scholarly journals A Case of Nonfatal Ventricular Arrhythmia Due to Thyrotoxic Periodic Paralysis in a Saudi Patient as an Initial Presentation of Graves’ Disease

2016 ◽  
Vol 9 ◽  
pp. CCRep.S34560 ◽  
Author(s):  
Osamah Hakami ◽  
Maswood M. Ahmad ◽  
Naji Al Johani

Thyrotoxic periodic paralysis (TPP) is a potentially lethal complication of hyperthyroidism characterized by recurrent muscle weakness and hypokalemia. It has been commonly reported in non-Asian populations. Four cases were reported in Saudis so far, and one had a life-threatening arrhythmia. We describe an additional case of a 28-year-old apparently healthy Saudi male patient, who presented with acute paraparesis associated with hypokalemia (K: 2.0 mmol/L), complicated by ventricular tachycardia and cardiac arrest. He was successfully resuscitated and his hypokalemia was corrected. A diagnosis of Graves’ disease associated with TPP was made. He was initially treated with carbimazole and β-blockers and then given a definitive therapy with radioactive iodine, which showed a good response. This case highlights the importance of early recognition and prompt treatment of TPP as a differential diagnosis for muscle weakness. A brief review of TPP and associated arrhythmia is included.

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Henrik Elenius ◽  
Marie Cesa ◽  
Corina C. Nava Suarez ◽  
Abhishek Nimkar ◽  
Prasanta Basak ◽  
...  

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.


2019 ◽  
Vol 104 (12) ◽  
pp. 6338-6344
Author(s):  
Shinsuke Noso ◽  
Naru Babaya ◽  
Yoshihisa Hiromine ◽  
Hiroyuki Ito ◽  
Yasunori Taketomo ◽  
...  

Abstract Context and Objectives Thyrotoxic periodic paralysis (TPP) is an acute complication of thyrotoxicosis that can be lethal. TPP is rare in Caucasians but often affects young men in East Asian populations. This study aimed to clarify the contribution of KCNJ18 to susceptibility to TPP in East Asian populations. Participants and Methods The study comprised 635 participants including 13 Japanese patients with TPP, 208 Japanese patients with Graves disease without TPP, and 414 healthy control subjects from the Japanese (n = 208), Korean (n = 111), and Caucasian populations (n = 95). DNA samples from 29 participants (13 with TPP, 8 with Graves disease, and 8 controls) were sequenced for KCNJ18, and all participants (n = 635) were genotyped for six variants of KCNJ18 and a polymorphism of KCNJ2 (rs312691). Results Six single-nucleotide variants (SNVs) with amino acid substitutions were identified by direct sequencing of KCNJ18. Among these, four SNVs comprised three haplotypes under strong linkage disequilibrium. Haplotype 1 (AAAG) of KCNJ18 was significantly associated with susceptibility to TPP in the Japanese population (OR = 19.6; 95% CI, 1.5 to 256.9; P = 0.013). Haplotype frequencies in the general East Asian (Japanese and Korean) and Caucasian populations differed significantly (haplotype 1: 80.8% vs 48.4%, P = 1.1×10−27). Conclusion A major haplotype of KCNJ18 in East Asian populations is significantly associated with susceptibility to TPP. The haplotype is much more common in East Asian than Caucasian populations, suggesting its contribution to the high prevalence of TPP in East Asian populations.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Luke He ◽  
Veronica Lawrence ◽  
Wayne V Moore ◽  
Yun Yan

