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We present a unique case of hypokalemic thyrotoxic periodic paralysis (TPP) in an adolescent girl in North America. TPP is a rare but dangerous complication seen in thyrotoxic patients characterized by hypokalemia and acute proximal symmetric lower-extremity weakness. It is an especially rare phenomenon in pediatrics, with roughly 20 case reports described in adolescents worldwide; the majority are male. Our patient is a 14-year-old Asian girl with biochemical hyperandrogenism and known Graves disease who presented with an acute episode of lower-extremity weakness after eating a carbohydrate-rich meal. Laboratory workup revealed hypokalemia, hypomagnesemia, an undetectable thyrotropin, and hyperthyroxinemia. Electrolyte derangements responded well to supplementation, and the muscle weakness resolved with electrolyte normalization. Following improvement in thyroid function, the patient underwent thyroidectomy for definitive management of Graves disease. As TPP is potentially exacerbated by higher androgen and insulin levels, we suspect that with increasing rates of obesity and polycystic ovary syndrome, the incidence of TPP among adolescents may increase. It is therefore critically important that there is awareness and recognition of this serious diagnosis among all health care providers. [ABSTRACT FROM AUTHOR]

Sporadic thyrotoxic periodic paralysis (TPP) is a rare muscle disorder that manifests with abrupt muscle weakness and hypokalemia associated with hyperthyroidism. It is mostly reported in the Asian population, and rare in Caucasians. Only few cases have been reported in people with black ancestry. Here, we report a rare case of thyrotoxic periodic paralysis revealing Graves' disease in a young Malian. A 17‐year‐old man was admitted in the Neurology clinic with rapid proximal tetraplegia that started after strenuous physical activities at the school. Clinical examination confirmed the proximal weakness. In addition, he had bilateral ptosis, exophthalmia, and horizontal ophthalmoplegia. Laboratory testing showed normal serum potassium and creatinine, low calcium and TSH levels. However, CK, FT4, thyroid stimulating hormone antibody, and acetylcholine receptor antibody levels were high. In addition, electrocardiogram was normal while thyroid Doppler‐ultrasound showed heterogeneous, hypoechogenic, hypertrophic, and hyper vascularized gland. Patient had completely recovered his limb weakness within the following hours with symptomatic treatment. The clinical findings were consistent with Graves' disease, and he was put on Neomercazole. He did not present another episode of paralysis after 4‐years of follow up. This is a first case of thyrotoxic periodic paralysis reported in Mali and one of the rare cases in sub‐Saharan Africa. Despite its scarcity, all patients with acute weakness consecutive to effort, whether recurring or not, should be screened for TPP. [ABSTRACT FROM AUTHOR]

Abstract Sporadic thyrotoxic periodic paralysis (TPP) is a rare muscle disorder that manifests with abrupt muscle weakness and hypokalemia associated with hyperthyroidism. It is mostly reported in the Asian population, and rare in Caucasians. Only few cases have been reported in people with black ancestry. Here, we report a rare case of thyrotoxic periodic paralysis revealing Graves' disease in a young Malian. A 17‐year‐old man was admitted in the Neurology clinic with rapid proximal tetraplegia that started after strenuous physical activities at the school. Clinical examination confirmed the proximal weakness. In addition, he had bilateral ptosis, exophthalmia, and horizontal ophthalmoplegia. Laboratory testing showed normal serum potassium and creatinine, low calcium and TSH levels. However, CK, FT4, thyroid stimulating hormone antibody, and acetylcholine receptor antibody levels were high. In addition, electrocardiogram was normal while thyroid Doppler‐ultrasound showed heterogeneous, hypoechogenic, hypertrophic, and hyper vascularized gland. Patient had completely recovered his limb weakness within the following hours with symptomatic treatment. The clinical findings were consistent with Graves' disease, and he was put on Neomercazole. He did not present another episode of paralysis after 4‐years of follow up. This is a first case of thyrotoxic periodic paralysis reported in Mali and one of the rare cases in sub‐Saharan Africa. Despite its scarcity, all patients with acute weakness consecutive to effort, whether recurring or not, should be screened for TPP.

