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1
Campana, Mario S., Maria Riofrio, Raja S. Jadav, and Mattan Rozenek. "An Unusual Presentation of Thyrotoxicosis: Leg Weakness and Hypokalemia in a 21-Year-Old Male." Case Reports in Endocrinology 2021 (October 23, 2021): 1–4. http://dx.doi.org/10.1155/2021/1776538.
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Patients with hyperthyroidism or thyrotoxicosis present with an unspecific constellation of signs or symptoms such as palpitations, tremors, weight loss, or diarrhea. In some severe cases, hyperthyroidism can predispose patients to metabolic abnormalities and arrhythmias. Thyrotoxic periodic paralysis (TTP) is a rare, life-threatening complication or variant of hyperthyroidism associated with hypokalemia and muscle weakness that affects young Asian or Hispanic males between 20–40 years. TTP is reversible, and the management consists of beta-blockers, antithyroid therapy, and conservative potassium correction to prevent severe cardiovascular events such as ventricular arrhythmias with the improvement of transient muscle paralysis. We present a case of a 21-year-old Hispanic male complaining with symptoms of thyrotoxicosis, marked hypokalemia, and severe generalized muscle weakness. Physicians must be aware of this uncommon complication of thyrotoxicosis called thyrotoxic periodic paralysis (TTP) to avoid potassium overcorrection and all the endocrine associations with this pathology.
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Acharya, Ratna, and Kiran Upadhyay. "Unmasking of Gitelman Syndrome during Pregnancy in an Adolescent with Thyrotoxic Crisis." Pediatric Reports 13, no. 4 (2021): 632–38. http://dx.doi.org/10.3390/pediatric13040075.
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Background. Gitelman syndrome (GS) is an inherited salt-losing renal tubulopathy characterized by hypokalemic metabolic alkalosis with hypomagnesemia and hypocalciuria. Patients can be asymptomatic until late adolescence or adulthood, and hence may be discovered incidentally during presentation with other illnesses. GS has been described in association with thyroid disorders and should be considered in patients with hyperthyroidism and persistent hypokalemia, especially in those with associated hypomagnesemia and hypocalciuria. Case summary. In this report, we describe an 18-year-old female who presented with hyperemesis gravidarum and thyrotoxicosis, and was incidentally found to have GS, confirmed by the sequence analysis of SLC12A3. Conclusions. Thyroid dysfunctions, such as hypothyroidism, thyrotoxicosis, and thyroid nodules, may develop during pregnancy. A structural homology between the beta-human chorionic gonadotropin and thyroid stimulating hormone molecules, as well as their receptors is probably the basis for the transient thyrotoxicosis crisis during pregnancy. Since hyperemesis in pregnancy can also lead to hypokalemia and alkalosis, a high index of suspicion for GS during pregnancy is required for timely diagnosis and management.
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Jackson, Ian, Yazan Addasi, Moeed Ahmed, et al. "Hypokalemic Periodic Paralysis Precipitated by Thyrotoxicosis and Renal Tubular Acidosis." Case Reports in Endocrinology 2021 (June 21, 2021): 1–4. http://dx.doi.org/10.1155/2021/4529009.
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Background. Hypokalemic periodic paralysis is a rare neuromuscular disorder characterized by transient episodes of flaccid paralysis due to a defect in muscle ion channels. Most cases are hereditary, but it can be acquired. We present a case of acquired hypokalemic periodic paralysis associated with hyperthyroidism and renal tubular acidosis. Clinical Case. A 38-year-old female with a history of Graves’ disease presented to the emergency department with generalized weakness and associated nausea, vomiting, and weight loss. Examination was significant for diffuse weakness in all extremities. Labs showed hypokalemia, hyperthyroidism, and nonanion gap metabolic acidosis with a positive urine anion gap. She was treated for hypokalemic periodic paralysis and renal tubular acidosis. Potassium replacement, propranolol, methimazole, and sodium bicarbonate were initiated. Her potassium gradually corrected with resolution of her symptoms. Further investigation revealed a history of dry eyes, dry mouth, and recurrent dental carries. She had positive ANA, SS-A, and SS-B antibodies. She was diagnosed with Sjögren’s syndrome, which may have been associated with her Graves’ disease and thus contributed to both her RTA and hyperthyroidism. Conclusion. Early recognition and treatment of thyrotoxic periodic paralysis are important to prevent cardiac complications. Management includes potassium replacement with careful monitoring to prevent rebound hyperkalemia. The definitive treatment is to achieve euthyroid status.
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Agu, Chinyere, Zimri Tan, and Ronald Cobbs. "ODP535 Thyrotoxic Periodic Paralysis (TPP) in A Young African American Male: Post Exercise." Journal of the Endocrine Society 6, Supplement_1 (2022): A790—A791. http://dx.doi.org/10.1210/jendso/bvac150.1634.
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Abstract Thyrotoxic periodic paralysis (TPP) is a rare fatal disorder with hypokalemia as the hallmark feature associated with thyrotoxicosis. Compared with existing studies that TPP is prevalent among younger men of Asian descent, this study intends to complement this area of study by addressing aspects currently not fully covered involving the existence of TPP among men of African descent. This study documents the case of a 37year old African American Man with no previous history of hyperthyroidism who presented with sudden onset lower extremity paralysis and hypokalemia. It is particularly important to note that while majority of patients with TPP have preexisting hyperthyroidism, our patient presented with no history of overactive thyroid. The finding of this work fills a gap in literature highlighting the importance of separating Familial Hypokalemic periodic paralysis (FPP) and TPP at its earliest detection. We find strong and robust evidence suggesting that patients may be easily termed FPP in view of its similarity to TPP thereby leading to a delay in the diagnosis and treatment. TPP has been linked with genetic mutations in specific ion channels (calcium channels and KIR) and increased Na-K ATPase pump activity. This leads to a massive intracellular shift in potassium causing hypokalemia under the influence of excess thyroid hormone. We find that both TPP and FPP have similar clinical presentations and same precipitants hence the need for a high index of suspicion in patients with hypokalemia and sudden onset paralysis with no history of hyperthyroidism to prevent lethal complications. Our results suggest that prompt correction of hypokalemia and treatment of hyperthyroidism is key in resolving attacks and preventing lethal complications. Presentation: No date and time listed
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Elenius, Henrik, Marie Cesa, Corina C. Nava Suarez, Abhishek Nimkar, Prasanta Basak, and Nandita Sinha. "Thyrotoxic Periodic Paralysis Causing Back Pain and Leg Weakness: An Unusual Presentation of Hyperthyroidism." Case Reports in Endocrinology 2021 (March 15, 2021): 1–4. http://dx.doi.org/10.1155/2021/6622658.
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Thyrotoxic periodic paralysis (TPP) is a rare muscular disorder, characterized by muscle weakness and hypokalemia triggered by thyrotoxicosis. In Asian populations, 2% of patients with thyrotoxicosis are affected, compared to only 0.1–0.2% of non-Asians. The vast majority of patients are male. Muscle weakness ranges in severity from very mild to life-threatening, due to respiratory compromise. We present a case of a previously healthy 39-year-old Hispanic male who presented with sudden quadriparesis and quickly recovered after being treated for hypokalemia and thyrotoxicosis. TPP, although unusual, is important to recognize as it is a potentially fatal condition that requires close monitoring and is readily reversible with appropriate therapy. Any cause of thyroid hormone excess can cause TPP, with Graves’ disease being the most common etiology. Acute treatment includes potassium repletion, while long-term management focuses on determining and treating the cause of thyrotoxicosis, since maintaining a euthyroid state will prevent further episodes of TPP.
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Ahmed ElKholi, Ali Haider, and Maryam Mahmood Ali. "Periodic Paralysis and the Emergency Department: A Case Series of Thyrotoxicosis Periodic Paralysis with Literature Review." Journal of Medical and Health Studies 5, no. 2 (2024): 119–24. http://dx.doi.org/10.32996/jmhs.2024.5.2.15.
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Thyrotoxic periodic paralysis is a rare but serious complication of thyrotoxic. It is an uncommon form of hypokalemic periodic paralysis characterized by proximal muscle weakness that may progress to involve distal muscle and respiratory muscle. Thyrotoxic periodic paralysis is commonly reported among Asian descent; especially the male population, between the ages of 20 and 40 years. The actual pathophysiology of Thyrotoxic periodic paralysis is unclear. However, hyperthyroidism, channelopathies, high-carbohydrate food, and hyperandrogenism are the most common predisposing factors associated with this condition. Hypokalemia and muscle weakness in Thyrotoxicosis patients result from increased shifting of K+ intracellularly. This is known to be related to increased sodium-potassium-a adenosine triphosphatase (Na/K-ATPase) pump number and activity. The proper aim of treatment in Thyrotoxicosis patients is to reach the euthyroid state. Management of Thyrotoxic periodic paralysis at the Emergency department includes establishing Intravenous potassium replacement, starting non-selective beta-blockers to reduce the phosphate and potassium intracellular shifting, and normalizing the underlying hyperthyroid state. Here, we present two cases of Thyrotoxic Periodic Paralysis. These cases reiterate the need to consider all the complications of Thyrotoxicosis, even rare ones, to treat the condition and reverse the effect of periodic hypokalemia within the Emergency Department, to prevent any inevitable complication.
