a disorder most commonly seen in Asian men which is characterised by abrupt onset of hypo-kalemia and paralysis and it is primarily affects lower extremities and is secondary to thyrotoxicosis. It is due to an intracellular shift of potassium induced by thyroid hormone sensitisation of Na/K ATPase rather than depletion of total potassium. The absence of a family history, male predilection and, presentation in second to fourth decade of life and signs of thyrotoxicosis and sinus tachycardia help in the diagnosis of the disorder. The age of onset is later and corresponded with age of incidence of thyrotoxicosis. It is very essential to diagnose TPP early and treat appropriately.

Code Pseudo Stroke - A Case of Hypokalaemic Periodic Paralysis Mimicking Stroke.

Hypokalaemic periodic paralysis is an acute flaccid paralysis secondary to hypokalaemia, triggered by hyperthyroidism, environmental elements such as a high carbohydrate intake or rest after intense exercise, and an underlying genetic component with mutations in the muscle ion channels.The pursuit of code stroke protocol in the in-patient setting must bear in mind reversible but potentially fatal and disabling alternative diagnoses such as stroke mimics including hypokalaemic periodic paralysis.Stroke mimics defined as acute onset neurological deficits that are not related to vascular cause are a true challenge, multiple scales have been created to distinguish them from an actual stroke, such as the Recognition of Stroke in the Emergency Room (ROSIER) scale.

A case of thyrotoxic hypokalaemic periodic paralysis presenting to the emergency department

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Gitelman syndrome with Graves’ disease leading to rhabdomyolysis: a case report and literature review

A 14-year-old male patient who suffered from limb numbness, fatigue, and hypokalemia was considered Graves’ disease (GD) complicated with thyrotoxic periodic paralysis (TPP) at the first diagnosis. Although with the treatment of antithyroid drugs, he developed severe hypokalemia and rhabdomyolysis (RM). Further laboratory tests revealed hypomagnesemia, hypocalciuria, metabolic alkalosis, hyperrenin, and hyperaldosteronemia. Genetic testing revealed compound heterozygous mutations in the SLC12A3 gene (c.506-1G > A, c.1456G > A) encoding the thiazide-sensitive sodium-chloride cotransporter, which presented a definitive diagnosis of Gitelman syndrome (GS). Moreover, gene analysis revealed his mother diagnosed with subclinical hypothyroidism due to Hashimoto’s thyroiditis carried the c.506-1G > A heterozygous mutation in the SLC12A3 gene and his father carried the c.1456G > A heterozygous mutation in the SLC12A3 gene. His younger sister who had hypokalemia and hypomagnesemia carried the same compound heterozygous mutations as the proband and was diagnosed with GS as well, but with a much milder clinical presentation and better treatment outcome. This case suggested the potential relationship between GS and GD, clinicians should strengthen the differential diagnosis to avoid missed diagnosis.

Thyrotoxic periodic paralysis: a presentation of hyperthyroidism increasing in frequency around the world

Thyrotoxic periodic paralysis (TPP) is a complication of hyperthyroidism commonly seen in Asian populations. It presents as sudden-onset muscle paralysis and hypokalaemia. Diagnosis is often delayed due to the rarity of the disease, the subtlety of the hyperthyroidism and the fleeting nature of the clinical presentation. With global expansion, physicians outside Asia should be aware of this disease for early recognition and treatment as severe cardiac arrhythmias, which may prove fatal, can occur. Several breakthroughs have been made in identifying the pathophysiological mechanism resulting in the severe hypokalaemia, including mutations in the Kir2.6 channel, an inwardly rectifying potassium channel, which results in a massive intracellular potassium shift. Treating the underlying hyperthyroidism is the definitive treatment; however, beta blockers and potassium supplementation are vital in acute management of this condition. This is a report of a case seen in Cape Town, South Africa with a review of the literature regarding the clinical features, pathophysiology and treatment.

An interesting case of thyrotoxic periodic paralysis

Hyperthyroidism rarely cause paralysis by redistributive hypokalemia, with periodic attacks of paralysis termed as thyrotoxic periodic paralysis (TPP). It is more commonly seen in the Asian or Hispanic populations, genetic variation in Kir2.6, a muscle specific thyroid hormone responsive potassium channel cause predisposition of TPP. It typically presents in the early morning with limb weakness. Hyperthyroidism signs and symptoms are need not to be present in all patients. TPP attacks can be triggered by factors such a high-carbohydrate diet, sternous activity, mental stress, and steroids. TPP should be suspected in young patients presenting with acute muscle weakness and severe hypokalemia. Arrhythmias can be noted but most of these will resolve with normalization of potassium.  