Abstract Background Thyrotoxic periodic paralysis (TPP) is a rare condition characterized by muscle paralysis, thyrotoxicosis, and hypokalemia. It presents with paralysis of both proximal and distal musculature in upper and lower limbs and may affect respiratory musculature and the cardiac conduction system. Early diagnosis is essential, as the condition is potentially reversible by oral or intravenous potassium treatment, leading to rapid resolution without lasting weakness. Overlooking the diagnosis may result in respiratory failure and cardiac arrhythmias including QT prolongation, Torsades de points, and ventricular arrhythmias. Case presentation A 19-year-old Caucasian man was admitted acutely with paralysis in upper and lower limbs and tachycardia. Over several months, he had experienced anxiousness, sweating more than usual, had daily palpitations, shortness of breath on exertion, and loose stools, and had lost 21 kg over the last year. Initial blood gas showed very low potassium of 1.4 mM, and blood tests showed decreased Thyroid-stimulating hormone (TSH)

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. [ABSTRACT FROM AUTHOR]

Background: Thyrotoxic periodic paralysis (TPP) is a rare condition characterized by muscle paralysis, thyrotoxicosis, and hypokalemia. It presents with paralysis of both proximal and distal musculature in upper and lower limbs and may affect respiratory musculature and the cardiac conduction system. Early diagnosis is essential, as the condition is potentially reversible by oral or intravenous potassium treatment, leading to rapid resolution without lasting weakness. Overlooking the diagnosis may result in respiratory failure and cardiac arrhythmias including QT prolongation, Torsades de points, and ventricular arrhythmias. Case presentation: A 19-year-old Caucasian man was admitted acutely with paralysis in upper and lower limbs and tachycardia. Over several months, he had experienced anxiousness, sweating more than usual, had daily palpitations, shortness of breath on exertion, and loose stools, and had lost 21 kg over the last year. Initial blood gas showed very low potassium of 1.4 mM, and blood tests showed decreased Thyroid-stimulating hormone (TSH) < 0.01 × 10− 3 IU/L, elevated free thyroxine (fT4) of 63.5 pM (reference interval (RI): 12.0–22.0 pM), and elevated total triiodothyronine (T3) of 8.2 nM (RI: 1.0–2.6 nM). He was diagnosed with TPP and treated with liquid oral potassium chloride (30 mmol every 30 minutes) and propylthiouracil (initial dose of 400 mg followed by 200 mg three times daily). TSH-receptor antibodies (TRAB) and thyroid-peroxidase antibodies (TPO-ab) were highly elevated. Thyroid ultrasound showed a normal-sized gland and color Doppler sonography showed increased vascularity throughout the gland, compatible with Graves' disease. He was discharged on day 4 with a normal potassium level and followed in the outpatient clinic where he received standard care for Graves' disease. Genetic testing using whole-genome sequencing found no genetic variants in genes previously associated with TPP. Conclusion: TPP is very rare in Caucasians but more often affects young men in East Asian populations. The case presents a Caucasian man with TPP where genetic testing of CACNA1S, KCNJ18, SCN4A, KCNJ2, KCNE3, and ABCC8 shows no pathogenic variants in genes previously associated with TPP. [ABSTRACT FROM AUTHOR]

Thyrotoxic periodic paralysis (TPP) is a rare disease seen predominantly in men of Asian origin. It should be considered in the differential diagnosis of patients with acute onset of weakness, and it is reversible after the correction of serum potassium. TPP can rarely be the initial presentation of Graves' disease. The clinician should investigate for hyperthyroidism in a patient presenting with thyrotoxic periodic paralysis, even in the absence of other features of thyrotoxicosis. [ABSTRACT FROM AUTHOR]

Patients 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. Our aim was to report our experience with TPP at a tertiary care center in the United States. A 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. Thirty-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%. Young 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. [ABSTRACT FROM AUTHOR]