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Mahali, Lakshmi Priyanka, and Amanda Pechman. "A Case of Thyrotoxic Periodic Paralysis." Journal of the Endocrine Society 5, Supplement_1 (2021): A911. http://dx.doi.org/10.1210/jendso/bvab048.1860.
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Abstract Introduction: Thyrotoxic periodic paralysis (TPP) is an uncommon disorder characterized by simultaneous thyrotoxicosis, hypokalemia, and paralysis. It is a rare complication of hyperthyroidism with a prevalence of 1 in 100,000. It has a higher prevalence in young Asian males, with much fewer cases reported in Hispanic patients. The majority of cases are seen in hyperthyroidism due to Grave’s disease, however other causes of thyrotoxicosis have been associated with TPP. Hypokalemia occurs when thyroid hormone stimulates the sodium-potassium-ATP pump by binding to the thyroid response elements upstream of the genes for this pump, increasing its activity and thereby causing a transcellular shift of potassium into the intracellular fluid. Attacks usually begin with proximal muscle weakness of the lower extremities and may progress to tetraplegia, with the degree of muscle weakness corresponding to serum potassium levels. Interestingly, no correlations with serum T3 or T4 levels have been found. Clinical Case: A 38-year-old Hispanic man with a history of GERD presented to the emergency department with an inability to move his extremities. Initial labs were significant for profound hypokalemia to 2.0 mEq/L (3.5-5) and hyperthyroidism, with TSH<0.05 uU/mL (0.3-4.2) and free T4 2.4 ng/dL (0.6-1.5). Additional workup revealed a positive thyroid stimulating immunoglobulin and a positive thyrotropin binding inhibitor, and thyroid ultrasound demonstrated a hyperemic thyroid with numerous subcentimeter hypoechoic nodules, all of which was suggestive of Grave’s disease. His symptoms resolved with potassium repletion, suggesting thyrotoxic periodic paralysis secondary to hyperthyroidism. Upon further evaluation, the patient endorsed several months of hyperthyroid symptoms such as tremors, heat intolerance, and weight loss. He also endorsed alcohol use, a high carbohydrate diet, and recent life stressors, a combination of which likely precipitated his thyrotoxic periodic paralysis. He was discharged on methimazole 10 mg daily and propranolol 40 mg BID, with a decrease in his free T4 and improvement in his symptoms. He has been educated to avoid alcohol consumption and high-carbohydrate meals to avoid precipitating another episode of periodic paralysis, and once his hyperthyroidism is under better control he plans to undergo radioactive iodine ablation (RAI) for definitive management. Conclusions: Thyrotoxic periodic paralysis is a rare but dangerous complication of hyperthyroidism, and should be considered in the differential diagnosis when young individuals present with otherwise unexplained hypokalemia and paralysis. Acute management is potassium repletion, long term management involves treatment of thyrotoxicosis and avoiding precipitating factors, and definitive therapy is RAI or thyroidectomy.
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Vijayakumar, Abhishek, Giridhar Ashwath, and Durganna Thimmappa. "Thyrotoxic Periodic Paralysis: Clinical Challenges." Journal of Thyroid Research 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/649502.
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Thyrotoxic periodic paralysis (TPP), a disorder most commonly seen in Asian men, is characterized by abrupt onset of hypokalemia and paralysis. The condition primarily affects the lower extremities and is secondary to thyrotoxicosis. The underlying hyperthyroidism is often subtle causing difficulty in early diagnosis. Factors like high-carbohydrate meal exercise, steroid, and stress can precipitate an attack of TPP. Evidence is building up showing role of genetic mutations in Kir2.6 channel in the pathogenesis of TPP. Loss of function of Kir2.6 together with increased activity of Na+/K+ATPase may trigger a positive feed-forward cycle of hypokalemia. Biochemical hyperthyroidism with normal urinary potassium excretion and ECG changes are characteristic of TPP. Treatment with low-dose potassium supplements and nonselective beta-blockers should be initiated upon diagnosis, and the serum potassium level should be frequently monitored to prevent rebound hyperkalemia.
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Rahesh, Jasmin, Layan Al-Sukhni, Baseer Quraishi, and Tarek Naguib. "Upper extremity deep venous thrombosis secondary to thyrotoxic periodic paralysis with accompanying hyperphosphatemia and severe hypomagnesemia." Southwest Respiratory and Critical Care Chronicles 9, no. 41 (2021): 47–49. http://dx.doi.org/10.12746/swrccc.v9i41.927.
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Thyrotoxic periodic paralysis is a rare but life-threatening complication of hyperthyroidism. Characteristic features involve thyrotoxicosis, acute paralysis, and hypokalemia. Mild hypomagnesemia and hypophosphatemia are also present in most cases due to the resulting transcellular shift of electrolytes. Complications of thyrotoxic periodic paralysis reported in the literature have included cerebral venous thrombosis as well as lower extremity deep venous thrombosis. We present a patient with an unusual presentation of thyrotoxic periodic paralysis as reflected by hyperphosphatemia, upper extremity deep venous thrombosis and severe hypomagnesemia. This is the first reported case of upper extremity deep vein thrombosis in association with a peripherally inserted central catheter line secondary to thyrotoxicosis.
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Chang, Chin-Chun, Chih-Jen Cheng, Chih-Chien Sung, et al. "A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants." European Journal of Endocrinology 169, no. 5 (2013): 529–36. http://dx.doi.org/10.1530/eje-13-0381.
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BackgroundA comprehensive analysis has not been performed on patients with thyrotoxic periodic paralysis (TPP) characterized by acute hypokalemia and paralysis in the setting of thyrotoxicosis.PurposeThe aim of this study was to analyze the detailed symptomatology of thyrotoxicosis and precipitating factors for the attack in a large cohort of TPP patients.Patients and methodsA prospective observational study enrolled patients with TPP consecutively over 10 years at an academic medical center. Clinical features, including signs/symptoms of thyrotoxicosis and precipitating factors, were analyzed. The Wayne's index was used to assess the severity of thyrotoxicosis at presentation. Patients who agreed to receive an oral glucose-loading test after recovery were evaluated.ResultsAmong the 135 TPP patients (male:female, 130:5), 70% of paralytic attacks occurred in the morning, especially during the seasons of summer and fall. Two-thirds of patients did not have a known family or personal history of hyperthyroidism. Only 17% of TPP patients manifested overt signs/symptoms of thyrotoxicosis (Wayne's index >19). A clear precipitating factor, such as high carbohydrate load, acute upper respiratory tract infection, strenuous exercise, high-salt diet, or the use of steroids or bronchodilators, was identified in only 34% of TPP patients. A glucose load to stimulate insulin secretion induced acute hypokalemia (K+2.47±0.6 mmol/l) with reparalysis in only 18% (10/55) of TPP patients.ConclusionsMost TPP patients have only subtle clinical signs/symptoms of thyrotoxicosis and only a small fraction has clear precipitating factors. In addition to the effects of hyperinsulinemia, other insulin-independent mechanisms may participate in the pathogenesis of TPP.
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Sethi, Prativa Priyadarshani, Ashwin Parchani, and Monika Pathania. "Respiratory Muscle Weakness in Thyrotoxic Periodic Palsy: A Lesson to Remember." Annals of Neurosciences 28, no. 3-4 (2021): 179–82. http://dx.doi.org/10.1177/09727531211051080.
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Thyrotoxic periodic palsy (TPP) is a sporadic form of hypokalemic periodic palsy that may occur in association with hyperthyroidism mostly with Graves’ disease. Acute thyrotoxic periodic palsy is a disorder most commonly seen in Asian men and characterized by abrupt onset of hypokalemia and paralysis. The disorder primarily affects the lower extremities and can involve all four limbs and presents as acute flaccid paralysis. The diagnosis of thyrotoxic periodic palsy is not difficult, but the disease's low incidence and many differentials for acute flaccid paralysis delay and complicate the diagnosis. TPP is not related to the etiology, severity, and duration of thyrotoxicosis. The treatment is similar to hypokalemic periodic palsy with potassium supplementation and initiation of antithyroid drugs and beta-blocker therapy. Here a similar case of quadriparesis is reported, which got precipitated after abrupt cessation of carbimazole in a young male. This initially was thought to be a case of hypokalemic periodic palsy and was later diagnosed to be TPP and recovered after initiating antithyroid drugs and potassium supplementation.