WCN23-0082 Clinical Features between Hypokalemic and Thyrotoxic Periodic Paralysis

WCN23-0082 Clinical Features between Hypokalemic and Thyrotoxic Periodic Paralysis

Thyrotoxic periodic paralysis associated with lactic metabolic acidosis: Case report of an African man and review of literature

BackgroundThyrotoxic periodic paralysis (TPP) is a rare and most often acquired subtype of hypokalemic periodic paralysis. The association of varying degrees of muscle weakness, hyperthyroidism and hypokalemia characterizes it. The treatment requires potassium supplementation, control of hyperthyroidism and prevention measures. It is a frequent disease in Asian men, but much rare in Caucasian or African populations. This is the first report of TPP associated with lactic metabolic acidosis in an African man. Case presentationA 23 year-old African man, native from Morocco, with recurrent episodes of tetraparesis for eleven months, and abdominal pain, was referred for evaluation. Biochemical investigations showed severe hypokalemia associated with hyperthyroidism and lactic metabolic acidosis. His EKG showed signs of hypokalemia such as sinus tachycardia and U waves. After potassium supplementation, neurological recuperation was quick and complete. Thyroid ultrasound identified a hypoechogenic and hypervascularized goiter, associated with high levels of thyroid antibodies, in favor of Grave's disease. With antithyroid drugs and life-style changes, the patient did not have any other attack. Review of literatureIn addition to the case report, this article presents an extended review of literature, from the first large study reporting the diagnosis and incidence of TPP in 1957 to nowadays. Are reported here the latest information concerning epidemiology, clinical manifestations, complementary examinations, management and genetic finding. The lactic acidosis observed initially is exceptional, never described in TPP. TPP is a diagnostic and therapeutic emergency, requiring careful potassium supplementation, in order to avoid the risk of the onset of rebound hyperkalemia, to be maintained until the etiological treatment is effective. Paraclinical assessment with emergency EKG and electromyogram are essential to assess the impact. DiscussionIt is essential in the face of any hypokalaemic periodic paralysis, including in non-Asian subjects, to search hyperthyroidism. ConclusionsThis report demonstrates the importance of thyroid testing in case of acute muscle weakness, even in non-Asian patients in order to diagnose TPP. This is a rare but possible etiology, to be distinguished from the familial form of hypokalemic periodic paralysis. It also questions on the impact of TPP on energetic metabolism, in particular on lactic metabolism.

Thyrotoxic Periodic Paralysis: An Under-Recognized Cause of Paralysis in Young Hispanic Men

BackgroundPatients presenting to the emergency department with paralysis can have a wide differential diagnosis. Thyrotoxic periodic paralysis (TPP) is a rare disorder causing transient flaccid paralysis in the setting of thyrotoxicosis and hypokalemia. It has been reported in Asian male populations predominantly, and the diagnosis is rarely considered in non-Asian populations. Recent research has identified cases in patients with diverse ethnic backgrounds, although epidemiologic data from the United States are very limited. ObjectiveOur aim was to report our experience with TPP at a tertiary care center in the United States. MethodsA retrospective chart review was conducted between January 2006 and February 2022 to identify cases of TPP and determine their demographic and clinical characteristics. Prevalence of TPP was estimated using the institutional hyperthyroidism registry. ResultsThirty-three patients with TPP were identified. All of the patients were male; median age was 28 years, and 85% were Hispanic. All patients had hypokalemia at presentation and 23% had rebound hyperkalemia after treatment. Prevalence of TPP in our population of patients with hyperthyroidism was approximately 0.5%. ConclusionsYoung Hispanic men presenting with paralysis should be evaluated for TPP, as the prevalence in this population may be higher than estimated previously. Management of TPP involves treatment of underlying hyperthyroidism and cautious potassium repletion, with an initial dose of no more than 60 mEq/L of potassium chloride to avoid rebound hyperkalemia.

A Work-Related Thyrotoxic Periodic Paralysis in A Worker Exposed to Heat Stress: A Case Report

Thyrotoxic Periodic Paralysis (TPP) is an uncommon disorder, characterized by the triad of acute hypokalemia, muscle paralysis, and thyrotoxicosis. Attacks are typically transient, last hours to days, and may be triggered by many conditions, including exposure to heat stress in both indoor and outdoor activities. Indoor workers, especially those working around furnaces, ovens, smelters, and boilers, are at a higher heat stress risk, even higher risk if they have other individual factors such as obesity, dehydration, slower heat acclimation, consume certain medications and presence of underlying diseases. A 48-year-old man presented a sudden onset weakness in all four limbs, associated with admission blood hypokalemia and thyrotoxicosis. No history of either alcohol or high carbohydrate intake consumption, infection, trauma, or heavy exercise. He has been working as a chef in the food procurement unit at a hospital for 28 years, 6 hours/day, six days/week. The results of the heat measurement at the cooking area where he works revealed that the heat stress index was 31,9º C Wet Bulb & Globe Temperature (WBGT).