Hypokalemic periodic paralysis (HPP) is a heterogeneous group of diseases characterized by intermittent episodes of delayed paralysis of skeletal muscle with episodes of hypokalemia, caused by variants in CACNA1S or SCN4A genes, or secondary to thyrotoxicosis, Sjogren syndrome, primary aldosteronism, etc. HPP may be the only presentation in Andersen--Tawil syndrome in which the majority of cases are caused by pathogenic variants in the KCNJ2 gene. We present a case of a 29-year-old male with hypokalemic periodic paralysis. The patient began to experience recurrent weakness of the extremities at the age of 26, which was effectively treated with potassium supplementation. He had recently developed dry mouth, palpitations, weight loss, and even dyspnea, with a serum potassium level as low as 1.59 mmol/L. The results of auxiliary examinations showed Graves' disease, and genetic testing indicated a missense variant, NM&lowbar;000334.4 (SCN4A):c.3404G>A (p.R1135H). He did not experience periodic paralysis during follow-up after lifestyle guidance and treatment of thyrotoxicosis with radioactive iodine. It is a rare case of SCN4A p.R1135H gene variant combined with hyperthyroidism resulting in HPP with respiratory muscle paralysis to raise awareness of the disease and avoid misdiagnosis and missed diagnosis. [ABSTRACT FROM AUTHOR]

We present a case of thyrotoxic periodic paralysis (TPP) presenting with stroke symptoms as a harbinger of Grave’s disease. A 61-year-old female presented with symptoms of abdominal pain and fatigue two weeks prior to admission and reported acute diarrhoea and unintentional weight loss. Investigation revealed thyrotoxicosis with undetectable thyroid stimulating hormone (TSH), elevated free T4 and elevated thyroid stimulating immunoglobulin (TSI). On the third day of admission, while undergoing physical therapy, code stroke was called on account of the onset of right-side predominant acute flaccid paralysis of upper and lower extremities, right-side facial droop, dysarthria and hyporeflexia bilaterally. The patient was alert and fully oriented with stable vitals with no increased labour in breathing at room air. An emergent head and neck CT, angiography, and magnetic resonance imaging (MRI) were negative. Serum potassium was 2.7 mmol/l, requiring prompt replacement. The patient’s paralysis and dysarthria improved over the following three days with a complete reversal of symptoms following the correction of serum potassium. Thyrotoxic periodic paralysis can occur in association with any of the causes of hyperthyroidism. It is due to a significant intracellular shift of potassium, subsequently manifesting clinically with hypokalaemia and muscle paralysis.

Abstract Thyrotoxic periodic paralysis (TPP) is a rare disease seen predominantly in men of Asian origin. It should be considered in the differential diagnosis of patients with acute onset of weakness, and it is reversible after the correction of serum potassium. TPP can rarely be the initial presentation of Graves' disease.

Hyperthyroidism can lead to thyrotoxic periodic paralysis (TPP), an infrequent yet fatal complication. It leads to a drop in the levels of serum potassium which in turn causes episodes of muscle weakness. This condition is exceptionally associated with respiratory insufficiency and arrhythmias, making it fatal. We present a rare case of a young male presenting with quadriparesis and ventricular tachycardia. A thorough laboratory work confirmed diagnosis of thyrotoxicosis and hypokalemia. This case further strengthens that recognition of TPP well before time is critical for early initiation of treatment.

Thyrotoxic periodic paralysis (TPP) is an endocrine emergency caused by thyrotoxicosis, mainly manifesting as periodic muscle weakness and hypokalemia, which seriously threatens the health of patients. The level of hypokalemia is closely related to the severity of muscle weakness in patients with TPP, and potassium supplementation can quickly alleviate the symptom of muscle weakness and hypokalemia. However, excessive potassium supplementation can lead to acute rebound hyperkalemia in patients with TPP, which also threatens the health of patients. This article reported 3 cases of TPP patients with acute rebound hyperkalemia caused by excessive potassium supplementation, and analyzed the risk factors for rebound hyperkalemia, in order to provide more information for the clinical treatment of TPP patients.