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Rivas, Ana M., Subhanudh Thavaraputta, Menfil Andres Orellana-Barrios, et al. "THYROTOXIC PERIODIC PARALYSIS AND COMPLICATED THYROTOXICOSIS, TWO PRESENTATIONS OF HYPERTHYROIDISM WITH NOTABLE DIFFERENCES IN THEIR CLINICAL MANIFESTATIONS: AN EXPERIENCE FROM A TERTIARY CARE HOSPITAL IN THE UNITED STATES." Endocrine Practice 26, no. 7 (2020): 699–706. http://dx.doi.org/10.4158/ep-2019-0454.
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Objective: Thyrotoxic periodic paralysis (TPP) is a muscular disorder characterized by sudden episodes of muscle weakness and hypokalemia in the setting of thyrotoxicosis. We aimed to report our experience with TPP in West Texas and compare its clinical presentation to that of patients admitted for complicated thyrotoxicosis. Methods: Retrospective review of records of adult patients with admission diagnosis of hyperthyroidism, thyrotoxicosis, and/or discharge diagnosis of periodic paralysis seen at our institution in a 6-year period. Results: Patients admitted for complicated thyrotoxicosis were more commonly females of a mean age of 44 years. Patients with TPP were more commonly Hispanic males of a mean age of 27 years. Despite no significantly different thyroid hormone levels, patients with TPP presented with less-severe signs and symptoms of hyperthyroidism, as reflected by lower Burch-Wartofsky score on admission (19 vs. 35; P<.001) and lower occurrence of atrial fibrillation in the TPP group (0% vs. 36%; P<.001). Finally, 89% of TPP patients presented with corrected QT (QTc) prolongation, whereas only 19% of thyrotoxic patient presented with a prolonged QTc. Conclusion: Hispanic patients with TTP seems to have relative resistance to the actions of thyroid hormones and commonly present with QTc prolongation, a risk factor for cardiac arrhythmias. Abbreviations: BWS = Burch-Wartofsky point scale; EKG = electrocardiogram; FT3 = free triiodothyronine; FT4 = free thyroxine; ICD = International Classification of Diseases; QTc = corrected QT; TPP = thyrotoxic periodic paralysis
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Shrestha, Bishow Chandra, Chheki Sherpa, Swarup sharma Rijal, Vasudev Magaji, and Vinita Singh. "Thyrotoxic Periodic Paralysis: A Rare Presentation of Graves’ Disease." Journal of the Endocrine Society 5, Supplement_1 (2021): A966—A967. http://dx.doi.org/10.1210/jendso/bvab048.1975.
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Abstract Background: Thyrotoxic periodic paralysis (TPP) is a rare but serious thyroid emergency characterized by hypokalemia, acute onset flaccid paralysis & thyrotoxicosis. Typically, seen in an Asian male with untreated hyperthyroidism symptoms, who awakens at night or in the early morning with flaccid ascending paralysis. This is precipitated by exercise, alcohol or carbohydrate rich meal. TPP is widely reported & studied in Asian population. Its prevalence is about 2 % in Asian hyperthyroid patients. However, incidence is 0.1-0.2% in non-Asian hyperthyroid patients. Clinical Case: 33-year-old Caucasian male with celiac disease and no thyroid disease sought emergency care for complaints of sudden onset severe weakness in all extremities. He reported 20-pound unintentional weight loss, intermittent palpitations and low-grade fever. He noticed leg cramps with numbness and unable to move his extremities. At initial evaluation, he had acute flaccid paralysis and tachycardia. Initial laboratory studies showed potassium at 1.9 mmol/l, Magnesium at 1.8, suppressed TSH &lt;0.005 uIU/ml with elevations in free T4 at 2.43 ng/dl and total T3 at 1.9 ng/ml. CT and MRI head were normal. Patient’s aldosterone level was normal. The patient’s paralysis and hypokalemia resolved after potassium replacement. Thyroid stimulating immunoglobulin was elevated and increased vascularity suggestive of Grave’s disease noted on thyroid Ultrasound. Methimazole and propranolol were initiated. His neurological workup was negative. After resolution of paralysis and hypokalemia he was discharged home. Since our patient presented with severe hypokalemia, flaccid paralysis and hyperthyroidism, that resolved promptly with potassium replacement, hence likely diagnosis of thyrotoxic periodic paralysis. Discussion: Thyrotoxic periodic paralysis is potentially reversible and mostly seen with Graves’ disease among Asian population. Early diagnosis & treatment prevents life threatening complications. Differential diagnosis of TPP includes familial periodic paralysis, Guillain-Barre Syndrome & acute intermittent porphyria. Diagnosis is based on family history, characteristic presentation, hyperthyroidism with low serum potassium level. Possible mechanism is increased sodium-potassium ATPase activity in the skeletal muscle membrane leading to intracellular shift of potassium causing hypokalemia and muscle inexcitability. Treatment includes potassium replacement, nonselective beta-blocker and definitive treatment of hyperthyroidism, to prevent further episodes.
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Reddy, Yavasani Neil Krishna, Harini Jayaraman, Himamshu Acharya, Gururaja Rao, and H. K. Ganesh. "Thyrotoxic periodic paralysis: A case series." IJEM Case Reports 2, no. 3 (2024): 106–8. http://dx.doi.org/10.4103/ijemcr.ijemcr_44_24.
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ABSTRACT Thyrotoxic periodic paralysis (TPP) is a disorder most commonly observed in Asian men. It is characterized by acute flaccid paralysis with hypokalemia. The condition primarily affects the lower limbs and can be secondary to thyrotoxicosis. The main characteristic features of TPP are increased thyroid hormone levels, hypokalemia and proximal muscle weakness, or paralysis. In this study, we report six cases of TPP. All the cases had potassium levels of <2.5 mEq/L and weakness of limbs, which were reversed after the correction of potassium levels. The etiology of elevated thyroid hormone levels was found to be Graves’ disease in all the cases. Upon treatment of hyperthyroidism, none of the subjects had a recurrence of weakness. In young subjects with sudden-onset weakness, it is important to consider TPP as one of the differential diagnoses.
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Fitriani, Fadlila, Vina Yanti Susanti, and Mohammad Robikhul Ikhsan. "COVID-19 Infection-Related Thyrotoxic Hypokalemic Periodic Paralysis." Case Reports in Endocrinology 2022 (August 24, 2022): 1–4. http://dx.doi.org/10.1155/2022/1382270.
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SARS-CoV-2 infection induces the dysfunction of many organs including the thyroid gland through the role of ACE2 receptors as well as the consequences of the cytokine storm. Thyroid diseases such as subacute thyroidism, Graves’ disease, thyrotoxicosis, and Hashimoto’s thyroiditis have been documented in patients with SARS-CoV-2 infection. However, there are limited reports about the consequences of SARS-CoV-2 infection-related thyroid complications. We describe a case of man who was admitted to the emergency department due to repeated lower limb weakness since diagnosed with COVID-19. He had refractory hypokalemia and was treated with potassium replacement therapy for 2 months. However, the complaints continued. The patient has no history of thyroid disease, yet the laboratory result showed hyperthyroidism. Accordingly, he received oral thiamazole. As the laboratory parameters of the thyroid hormones improved, potassium levels returned to normal and the limb weakness stopped. This unusual thyroid complication should be considered in SARS-CoV-2 infection. The prompt diagnosis and appropriate therapy can reduce the burden of the disease.
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Seetharaman, Kavita. "Thyrotoxic Periodic Paralysis." Journal of the Endocrine Society 5, Supplement_1 (2021): A965—A966. http://dx.doi.org/10.1210/jendso/bvab048.1973.