Graves' disease is an autoimmune thyroid disease with several characteristic symptoms and signs. Graves' ophthalmopathy, an inflammatory disease in the orbital area, is the main extrathyroid manifestation of Graves' disease. About 5% of Graves' ophthalmopathy patients have moderate to severe severity requiring high doses of systemic corticosteroid therapy. Graves' disease also has few complications, one of which is thyrotoxic periodic paralytic characterized by hypokalemia and muscle paralysis. Chronic hepatitis B virus infection has the potential to be co-incidence with other diseases (eg Graves ophthalmopathy). The need of high dose of corticosteroid therapy in treating Graves’ ophthalmopathy is a risk of reactivation in hepatitis B infection patient. This paper presented a Graves' disease patient complicated with Graves’ ophthalmopathy who developed limb muscle weakness. Patient will receive high doses of corticosteroids and prophylactic lamivudine therapy to prevent hepatitis B virus reactivation.

Thyrotoxic periodic paralysis (TPP) is a clinical condition characterized by hypokalemia, muscle paralysis, and hyperthyroidism. TPP can be challenging to diagnose due to its low disease prevalence and the similarity of paralysis to other common conditions. Through this case report, we highlight the importance of considering hyperthyroidism as a cause of recurrent attacks of muscle paralysis, particularly in the setting of other signs of hyperthyroidism. A 32-year-old Hispanic man with a history of recurrent episodes of muscle weakness presented to the hospital with the acute onset of bilateral lower extremity weakness and an inability to ambulate. Additionally, the patient was experiencing symptoms of hyperthyroidism, including heat intolerance, weight loss, anxiety, and tremors. Lab evaluation showed hypokalemia, and the thyroid panel indicated hyperthyroidism due to Graves disease. His symptoms resolved after the replacement of potassium orally and intravenously, and he was discharged home on methimazole and propranolol. The presented case emphasizes that endocrinological and metabolic causes should be considered in the differential diagnosis of acute flaccid paralysis. The symptoms of hyperthyroidism can be subtle in many cases, which can make the diagnosis very challenging., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Renganathan et al.)

Thyrotoxic periodic paralysis (TPP) is a rare disorder characterized by muscle paralysis, thyrotoxicosis, and hypokalemia. It commonly manifests as paralysis of both proximal and distal upper and lower limbs, and if left untreated, may progress to respiratory failure or cardiac arrhythmias. It is most common in Asian males and is frequently precipitated by strenuous exercise, high carbohydrate diet, stress, corticosteroid therapy, or alcohol. Early diagnosis of TPP is crucial as the condition may be reversible with oral or IV potassium replacement therapy, and management of the underlying hyperthyroidism. We describe a Samoan man in his 30s who presented with acute onset lower extremity paralysis. Laboratory investigations revealed low serum potassium of 2.2 mEq/L (reference range 3.5-5.0 mEq/L) and thyrotoxicosis with a low (thyroid stimulating hormone (TSH) of <0.07 uIU/mL (reference range 0.27-4.20 uIU/mL) and an elevated free T4 of 5.4 ng/dL (reference range 0.9-2.1 ng/dL). He was treated with both oral and IV potassium chloride as well as propranolol and regained full strength in his extremities. While rare, TPP is a reversible complication of thyrotoxicosis and a high index of suspicion in clinical practice is essential to prevent adverse outcomes., Competing Interests: Human subjects: Consent was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Nguyen et al.)

A rare complication of thyrotoxicosis among Asians is Thyrotoxic Periodic Paralysis (TPP), with an incidence of approximately 2% in patients with thyrotoxicosis from any cause. TPP is characterized by sudden onset of hypokalemia and muscle paralysis. Hypokalemia in TPP results from an intracellular shift of potassium induced by the thyroid hormone sensitization of Na+/K+–ATPase rather than depletion of total body potassium. Treatment of TPP includes correcting the underlying hyperthyroid state, prevention of potassium shift by using non-selective beta-blockade, and replacing potassium. TPP is curable once a euthyroid state is achieved. We describe here a rare case of TPP in a young Chinese man who presented with sudden bilateral lower limb weakness.

Graves' disease is an autoimmune thyroid disease with several characteristic symptoms and signs. Graves' ophthalmopathy, an inflammatory disease in the orbital area, is the main extrathyroid manifestation of Graves' disease. About 5% of Graves' ophthalmopathy patients have moderate to severe severity requiring high doses of systemic corticosteroid therapy. Graves' disease also has few complications, one of which is thyrotoxic periodic paralytic characterized by hypokalemia and muscle paralysis. Chronic hepatitis B virus infection has the potential to be co-incidence with other diseases (eg Graves ophthalmopathy). The need of high dose of corticosteroid therapy in treating Graves’ ophthalmopathy is a risk of reactivation in hepatitis B infection patient. This paper presented a Graves' disease patient complicated with Graves’ ophthalmopathy who developed limb muscle weakness. Patient will receive high doses of corticosteroids and prophylactic lamivudine therapy to prevent hepatitis B virus reactivation. [ABSTRACT FROM AUTHOR]

Introduction : Thyrotoxic periodic paralysis (TPP) is a type of hypokalemic periodic paralysis that is caused by an underlying thyrotoxicosis. It is a rare cause of hypokalemia due to intracellular potassium shift, causing acute muscle weakness. Case presentation : We present a case of a 19-year-old male of Thai descent with acute proximal symmetric lower limb weakness. The combination of these symptoms with profound hypokalemia, rapid recovery after normalization of serum potassium, and evidence of hyperthyroidism led to the diagnosis of thyrotoxic periodic paralysis, in this case due to an underlying Graves' disease. Conclusion : Clinicians should consider the diagnosis of TPP when a patient presents with the triad of acute paresis, profound hypokalemia and hyperthyroidism.

Thyrotoxic periodic paralysis (TPP) is a rare presentation of thyrotoxicosis most commonly associated with Graves' disease. It is rare in Caucasians, but it affects approximately 2% of Asians (occurring in those of Chinese, Japanese, Vietnamese, Filipino, and Korean descent) with thyrotoxicosis of any cause. Typical thyrotoxic features may be absent despite biochemical thyrotoxicosis. Hypokalemia and muscle paralysis are the result of an acute intracellular shift of potassium and not due to total body potassium deficiency. TPP is a self-limiting condition that is easily corrected by treatment of the thyrotoxicosis. We present a case of a Filipino man, aged 47 years, who presented to the emergency department with acute bilateral lower extremity weakness and hypokalemia who was subsequently diagnosed with TPP due to Graves' disease. [ABSTRACT FROM AUTHOR]

Context Thyrotoxic periodic paralysis (TPP) characterized by acute weakness, hypokalemia, and hyperthyroidism is a medical emergency with a great challenge in early diagnosis since most TPP patients do not have overt symptoms. Objective This work aims to assess artificial intelligence (AI)-assisted electrocardiography (ECG) combined with routine laboratory data in the early diagnosis of TPP. Methods A deep learning model (DLM) based on ECG12Net, an 82-layer convolutional neural network, was constructed to detect hypokalemia and hyperthyroidism. The development cohort consisted of 39 ECGs from patients with TPP and 502 ECGs of hypokalemic controls; the validation cohort consisted of 11 ECGs of TPP patients and 36 ECGs of non-TPP individuals with weakness. The AI-ECG–based TPP diagnostic process was then consecutively evaluated in 22 male patients with TTP-like features. Results In the validation cohort, the DLM-based ECG system detected all cases of hypokalemia in TPP patients with a mean absolute error of 0.26 mEq/L and diagnosed TPP with an area under curve (AUC) of approximately 80%, surpassing the best standard ECG parameter (AUC = 0.7285 for the QR interval). Combining the AI predictions with the estimated glomerular filtration rate and serum chloride boosted the diagnostic accuracy of the algorithm to AUC 0.986. In the prospective study, the integrated AI and routine laboratory diagnostic system had a PPV of 100% and F -measure of 87.5%. Conclusion An AI-ECG system reliably identifies hypokalemia in patients with paralysis, and integration with routine blood chemistries provides valuable decision support for the early diagnosis of TPP. [ABSTRACT FROM AUTHOR]

Abstract When clinical presentation is atypical, especially in a non‐Asian population, the finding of recurrent and refractory hypokalemia can serve as a key diagnostic clue for timely diagnoses and management of thyrotoxic periodic paralysis. In suspected cases, complete thyroid laboratory panel should be measured so that T3 toxicosis is not missed.