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Abstract Thyrotoxic Periodic Paralysis (TPP) is an emergency associated with flaccid paralysis in which the paralysis is reversible with prompt potassium replacement and the attacks are terminated when hyperthyroidism is cured. Timely diagnosis and treatment are therefore prudent. While managing patients with flaccid paralysis, physicians should be aware of TPP as potential etiology and investigate history to identify the triggering factors and provide timely and cautious treatment with replacement of potassium, further addressing permanent approaches to treating thyrotoxicosis to prevent future recurrences of TPP. We report a clinical scenario of a patient who experienced TPP.22-year-old male, laying down at home at around 1:45pm developed sudden onset bilateral lower extremity weakness and was unable to stand up. His weakness was associated with thigh pain with exertion. He was eventually able to walk a few steps, but then fell onto his knees. He reported having a carbohydrate rich lunch at noon. Notably, patient underwent surgery under general anesthesia for a deviated nasal septum the day before. His neurological examination was remarkable for giveaway proximal lower extremity weakness involving only select muscle groups. Examination and CT/CTA of head and neck findings was not consistent with acute stroke. Myopathy secondary to electrolyte imbalance, drug/toxin, infection, or inflammatory disorders, myelopathy and myasthenia gravis were considered in the differential. Labs revealed suppressed TSH &lt;0.01uIU/mL, elevated FT4 of 6ng/dL and low serum potassium of 2.6mmol/L. CT scan of the neck revealed enlarged thyroid gland and thymic enlargement. Patient was given intravenous bolus of potassium chloride 20 mEq and serum potassium normalized in 4 hours to 3.8mmol/L. His lower extremity weakness resolved within 3hours of potassium replacement. The next day his serum potassium was 5.2mmol/L. His thyroid stimulating immunoglobulin index was elevated at 1.4 (normal &lt;1.3). He was started on propranolol, methimazole and advised to return to the endocrinology clinic to discuss permanent treatment options for hyperthyroidism to prevent TPP. Reviewing his prior medical history, he was diagnosed with Graves’ disease 5 months prior to the emergency room evaluation and was started on methimazole. He took methimazole for 2 months and did not return to follow up until the occurrence of TPP. He did not experience symptoms of hyperthyroidism in the interim. Discussion: TPP is a rare disorder with a prevalence of 0.1-0.2% in North America. TPP commonly affects Asian and Latin Americans males. The episodes of TPP are influenced by genetic, environmental, and ethnic factors. Common environmental triggers include carbohydrate rich meals, rest after intense physical exertion, fever, infection, trauma, emotional stress, and smoking. Thymic hyperplasia has also been reported to be associated with hypokalemic periodic paralysis. Clinical Presentation: The motor weakness tends to affect proximal lower extremities as noted in our patient’s presentation and is usually associated with hyporeflexia and is painless. Cardiac arrhythmias due to hypokalemia are rare, though ventricular fibrillation have been reported, and respiratory failure requiring mechanical ventilation is a possibility. Pathophysiology: TPP has been thought to be a channelopathy associated with increased Na+–K+ ATPase activity and loss of function mutation of the Kir 2.6 potassium efflux channel resulting in intracellular pooling of potassium and transient hypokalemia. The attacks are stimulated by thyroid hormone excess and/or hyperadrenergic activity and hyperinsulinemia, most commonly due to carbohydrate load or intravenous fluids containing dextrose. Treatment should include:1.Potassium supplementation to reverse paralysis and prevent life threatening cardiac arrhythmias. Care must be taken to not over replace potassium, as it could result in hyperkalemia when potassium channels revert to functioning normally.2.Propranolol, a non-selective betablocker works by blocking the thyroid hormone mediated adrenergic overstimulation of the Na-K ATPase channel, there by limiting the intracellular pooling of potassium.3.Definitive treatment of thyrotoxicosis should be offered. Studies comparing various modalities of treatment of thyrotoxicosis in the setting of TPP indicate permanent treatment with either radioactive iodine or thyroidectomy are often successful in preventing recurrence of TPP, as relapse events are higher in treatment with antithyroid drugs. Caution should be taken to prevent surge of thyroid hormone release following radioactive iodine treatment, as this can trigger TPP. Higher doses of radioactive iodine might be required to render hypothyroidism and prevent TPP recurrences. There is one case report of hypokalemic periodic paralysis associated with thymic hyperplasia that was treated with thymectomy. Our patient had multiple triggers leading to periodic paralysis, including a prior untreated Graves’ disease due to non-adherence to treatment during COVID-19 pandemic, general anesthesia for nasal septal surgery the day before presenting with TPP, having a carbohydrate rich meal one hour before the episode, and thymic enlargement on neck CT scan. He responded well to potassium replacement, and propranolol. He was started on methimazole and offered permanent treatment options to address hyperthyroidism. References: 1.K Shizume1, Y Shishiba, K Kuma, S Noguchi, J Tajiri, K Ito, J Y Noh. Comparison of the incidence of association of periodic paralysis and hyperthyroidism in Japan in 1957 and 1991. Endocrinol Jpn1992 Jun;39(3):315-8, doi: 10.1507/endocrj1954.39.315 2. R C Griggs, J Resnick, W K Engel. Intravenous treatment of hypokalemic periodic paralysis. Arch Neurol 1983 Sep;40(9):539-40.3. Maciel, R., Lindsey, S. & Dias da Silva, M. Novel etiopathophysiological aspects of thyrotoxic periodic paralysis. Nat Rev Endocrinol7, 657–667 (2011). https://doi.org/10.1038/nrendo.2011.58 4. Chang RY, Lang BH, Chan AC, Wong KP. Evaluating the efficacy of primary treatment for graves’ disease complicated by thyrotoxic periodic paralysis. Int J Endocrinol. 2014; 2014:949068 doi:10.1155/2014/949068 5.Yang R, Jurkat-Rott K, Cao J, et al. Hypokalemic Periodic Paralysis Induced by Thymic Hyperplasia and Relieved by Thymectomy. JAMA Neurol. 2013;70(11):1436–1439. doi:10.1001/jamaneurol.2013.3918
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hâmalla, Amaral Gonçalves, Abero Vale Luísa, Lima Rosa Mendes lice, Elisabeth Sousa Martins Freitas Joana, Moura Melo Suely, and Batista de Montalvão Cunha Diego. "PARALISIA PERIÓDICA HIPOCALÊMICA TIREOTÓXICA: RELATO DE CASO." REVISTA FT 27, no. 125 (2023): 16. https://doi.org/10.5281/zenodo.8265716.
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O presente estudo objetivou descrever um caso de paralisia periódica hipocalêmica tireotóxica (PHTT) de um paciente com diagnóstico de hipertireoidismo. O paciente abandonou o tratamento e foi necessário discutir a importância do reconhecimento e tratamento adequado para evitar complicações em seu quadro de saúde. Foi realizada uma pesquisa aplicada, qualitativa, descritiva, retrospectiva e observacional de caso único. O projeto de pesquisa foi submetido ao Comitê de Ética e Pesquisa e foi aprovado sob o CAAE 63457122.3.0000.5211. O participante do estudo, é um paciente que se apresentou com PPHT atendido em hospital privado de Teresina e os dados foram coletados através do prontuário eletrônico do mesmo. Detalhamento do caso: homem de 22 anos, pardo, com diagnóstico prévio de hipertireoidismo que abandonou o tratamento por 4 anos, acometido por PPHT que em seu primeiro atendimento não foi diagnosticado e retornou posteriormente com piora do quadro, apresentando tetraparesia flácida e arritmia grave que, após reconhecimento e manejo apropriados da equipe, apresentou melhora total do quadro e recebeu alta hospitalar com diagnóstico firmado e com tratamento adequado. Em seguida, realizou-se uma revisão da literatura quanto aos aspectos clínicos, fisiopatologia e diagnóstico, além da discussão acerca de diagnóstico diferencial e princípios do tratamento já publicados. Dado o exposto, diante da dificuldade e falta de conhecimento sobre essa complicação por profissionais de saúde, vê-se que o diagnóstico precoce e manejo adequado são imprescindíveis para prevenir desfechos desfavoráveis causados pela PPHT. A conduta adequada muda a evolução do paciente, evita condutas iatrogênicas, procedimentos desnecessários, internação prolongada e complicações potencialmente fatais.
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Boon, Tay Seng, Tan Yen Yun, and Gerard Jason Mathews. "A CASE REPORT OF THYROTOXIC PERIODIC PARALYSIS." Journal of the ASEAN Federation of Endocrine Societies 40, S1 (2025): 48. https://doi.org/10.15605/jafes.040.s1.078.