When clinical presentation is atypical, especially in a non-Asian population, the finding of recurrent and refractory hypokalemia can serve as a key diagnostic clue for timely diagnoses and management of thyrotoxic periodic paralysis. In suspected cases, complete thyroid laboratory panel should be measured so that T3 toxicosis is not missed. [ABSTRACT FROM AUTHOR]

Thyrotoxic hypokalemic periodic paralysis (THPP) is a disease characterized by recurrent episodes of muscle weakness due to intracellular potassium shifting in the presence of high levels of thyroid hormone. It occurs more commonly amongst young Asian men with underlying Graves’ disease. Attacks are commonly precipitated by ingestion of carbohydrate-rich meals or alcohols, stress or strenuous exercise. Herein, we describe an adult Thai man suffering from a hypokalemic periodic paralysis attack after receiving a dexamethasone injection. The diagnosis of Graves’ disease was confirmed by his thyroid function test and a presence of thyrotropin-receptor antibody. His weakness and hypokalemia responded well to potassium supplement and a non-selective beta blocker, while his thyrotoxicosis was initially controlled by an anti-thyroid medication and subsequently with a subtotal thyroidectomy. Clinicians should beware of this manifestation when administering steroids in the thyrotoxic patients, especially of Asian male descent.

Thyrotoxic periodic paralysis (TPP) is a disorder comprising acute hypokalaemia, intermittent muscle weakness and thyrotoxicosis. TPP is a rare manifestation of thyrotoxicosis predominantly seen in Asian people. We reported a patient who was brought to the emergency department with acute onset of weakness of her lower limbs. After a series of investigations, the patient was diagnosed as a case of thyrotoxicosis. The patient was placed on carbimazole, which prevented further attacks. The patient's improvement was satisfactory, and she is currently symptom free. Because of the presenting feature, its precipitating factor, the absence of a family history of periodic paralysis and the improvement of a clinical parameter after the starting of the antithyroid treatment, the condition was diagnosed as thyrotoxic periodic paralysis. The physician should concern about thyrotoxic periodic paralysis in people who present with weakness and features of thyrotoxicosis. A high prediction, early diagnosis and treatment of the condition can prevent severe complications, such as cardiac dysrhythmia.

Thyrotoxic periodic paralysis (TPP) is a notable and potentially lethal complication of thyrotoxicosis, and Graves’ disease is the most common cause of TPP. TPP is commonly reported in Asian males between 20–40 years of age, but it is rare in children and adolescents. We report 2 Korean adolescents (a 16-year-old male and a 14-year-old female) with episodes of TPP who were previously diagnosed with Graves’ disease. These 2 patients presented with lower leg weakness in the morning after waking up. They were diagnosed with TPP-associated with thyrotoxicosis due to Graves’ disease. After they were initially treated with potassium chloride and antithyroid drugs, muscle paralysis improved and an euthyroid state without muscle paralytic events was maintained during follow-up. Therefore, clinicians should consider TPP when patients have sudden paralysis and thyrotoxic symptoms such as goiter, tachycardia, and hypertension.

Background: Thyrotoxic periodic paralysis (TPP) is a unique manifestation of Graves’ disease. While it is uncommon in Asian, it is extremely rare in Caucasian patients (0.1–0.2%). Previous studies suggested that TPP indicate more severity of Graves’ disease and definitive treatments should be used to prevent relapses. Aim: To describe clinical features and impact of first-line treatment on long-term outcomes of TPP patients. Method: A retrospective cohort study over 35 years (1985–2019) of TPP from Graves’ disease patients was conducted. All cases were analyzed and their clinical courses were compared between those who received anti-thyroid drugs (ATD) versus radioactive iodine (RAI) as a primary treatment. None of them underwent surgery. Results: A total of 2964 hyperthyroid Graves’ disease patients were treated and followed-up at least 3 months over the study period. TPP was identified in 63 cases (2.1%) of all patients. There were 60 males and only 3 females with age at presentation of 35.0 ± 8.2 years. TPP was the first presentation of hyperthyroid Graves’ disease in 82.5% of them. During the acute attack of TPP, all patients presented with bilateral lower limb flaccid weaknesses with median serum potassium of 2.1 mmol/L. No fatal TPP cases were found. RAI was selected as primary treatment in 27 patients (42.9%). Nearly all RAI-treated patients rendered hypothyroidism with the median RAI dose at 15 mCi. No patients who were in remission after RAI treatment developed recurrent attack of TPP. In the remaining 36 ATD-treated patients with mean follow-up time at 9.1 years, relapse was found in 10 patients (27.8%) after the drug discontinuation and 6 patients suffered recurrent TPP. Only 8 ATD-treated TPP patients (22.2%) went into remission. Conclusions: TPP is a rare complication of hyperthyroid Graves’ disease. Definitive treatment with RAI or thyroidectomy should be employed to prevent relapse and further attacks of TPP.

Abstract Background Hypokalemia is one of the most common clinical electrolyte imbalance problems, and thyrotoxic periodic paralysis (TPP) is a leading cause of presentation to the emergency department. Low renal potassium secretion rates, a normal acid–base balance in the blood, and hyperthyroidism are the hallmarks of suspected TPP. Case presentation Here we report the case of a 36-year-old man who presented to the emergency department with a sudden onset of acute muscle weakness at 5 h prior to admission. Biochemistry tests revealed hypokalemia with hyperthyroidism and renal potassium wasting. TPP was initially not favored due to the presence of renal potassium wasting. However, his serum potassium level rebounded rapidly within several hours after potassium supplementation, indicating that the intracellular shifting of potassium ions was the main etiology for his hypokalemia. The early stage of TPP development may have contributed to this paradox. Conclusion Therefore, it is premature to rule out TPP based on the presentation of high renal potassium secretion rates alone. This finding may result in an incorrect impression being made in the early stage of TTP and may consequently lead to an inappropriate potassium supplementation policy.

We present a case of fatal rebound hyperkalemia in a patient with thyrotoxic periodic paralysis (TPP) treated with potassium supplementation. Although TPP is a rare hyperthyroidism-related endocrine disorder seen predominantly in men of Asian origin, the diagnosis should be considered in patients of non-Asian origins presenting with hypokalemia, muscle weakness or acute paralysis. The condition may present as a life threatening emergency and unfamiliarity with the disease could result in a fatal outcome. Immediate therapy with potassium chloride supplementation may foster a rapid recovery of muscle strength and prevent cardiac arrhythmias secondary to hypokalemia, but with a risk of rebound hyperkalemia. [West J Emerg Med. 2010; 11(1):57-59.]

Background: Thyrotoxic periodic paralysis is a rare complication of hyperthyroidism and is associated with hypokalemia and muscle paralysis. This condition is most commonly seen in Asian men. Case presentation: We report on a 14-year-old African American male with Graves' disease and intermittent asthma who presented with bilateral leg weakness. The patient demonstrated signs of thyrotoxicosis and laboratory evaluation revealed hypokalemia and hyperthyroidism. Following the administration of potassium supplementation clinical status improved and the patient was discharged home on a high dose of methimazole and propranolol. At a 6-month follow up visit, he was found to be clinically euthyroid and demonstrated no signs of hyperthyroidism or muscle weakness. Conclusion: Children presenting with weakness and hypokalemia should be investigated for thyroid dysfunction. Correction of hypokalemia improves acute presentation, but the patient will remain at risk for paralysis until euthyroid state is achieved. [ABSTRACT FROM AUTHOR]