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INTRODUCTION/BACKGROUND Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening clinical manifestation of thyrotoxicosis predominantly seen in those of Asian descent between the ages of 20 and 40 years. The attack is characterised by acute and reversible severe muscle weakness with hypokalemia that resolves with the treatment of hyperthyroidism. CASE A 22-year-old Chinese male with no previous medical illness presented to the emergency department with sudden onset bilateral lower limb weakness associated with intermittent palpitations for the past month. Lower limbs neurological examination revealed proximal muscle weakness but preserved tone, reflexes and sensation. There was a small diffuse goitre and fine tremors on the bilateral hands. He did not have features of thyroid eye disease or a thyroid bruit. Additionally, he denied any family history of thyroid disorders. Electrocardiogram showed sinus tachycardia, flattened T-waves and generalised U-waves. Laboratory assessments showed severe hypokalemia with a serum potassium level of less than 1.5 mmol/L (NR: 3.4–4.5). He was given intravenous potassium correction (KCl) twice (4 g in total) and 4 pints maintenance drips at 1.5 g KCl per pint. Thyroid function tests and TSH receptor antibodies were suggestive of Graves’ Disease. He was discharged home with carbimazole and propranolol and remains well after discharge. CONCLUSION Thyrotoxic periodic paralysis should be considered in the differential diagnosis of neuromuscular weakness in the context of hypokalaemia by the treating physicians. In TPP, hypokalaemia results from an intracellular shift of potassium induced by thyroid hormone sensitisation of the Na⁺/K⁺–ATPase pump, triggering muscle weakness and paralysis. The importance of prompt recognition, early diagnosis and treatment of the condition can prevent severe complications, such as cardiac dysrhythmia and respiratory failure. The addition of non-selective beta-blockers, such as propranolol, is utilised to treat and prevent paralytic attacks by mitigating hyperadrenergic activity and improving hypokalaemia.
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Weinstein, Robert, Arwa Albashaireh, Aashka Shah, Sabah Syed, and Syeda Naqvi. "PSAT356 Propranolol Improves Bulbar Dysfunction Seen in Hyperthyroidism." Journal of the Endocrine Society 6, Supplement_1 (2022): A838. http://dx.doi.org/10.1210/jendso/bvac150.1732.
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Abstract Background Many symptoms of hyperthyroidism are mediated by the augmented activity of the adrenergic central nervous system. Rarely, symptoms of bulbar dysfunction are seen with thyrotoxicosis such as dysphagia and dysarthria. Beta blockers can abort or reduce these symptoms before anti-thyroid drugs are used. Case A 59-year-old woman with hypertension and gout, presented to the emergency department with poor oral intake and difficulties swallowing. Symptoms initially started as hoarseness of voice for 3 weeks then progressed to Globus sensation, difficulties swallowing and aspiration of solids and liquids. She also reported generalized muscle weakness, palpitations, increased sweating, tremors and 20 pounds weight loss in the preceding 2 months. Physical exam showed an ill-appearing, catechetic woman. Luedde exophthalmometry showed an absence of proptosis measuring 15 mm bilaterally without lid lag or stare and extraocular muscles were intact. The skin was silky without edema. The strength in the lower extremities was decreased and she was unable to squat or raise from a seated position. Labs showed creatinine of 2.7 mg/dL (0.4–1 mg/dL), BUN 49 (6–20 mg/dL), potassium of 3.1 (3.5–5.1 mmol/L), TSH &lt; 0.02 (0.34–5.60 uIU/mL), FT4: 3.72. CT of the neck was obtained and multiple sub-centimetric hypodense thyroid nodules with calcifications were noted in the left thyroid lobe. Intravenous potassium chloride was given without improvement of dysphagia. 10 milligrams (mg) of propranolol were ordered to be given every 8 hours. After the first dose and over the next 24 hours she reported rapid improvement in dysphagia and muscle weakness. She was discharged on 15 mg of methimazole twice daily and propranolol 10 mg thrice daily. TSI and TRAB were elevated at 1.03 (normal &lt; 0.54 IU/L) and 2.20 (normal&lt;1.75 IU/L) respectively and the diagnosis of Graves’ disease was made. At her 3 weeks follow up, TSH was &lt;0.02 (0.34–5.60 uIU/mL) with normal FT4. She reported complete resolution of dysphagia and improvement in lower extremities weakness. Discussion Hyperthyroidism may exert powerful effects on the neuro-muscular system. The pathogenesis of myopathy in hyperthyroidism is not fully understood. In hyperthyroid periodic paralysis, hypokalemia is present, and paresis is corrected with potassium supplementation. Our patient's symptoms did not improve with potassium supplement but dramatically improved after propranolol use and before the thyroid function was normalized. This implies a role of adrenergic overactivity in myopathy of hyperthyroidism. A study1 was conducted to quantify muscular weakness in hyperthyroidism and assess the response to therapy concluded that propranolol improves muscular weakness. Conclusion Prior to normalization of thyroid function, the use of beta blockers can alleviate symptoms of bulbar dysfunction. (1)Olson BR, Klein I, Benner R, Burdett R, Trzepacz P, Levey GS. Hyperthyroid myopathy and the response to treatment. Thyroid. 1991;1(2): 137-41. doi: 10.1089/thy.1991.1.137. PMID: 1688015. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.
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Yamada, Kota, Akiyo Tanabe, Makiko Hashimoto, Mitsuru Ohsugi, Kohjiro Ueki, and Hiroshi Kajio. "A single-center retrospective study on the clinical features of thyrotoxic periodic paralysis." PLOS ONE 19, no. 8 (2024): e0308076. http://dx.doi.org/10.1371/journal.pone.0308076.
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Purpose Thyrotoxic periodic paralysis (TPP) is characterized by muscle paralysis and significant intracellular potassium movement resulting in hypokalemia. Since TPP is a rare condition, only a few studies have explicated the clinical characteristics of patients with this disease. This study aimed to elucidate the clinical characteristics of patients with TPP by comparing them with those with thyrotoxicosis without paralysis (non-TPP) and sporadic periodic paralysis (SPP). Methods This was a single-center retrospective cohort study. Clinical data of patients with hyperthyroidism (n = 62) or periodic paralysis (n = 92) who were emergently admitted to our hospital was extracted from the electronic medical records and analyzed. Results All patients in the TPP group (15 males and 2 females) had Graves’ disease, with 14 being newly diagnosed. The average serum potassium level on admission was 2.3±0.75 mEq/L. No significant correlation was observed among serum potassium level, amount of potassium required for normalization, and thyroid hormone levels. The TPP group showed significantly younger age, higher male ratio and body mass index (BMI), and lower serum potassium and phosphorus levels than the non-TPP group, which comprised 36 patients with Graves’ disease. No significant differences were observed between the TPP and SPP (n = 11) groups in terms of age, sex, BMI, serum electrolyte levels, potassium requirement for normalization, and recovery time. Main conclusions Considering that most patients with TPP have undiagnosed Graves’ disease, distinguishing TPP from SPP based on clinical information and course alone is difficult in emergency settings. Therefore, for early detection and launch of specific treatment of Graves’ disease, screening for thyroid hormone and anti-thyroid stimulating hormone receptor antibody levels is necessary when treating patients with periodic paralysis.
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Joshi, Mugdha, Wael Salameh, Janine Vintch, and Elizabeth Leigh Goodman. "Hypokalemic periodic paralysis presenting as cardiac arrest." BMJ Case Reports 17, no. 11 (2024): e259889. http://dx.doi.org/10.1136/bcr-2024-259889.
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Hypokalemic periodic paralysis (HPP) is a channelopathy with a genetic predisposition which may occur in the presence or absence of hyperthyroidism. We present a unique case of severe HPP associated with both Grave’s thyrotoxicosis and pemphigus vulgaris. The patient developed proximal limb weakness after treatment with rituximab. He then subsequently presented with witnessed ventricular fibrillation arrest. Cardiopulmonary resuscitation was initiated in the field and return of spontaneous circulation was achieved. His initial potassium was 1.9 mmol/L with a marked metabolic acidosis.
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Menon, Saieehwaran, Xin Yi Ooi, Sue Wen Lim, Hui Chin Wong, and Sy Liang Yong. "WHEN THE CURE BITES BACK." Journal of the ASEAN Federation of Endocrine Societies 40, S1 (2025): 60. https://doi.org/10.15605/jafes.040.s1.100.