Thyrotoxic periodic paralysis (TPP) is a rare but potentially life-threatening entity, which is characterized by sudden onset of muscle weakness and can in exceptional cases be associated with more severe symptoms, such as severe hypokalemia. We present the rare case of a young patient presenting with monomorphic ventricular tachycardia secondary to hypokalemia due to TPP. This case report highlights the importance of recognition of TPP as a rare cause of VT. A high index of suspicion is needed since signs of hyperthyroidism may be subtle. However, early diagnosis is crucial in order to avoid cardiovascular complications and improve outcomes. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Despite its’ life-threatening potential due to cardiac severe dysrhythmia in the context of severe hypokalemia, thyrotoxic periodic paralysis (TPP) often goes unrecognized. Although classically confined to young Asian men, it can occur irrespective of age, sex, and race. We report a short series of three cases of TPP as first presentation of Graves’ disease in a young Caucasian male and in two Caucasian elderly and middle-aged women, respectively. The first patient developed malignant ventricular arrhythmias due to severe hypokalemia and was defibrillated, with recovery after prompt potassium correction and administration of antithyroid agents and propranolol. The other two cases developed persistent hypokalemia despite adequate potassium chloride (KCl) repletion, with slow recovery of motor deficit and serum potassium normalization up to day 5. In the first case, long-term euthyroid state was achieved via total thyroidectomy due to the presence of a suspicious nodule that proved to be malignant. In the other two cases, medical treatment was the choice of therapy for thyrotoxicosis. None experienced recurrent TPP. Thyroid hormone evaluation is mandatory in the presence of hypokalemic paralysis, even in the absence of clinical signs of thyrotoxicosis. If TPP is confirmed, initial therapy should comprise antithyroid drugs and propranolol, besides hypokalemia correction.

Thyrotoxic periodic paralysis is an uncommon disorder characterized by hypokalaemia, thyrotoxicosis and paralysis, most commonly seen in South Asian males. Aim of our case series is to highlight the significance of this reversible cause of patients presenting with neuromuscular paralysis. We present case series of 1 Asian and three Caucasian patients with thyrotoxic periodic paralysis who came with neuromuscular weakness secondary to thyrotoxicosis. All made a swift and uneventful recovery with no recurrence. Thyrotoxic periodic paralysis (TPP) is an infrequent condition having recurrent episodes of muscle weakness as main feature. Hypokalaemia is a common finding seen in these patients. Resolution of the attacks is achieved with correction of hypokalaemia and hyperthyroidism. [ABSTRACT FROM AUTHOR]

Background: Thyrotoxic 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 Presentation: A 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 Literature: In 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., Discussion: It is essential in the face of any hypokalaemic periodic paralysis, including in non-Asian subjects, to search hyperthyroidism., Conclusions: This 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., (Copyright © 2023 Elsevier Masson SAS. All rights reserved.)

Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare but potentially serious complication of thyrotoxicosis. The resulting muscle weakness is profound, associated with more severe hypokalemia, yet reversible. However, clinicians must be cautious because patients can develop life-threatening hyperkalemia during treatment. Underlying causes should be investigated as repeated episodes of THPP may occur. [ABSTRACT FROM AUTHOR]

Introduction: Thyrotoxic periodic paralysis (TPP) is characterized by recurrent episodes of reversible paralysis with hyperthyroidism. It is clinically similar to hypokalemic periodic paralysis (HOPP), which features significant ion-channel dysfunction and reduced muscle fiber conduction velocity (MFCV). However, the muscle membrane function in TPP is not known.Methods: For 13 patients with TPP and 15 age-matched controls, clinical assessment and serial neurophysiological testing, including nerve conduction, prolonged exercise (PE) testing, and MFCV. were performed.Results: MFCV values were elevated up to 1 year from the paralytic attack in TPP patients. In the group with a positive PE test, MFCV values were higher. There was no significant relationship between MFCV values and either hypokalemia or hyperthyroidism.Conclusions: Although clinical manifestations in TPP are similar to those observed in HOPP, TPP appears to feature an alternate pathogenic mechanism. Specifically, MFCV values increased rather than decreased. Further studies are needed to support these findings. Muscle Nerve, 2016 Muscle Nerve 56: 780-786, 2017. [ABSTRACT FROM AUTHOR]