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INTRODUCTION/BACKGROUNDMusculoskeletal complaints, including myositis, are common in thyroid disorders. However, it is a rare and non-classical side effect of antithyroid drugs. CASEA 35-year-old male with Graves' disease was admitted for symptomatic thyrotoxicosis despite treatment with high-dose carbimazole, lithium and dexamethasone for direct observed therapy (DOTS). On examination, he exhibited signs of thyrotoxicosis, including tremors, sweaty palms, proptosis and a large goitre. Thyroid function tests revealed overt thyrotoxicosis (TSH <0.001 mIU/L, T4 122.5 pmol/L). He responded well to DOTS on the same treatment, with T4 decreasing to 27 pmol/L by Day 10 of admission. However, he developed severe proximal muscle aches on day 10. Laboratory investigation revealed an elevated creatinine kinase (CK) level of 5662 IU/L. A diagnosis of carbimazole-induced myositis was made, prompting the discontinuation of carbimazole and initiation of intravenous hydration and cholestyramine while continuing lithium and steroids. The myositis improved, but there was a rebound in his thyrotoxicosis (T4 52 pmol/L), prompting a trial of propylthiouracil, which led to a flare of the myositis (CK 1328 IU/L). He was planned for urgent total thyroidectomy then and was started on Lugol’s iodine. Myalgia and elevated CK levels are rare but recognised manifestations of hyperthyroidism. These can be due to direct effects of thyrotoxicosis on skeletal muscle, thyrotoxic hypokalemic periodic paralysis and drug-induced myositis by carbimazole and propylthiouracil. The pathophysiology of drug-induced myositis may be due to the abrupt decrease in circulating thyroid hormones, leading to a relative hypothyroid state in the peripheral tissues and resulting in myositis. Thioamides may also have a direct toxic effect on myocytes and trigger a local immune response at myocytes, leading to myositis. CONCLUSIONThis case highlights myositis as a rare side effect of anti-thyroid drugs and can cause significant morbidity. Early recognition and close monitoring are essential for managing this condition.
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Kotaru, Rakesh Chowdary, and Suresh Kumar Paidi. "Atrial Arrhythmia: A Rare Presentation of Thyrotoxic Hypokalemic Periodic Paralysis." Indian Journal of Clinical Cardiology, December 30, 2024. https://doi.org/10.1177/26324636241307427.
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Thyrotoxic hypokalemic periodic paralysis is a rare but life-threatening complication of hyperthyroidism characterized by hyperthyroidism, hypokalemia, and transient episodes of acute proximal muscle weakness. Incidence of thyrotoxic hypokalemic periodic paralysis is more common in Asian men and extremely rare in blacks. The basic mechanism includes thyrotoxicosis-induced hypokalemia leading to muscle weakness associated with respiratory insufficiency and fatal arrhythmias. We present a rare case of atrial arrhythmia as the initial presentation of thyrotoxic hypokalemic periodic paralysis.
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ALakkad, Ashraf. "Hypokalemic Paralysis Due to Thyrotoxicosis." International Journal of Advances in Nephrology Research Page 8-13 (January 5, 2022). https://doi.org/10.5281/zenodo.7361762.
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Thyrotoxicosis hypokalemic paralysis is a relatively uncommon, life-threatening complication of hyperthyroidism that is most frequently seen in young Asian males but can occur sporadically in other races. The present case report discusses a 33-year-old non-diabetic non-alcoholic male admitted to the emergency room with complaints of lower limb weakness, generalized body aches, and palpitations. Laboratory investigations showed extremely low levels of potassium. An ECG showed ST depression, T-wave inversion, a prolonged Q-T interval, and the presence of a U-wave. T4 and thyroid antibody levels were found to be abnormally raised, indicating thyrotoxicosis. On a thyroid ultrasound image, enlargement of both thyroid lobes with homogenous texture and marked vascularity was noted. This hidden thyrotoxicosis led to hypokalemia which caused paralysis, palpitations, and associated symptoms. The patient was treated with intravenous potassium and other medications accordingly. The above-mentioned case was a unique presentation, one that was not commonly found in the hospital with such evident indications resulting in an absolute diagnosis. This case study will explore how the patient was diagnosed and managed with intravenous potassium to relieve hypokalemic paralysis caused by thyrotoxicosis.
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Mohamed, Hawa Nuradin, Abdi Karim Ahmed Ghedi, Sevgi Ozturk, Mohamed Osman Omar Jeele, and Ahmed Muhammad Bashir. "Hypokalemic periodic paralysis as the first sign of thyrotoxicosis- a rare case report from Somalia." Thyroid Research 16, no. 1 (2023). http://dx.doi.org/10.1186/s13044-023-00158-4.
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Abstract Background Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare complication of hyperthyroidism characterized by thyrotoxicosis, hypokalemia, and paralysis. It is the most common form of acquired periodic paralysis. THPP is precipitated by strenuous exercise, a high carbohydrate diet, stress, infection, alcohol, albuterol, and corticosteroid therapy. It is most common in Asian men with hyperthyroidism and exceptionally rare in black people. Case Presentation A 29-year-old man was admitted to the emergency department in Somalia with a sudden onset of paralysis after a high carbohydrate meal. Laboratory investigations showed low serum potassium 1.8 mEq/l (3.5–4.5), and biochemical thyrotoxicosis with TSH 0.006 miu/l (0.35–5.1), total T3 3.2 ng/ml (0.9–2.8) and total T4 13.5 ng/ml (0.6–1.2). He was successfully treated with potassium chloride infusion and an antithyroid drug, methimazole. Conclusion To prevent life-threatening cardiac and respiratory complications, it is critical to consider and diagnose THPP early, even in populations where the condition is rare.
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Kadek Reisya Sita Damayanti and Rizaldy Taslim Pinzon. "Acute Hypokalemia Related with Thyrotoxicosis Periodic Paralysis: A Case Report." Acta Neurologica Indonesia 2, no. 02 (2024). http://dx.doi.org/10.69868/ani.v2i02.26.
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Introduction : Hypokalemia paralysis is a rare condition. Thyrotoxic periodic paralysis (TPP) is a condition of hyperthyroidism characterized with acute muscle weakness and hypokalemia. TPP is commonly found in young Asian male. TPP is an uncommon clinical entity and might be a life threatening complication of thyrotoxicosis. We report a rare case of TPP with ECG abnormality related with severe hypokalemia. Case Report : A-21-year old Javanese male was presented to emergency department with acute onset of lower bilateral extremities weakness with proximal muscle predominant. Weakness progressed to his bilateral upper limb. Patient denied any significant trauma, vomiting, diarrhea, chest pain. Patient was fully conscious. Neurological examination revealed four limb weakness (lower limb muscle strength 2 from 5 scale MRC), diminished deep tendon reflexes, and intact sensory. Laboratory were remarkable for severe hypokalemia of 1.86 mEq/L. Further tests showed low TSH (0.022 mU/L), increased FT4 (23,68 mmol/L). ECG test showed abnormality related with hypokalemia. Thyroid ultrasound revealed multiple thyroid swelling, mass, and calcification. Patient was admitted to ICU and administered with 25mEq Potassium IV. Hypokalemia resolved after 3 days (Serum Potassium 3.76 mEq/L), followed by normal ECG feature without any AV block. He was discharged without any neurological abnormaliy. Conclusion : We report a rare case of acute onset paralysis and markedly low potassium level and high free T4 in previously health Asian male. This case highlights the paralysis related with hyperthyroidism that resolved completely following potassium replacement. Keywords: hypokalemia; paralysis; hyperthyroid; thyrotoxicosis periodic paralysis
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Scheive, Melanie, Neha Patel, and Zeb Saeed. "High-dose intravenous hydrocortisone for the treatment of hyperthyroidism: a rare precipitant of thyrotoxicosis periodic paralysis." Endocrinology, Diabetes & Metabolism Case Reports 2023 (February 1, 2023). http://dx.doi.org/10.1530/edm-22-0358.
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Summary Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism triggered by precipitants that increase the activity of the sodium-potassium pump in the skeletal muscle. In our case study, a previously healthy 34-year-old male presented to the emergency department with new onset thyrotoxicosis, secondary to Graves’ disease. Given the severity of his triiodothyronine (T3) thyrotoxicosis, he was admitted and started on a high dose of beta-blocker, thioamides, and intravenous hydrocortisone. On the second day of his hospitalization, he developed acute flaccid paralysis of his lower extremities. Subsequent stroke workup was negative, and his electrolytes revealed severe hypokalemia and hyperglycemia consistent with TPP. He was treated with potassium and had a complete recovery of his paralysis and hypokalemia within hours. The patient has not had any recurrence since this singular episode in the hospital. This case highlights the scenario where the treatment of hyperthyroidism with high-dose corticosteroids to reduce the conversion of thyroxine to T3 inadvertently resulted in TPP. Clinicians should be aware of this potentially rare but serious consequence of using steroids to manage hyperthyroidism. Learning points High-dose steroids used to treat hyperthyroidism in hospitalized patients may rarely precipitate thyrotoxic periodic paralysis (TPP) by inducing hypokalemia and hyperglycemia. TPP should be included in the differential diagnosis for acute flaccid paralysis in hospitalized patients with hyperthyroidism. Since TPP is associated with trans-cellular shifts in potassium instead of total body potassium depletion, conservative repletion of potassium is recommended to avoid rebound hyperkalemia.
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Maltese, Virginia, Elisa Gatta, Irene Silvestrini, et al. "An Unusual and Severe Thyrotoxicosis in a Twin Pregnancy: Fortune Favors the Brave." Case Reports in Endocrinology 2025, no. 1 (2025). https://doi.org/10.1155/crie/6298137.
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Graves’ disease (GD) and gestational transient thyrotoxicosis (GTT) are the most common causes of thyrotoxicosis during pregnancy, with prevalence ranging from 0.1% to 1% and from 1% to 3%, respectively. Hyperthyroidism during pregnancy can have severe consequences if not promptly recognized and treated. Even more severe, if possible, is the thyroid storm, a life‐threatening complication of hyperthyroidism, characterized by severe and dramatic clinical manifestations of thyrotoxicosis. No prior history of thyroid disease, absence of GD stigmata, negative thyrotropin (TSH) receptor antibody levels, serum human chorionic gonadotropin (hCG) higher on average, and symptoms of emesis may lead to the diagnosis of GTT. Few cases of thyroid storm during pregnancy are reported in literature, mainly due to gestational trophoblastic disease. We report a rare and severe case of thyroid storm in a 24‐year‐old woman at 15 weeks’ gestation with twins, likely due to GTT, precipitated by acute myocarditis. Initially presenting with weakness, vomiting, and sinus tachycardia, the patient rapidly deteriorated into a life‐threatening condition characterized by hypokalemia, myocardial injury, and severe thyrotoxicosis. Cardiac imaging later revealed acute myocarditis. Thyroid function stabilized at the end of the pregnancy, allowing discontinuation of methimazole. Both fetuses were delivered via emergency cesarean section at 36 weeks, with no significant congenital abnormalities. This case highlights the complexity of diagnosing and managing hyperthyroidism in twin pregnancies, particularly in the context of hyperemesis gravidarum (HG).
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Zhang, Zhi, and Banghui Xiao. "Case report: SCN4A p.R1135H gene variant in combination with thyrotoxicosis causing hypokalemic periodic paralysis." Frontiers in Neurology 13 (January 17, 2023). http://dx.doi.org/10.3389/fneur.2022.1078784.
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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_000334.4 (SCN4A):c.3404G&gt;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.
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Sinha, Suresh, and Nagarajan Raghupathy. "Thyrotoxic Periodic Paralysis." JOURNAL OF CLINICAL AND DIAGNOSTIC RESEARCH, 2020. http://dx.doi.org/10.7860/jcdr/2020/44218.13836.
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Thyrotoxic periodic paralysis is not uncommon in people of Asian origin. It presents as sudden onset paralysis resulting from hypokalemia due to intracellular shift of potassium because of thyroid hormone sensitive Sodium-Potassium ATPase. A 34-year-old male with history of weight loss, palpitation and increased sweating for three months presented with sudden onset weakness of both lower limbs, two hours post-dinner. On investigation, he was found to be having hypokalemia as well as thyrotoxicosis. His potassium was corrected and was put on non-selective beta blocker and carbimazole. The patient improved within 24 hours and was discharged with advice to continue with Inderal and Carbimazole and report after one month. Hyperthyroidism should be included in differential diagnosis of sudden onset lower limb weakness.
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Bayrak Demirel, Ozge, Cansu Koc, Ummahan Tercan, et al. "Thyrotoxic hypokalemic periodic paralysis induced by high-dose insulin in an adolescent male with type 1 diabetes mellitus." Hormone Research in Paediatrics, December 24, 2024, 1–8. https://doi.org/10.1159/000543329.
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Introduction: Thyrotoxic hypokalemic periodic paralysis (THPP) is a rare but severe complication of hyperthyroidism characterized by acute muscle weakness. This study reports the first case of THPP in an adolescent with type 1 diabetes mellitus (T1DM) and Graves' disease, triggered by high-dose insulin, high carbohydrate intake, and strenuous exercise. It highlights the clinical presentation, management, and implications of THPP in this context. Case presentation: A 17-year-old male patient with T1DM and Graves’ disease presented to the emergency department with weakness in the extremities. The patient had engaged in strenuous exercise, high dose rapid-acting insulin, and consumed a large amount of rice shortly before the onset of the symptoms. He exhibited hypertension and tachycardia, with diminished muscle strength and deep tendon reflexes with severe hypokalemia (1.6 mmol/L). Treatment with potassium and magnesium replacements was initiated. The patient's symptoms resolved within five hours, and his neurological examination was normalised. Hypokalemia did not recur during follow-up. All symptoms improved rapidly with potassium replacement, beta-blocker therapy, and antithyroid treatment. Conclusion: This case represents the first documented instance of THPP in an adolescent with T1DM and Graves' disease. This entity should be included in the differential diagnosis of acute paralysis in patients with known thyrotoxicosis or those exhibiting symptoms such as tachycardia and hypertension. Insulin treatment in a hyperthyroid diabetic patient may increase the risk of THPP.
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Wang, Yan-Li, and Jian Li. "Insulin-induced severe thyrotoxic periodic paralysis: A case report." World Journal of Clinical Cases 13, no. 7 (2025). http://dx.doi.org/10.12998/wjcc.v13.i7.101214.
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BACKGROUND Thyrotoxic periodic paralysis (TPP) is an endocrine emergency caused by thyrotoxicosis, manifesting mainly as periodic myasthenia and hypokalemia, and posing a serious threat to the patient's health. Fatigue, strenuous exercise, alcohol abuse, high carbohydrate intake and insulin injections are common triggers of paralysis. This article reports a case of severe TPP induced by insulin injection, elucidates the characteristics and pathogenesis of the disease, analyses the risk factors for triggering TPP, and hopefully provides more clinical data for TPP patients. CASE SUMMARY A 38-year-old Asian man presented to the emergency department with a one-week history of limb weakness and worsening half-day. His medical history included poorly controlled type 2 diabetes and he had been switched to Aspart50 a week earlier. He was alert and oriented with upper extremity strength grade 3 and lower extremity strength grade 1. Emergency department tests showed hypokalemia of 1.6 mmol/L. The paramedics administered 1.5 g of potassium intravenously, followed by 4.0 g orally. Weakness in the arms and legs improved. He was referred to endocrinology where he was diagnosed with Graves' disease, with suboptimal control and insulin injections possibly causing TPP. We stopped his insulin and he was discharged with a potassium level of 4.0 mmol/L. CONCLUSION Insulin is a trigger for TPP and should be avoided in patients with hyperthyroidism. Early recognition and treatment of TPP is crucial, especially in patients presenting with hypokalemic periodic paralysis.
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Mathew, Jilcy Joy, and Ariana R. Pichardo-Lowden. "SUN-507 Fueling the Fire: A Case of Hypokalemic Periodic Paralysis Associated with Type I Renal Tubular Acidosis and Thyrotoxicosis in Pregnancy." Journal of the Endocrine Society 4, Supplement_1 (2020). http://dx.doi.org/10.1210/jendso/bvaa046.952.
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Abstract Background: Hypokalemic periodic paralysis (HPP) related to thyrotoxicosis, though rare, is more often seen in Asian males. Type 1 renal tubular acidosis (T1 RTA), which can also cause HPP, is typically managed with alkali therapy and potassium supplementation, though there are no well-established guidelines for management in pregnancy. Clinical Case: A 27-year-old Puerto Rican woman, at 32 weeks gestation, presented to the hospital with sudden onset muscle weakness, and was found to have 1/5 muscle strength in her lower extremities. She had no personal or family history of similar illness. Laboratory analysis revealed hypokalemia (potassium 2.0 mmol/L, range: 3.5 – 5); non-gap metabolic acidosis (sodium 137mmol/L, range 136 – 145; chloride 113 mmol/L, range 98- 107; and bicarbonate 8 mmol/L, range 22 – 29); and an arterial pH of 7.09. Urine studies demonstrated a urine pH of 6.5 and a urine sodium of 32 mmol/L which was diagnostic of T1 RTA in the context of her metabolic derangements. She was treated emergently with potassium and bicarbonate infusions, with improvement in her symptoms. Subsequent thyroid function testing revealed: a low TSH of 0.01 uIU/ml, normal free T4 of 1.66 (range: 0.9 - 1.7) ng/dl, normal free of T3 3.7 (range: 2.0 -4.4) pg/ml and elevated total T4 of 16.5 (range: 4.5 - 11.7) ug/dl. Renal ultrasound demonstrated medullary nephrocalcinosis. She was discharged on potassium and sodium citrate tablets. At 37 weeks, the patient was readmitted for induction of labor due to pre-eclampsia, and delivered a healthy male baby. Several months later, she presented to the Endocrinology clinic with symptoms of increased frequency bowel movements, palpitations and heat intolerance, which had been ongoing since pregnancy. On review, a metabolic panel prior to pregnancy had demonstrated non-gap acidosis and mild hypokalemia. Further testing demonstrated the following: TSH &lt; 0.01 uIU/ml, Free T4 1.71 ng/dl, Free T3 4.8 pg/ml, TSI 280%, and a thyroid uptake scan with homogenous radiotracer uptake, with a 24-hour uptake of 40%. She was started on methimazole therapy, and continued on potassium and sodium citrate tablets with clinical and biochemical improvement. Conclusion: Thyrotoxicosis can augment hypokalemia in T1 RTA, and can increase the risk of HPP. Our patient had biochemical evidence of RTA prior to pregnancy, though without episodes of HPP, and we believe that her hyperthyroidism, triggered by pregnancy, may have been the additional insult that precipitated her paralysis. This is the first reported case of HPP related to co-existing thyrotoxicosis and T1 RTA in a pregnant individual. Reference:1. Tu ML, Fang YW, Leu JG, Tsai MH. An atypical presentation of high potassium renal secretion rate in a patient with thyrotoxic periodic paralysis: a case report. BMC Nephrol. 2018;19(1):160. Published 2018 Jul 4. doi:10.1186/s12882-018-0971-9
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Godfrey, Sean, Victoria Hudspeth, Patricia Amoako, and Michael Drewno. "SUN-519 Hypokalemic Periodic Paralysis." Journal of the Endocrine Society 4, Supplement_1 (2020). http://dx.doi.org/10.1210/jendso/bvaa046.395.
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Abstract Background:Hypokalemic periodic paralysis is a rare disorder associated most often with a genetic defect in electrolyte channels, which can also occur in the setting of thyrotoxicosis. The presenting state in the acquired form has a low potassium, low TSH, high free T4 or high T3. It is more common in men, and in the Asian population with an approximate incidence of 2%. Symptoms can last from hours to days and are often precipitated by stress, exercise, and/or high carbohydrate intake. It is believed that the excess thyroid hormone creates an increased catabolic state which drives potassium inward and hyperpolarizes the muscle membrane to create a paralytic state. Case:A 23 year old African American male presented with chest discomfort and palpitations. TSH was &lt;0.01 μU/mL (normal 0.530 - 6.340) with a free T4 of 3.31 ng/dL (normal 0.60–1.60). EKG showed ventricular conduction delay and he was sent home on propranolol 20mg daily and methimazole 5mg three times daily. He returned 5 days later with worsening palpitations and now new onset weakness. He was found to have a potassium of 1.4 mmol/L (normal 3.5–5.1) and magnesium of 1.2 mg/dL (normal 1.6–2.5). EKG showed normal sinus rhythm at a rate of 97, prolonged QT at 524msec (normal 330–470 msec), with repeat EKG 20 minutes later showing atrial tachycardia with a rate of 114 (normal 60–100). He was not able to move anything beyond his head, other than minor upper extremity hand movements, and could not sit up in bed. His potassium was initially repleted with eight doses of 10mEq KCl given q1h. His paralysis significantly improved within the first 4hrs, and was completely resolved by the next morning. Additional lab workup revealed thyroid stimulating antibody level of 13.00% (normal 0.0–0.55). He was discharged on methimazole 10mg twice daily and propranolol 10mg twice daily with instruction to follow up closely with his primary care physician and endocrinology. Conclusion:This patient presented with acute onset of weakness and palpitations in the setting of hyperthyroidism from Graves’ disease and hypokalemia consistent with thyrotoxic periodic paralysis. The physiology behind the presentation is not clear, but the current hypothesis is that depolarization of the neuromuscular junction leads to a tonic state from hyper-polarization. Thyroid hormone increases the metabolic demand, which along with an increase in sympathetic tone drives the sodium-potassium ATPase activity into overdrive, thus decreasing extracellular potassium. Thyrotoxic periodic paralysis is rare presentation, but should be considered for any patient that presents potassium abnormalities and symptoms of thyrotoxicosis.
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Nosova, Emily V., Emily Japp, Sheldon T. Brown, Alan J. Cohen, and Pietra D. Greenberg. "SUN-518 Graves’ Disease Newly Diagnosed in the Setting of Hypokalemic Periodic Paralysis in an HIV+ Patient." Journal of the Endocrine Society 4, Supplement_1 (2020). http://dx.doi.org/10.1210/jendso/bvaa046.812.
Full textAbstract:
Abstract Relevance: A rare yet distinct cause of sudden onset paralysis is severe hypokalemia associated with thyrotoxicosis. This is thought to be associated with mutations in genes encoding cellular potassium channels. We report a case of acute onset paralysis with profound hypokalemia and a new diagnosis of Graves’ thyrotoxicosis in a previously asymptomatic African American, HIV+ man on highly active antiretroviral therapy (HAART) for over 8 years. Clinical case: A 49-year-old man with hypertension and HIV presented with acute paralysis of his bilateral upper and lower extremities. His initial potassium was 1.8 mEq/L (3.5-5.0). Prior to sudden onset loss of motor strength, he denied any preceding palpitations, tremor, anxiety, diaphoresis, hyper-defecation, weight loss, heat or cold intolerance, neck pain, increase in neck girth or difficulty swallowing, proptosis or other ocular symptoms. He has no family history of thyroid disease. He had an enlarged palpable thyroid without nodules and no audible bruit. There was no periorbital edema or proptosis, and no signs of dermopathy. A thyroid ultrasound showed a hyperemic and diffusely enlarged thyroid gland without nodules. Labs included a TSH of 0.007 mCU/mL (0.43-3.8), Free T4 2.1 ng/dL (0.71-1.85), Total T3 229.6 ng/dL (58-194), and thyrotropin receptor antibody 2.6 IU/L (0-1.75). The CD4+ count was 146 in 2010 with a slow gradual rise to 673 in 2019, and HIV viral load was undetectable. There were no offending medications or supplements identified. With aggressive potassium repletion, the serum potassium improved to 4.6 mEq/L and he regained normal strength within several hours. He was started on Methimazole 10mg daily and propranolol 10mg TID. At one month, the thyroid function tests normalized. Methimazole 10mg daily was continued and propranolol was tapered off. He remains euthyroid. Genetic testing is pending. Conclusions: Graves’ disease is the most common thyroid disease triggered by immune reconstitution in HIV + individuals on HAART. The incidence of thyroid disease in HIV patients on HAART is higher in women and Africans with a 1.5-2 fold increase compared with the general population [Muller et. al, Eur Thyroid J 2019;8:173-185]. Despite a higher incidence of hyperthyroidism in women, over 95% of cases of hypokalemic periodic paralysis have been reported in men, with a 10-fold higher incidence among Asians compared to Westerners. There has been one prior case report of Thyrotoxic Periodic Paralysis in an HIV + patient and this was in a Polynesian male (Brown JD et al. Hawaii Med J 2007). To our knowledge, this is the first case report of an African American HIV+ patient with this disorder. An association with mutations in the Kir2.6 gene (encodes a potassium channel, is expressed in skeletal muscle, and is transcriptionally regulated by thyroid hormone) has been proposed [Ryan et. al, Cell 2010 January 8; 140(1):88-98].
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Case, James, Devi Suravajjala, and Vijay Eranki. "FRI507 Thyrotoxic Periodic Paralysis: A Rare Occurrence Of Exogenous Thyroid Replacement." Journal of the Endocrine Society 7, Supplement_1 (2023). http://dx.doi.org/10.1210/jendso/bvad114.1853.
Full textAbstract:
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 &lt;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
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Sanchez-Nadales, Alejandro, Valentina Celis-Barreto, Alejandra Diaz-Sierra, Andres Sanchez-Nadales, Antonio Lewis, and Jose Sleiman. "When cardiology meets endocrinology: sustained atrial flutter associated with thyrotoxic periodic paralysis." Oxford Medical Case Reports 2022, no. 3 (2022). http://dx.doi.org/10.1093/omcr/omac020.
Full textAbstract:
ABSTRACT Periodic paralysis is a rare muscle disease that manifests as episodes of painless muscle weakness, and the hypokalemic form is commonly associated with hyperthyroidism. Most tachyarrhythmias related with thyrotoxicosis include sinus tachycardia and atrial fibrillation, but an association between thyrotoxic hypokalemic periodic paralysis and typical atrial flutter has seldomly been documented. Here, we present the case of a young male who was diagnosed with thyrotoxic periodic paralysis causing cavotricuspid isthmus-dependent atrial flutter, successfully treated with diltiazem, propranolol, methimazole, potassium iodine (SSK) and rivaroxaban.