Abstract BACKGROUND: Thyrotoxic periodic paralysis (TPP) is an uncommon disorder characterized by acute flaccid paralysis due to hypokalemia. It is diagnosed primarily in Asian adult males and is rare in children and adolescents. Here we report an adolescent male patient of Vietnamese descent who presented to the emergency department with an episode of syncope, muscle weakness, and shortness of breath one day after the initiation of methimazole treatment for Graves’ disease. The laboratory revealed significant hypokalemia. In this report we also included and summarized the reported cases of TPP in adolescent patients since 1997. Clinical Case: A 17-year-old Vietnamese American male who was recently diagnosed with Graves’ disease presented to the emergency department after an episode of syncope, muscle weakness, and difficulty breathing. Two months previously, he began having episodes of tachycardia. He was diagnosed with hyperthyroidism with a TSH of 0.007 mIU/mL and free T 4 > 7 ng/dL (0.8-1.9). He was subsequently evaluated by Cardiology and started on atenolol. He was then seen by Endocrinology 5 days after and started on methimazole 15 mg twice daily. On the next morning after starting methimazole, he reported feeling weak and passed out. His father had found him on the floor, weak and unable to move, approximately 30 minutes after his father “heard a thud upstairs”. The patient recalled that his legs gave out and he “hitting his face on a table”. In the emergency department, he was tachycardic at 116 bpm, widened pulse blood pressure of 131/50 mmHg with normal respiratory rate 24 BR/min. He had diffused and significant muscle weakness on his all extremities including grip strength. His potassium was 1.6 mmol/L (3.5 - 5.2) and magnesium 1.6 mmol/L (1.6-2.3). The rest of his chemistry panel was unremarkable. He had EKG changes consistent with hypokalemia with U waves, also revealing atrial rhythm with first degree AV block, intraventricular conduction delay, and QTc prolongation at 588 (<450). His chest x-ray was normal. Normal saline was administered, and potassium replacement was given with 40 mEq of KCl followed by D5 NS with 40 meq/L KCl at maintenance. He continued taking atenolol and methimazole. He was also given an IV dose of magnesium. His muscle strength returned completely and potassium level returned to normal range at 4.6 mmol/L after 24 hours of treatment. Conclusion: TPP is a rare cause of acute paralysis and can lead to cardiac arrhythmia and death without accurate diagnosis and prompt treatment. Our case should raise awareness of this disorder among pediatricians, emergency department physicians and endocrinologists. Acute paralysis with hypokalemia should also prompt the physician to consider evaluating thyroid function as a differential diagnosis in young Asian men.


2018 ◽  
Vol 2018 ◽  
pp. 1-3 ◽  
Author(s):  
Nick Si Rui Lan ◽  
P. Gerry Fegan

Thyrotoxic periodic paralysis is an infrequent manifestation of hyperthyroidism and an uncommon cause of muscle weakness in western countries. The diagnosis should be considered in the differential when a patient presents with transient and recurrent weakness associated with hypokalaemia. We present a case of a 26-year-old Asian male presenting with sudden onset muscle weakness affecting predominantly his lower limbs on a background of weight loss. Physical examination demonstrated symmetrical proximal muscle weakness with normal sensation and reflexes. Initial biochemical investigations revealed hypokalaemia, hypomagnesaemia, and hyperthyroidism. Intravenous electrolyte replacement was administered in the emergency department. The patient’s symptoms resolved during inpatient admission. Subsequent TSH receptor antibody testing and radionuclide thyroid scan confirmed a diagnosis of Graves’ disease. The patient was discharged on antithyroid medication with no further episodes of weakness on follow-up. Therefore, thyrotoxic periodic paralysis can be the presenting feature of previously undiagnosed Graves’ disease and should be considered in the differential diagnosis in patients presenting with weakness.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A966-A966
Author(s):  
Sujata Panthi ◽  
Rajib Kumar Bhattacharya

Abstract Background: Thyrotoxic periodic paralysis (TPP) can be a medical emergency as delay in diagnosis can lead to life-threatening arrhythmia. Periodic paralysis is more prevalent in the Asian population. We report a case of thyrotoxic periodic paralysis in a young Caucasian male. Case: A 24-year-old male with a past history of Graves’ disease, hypertension, and asthma was brought to the hospital due to leg weakness and fall. He was initially diagnosed with Graves’ disease 2 years ago. The patient could not take methimazole or metoprolol due to the affordability issue for the last 18 months. On presentation, he fell on the floor while attempting to stand up from the couch. He could not stand up or pick his cell phone. He remained on the floor for 2-3 hrs. A review of the system was positive for palpitation and fatigue and negative for diarrhea, weight loss, anxiety, sleep problem, and dry eyes. On arrival, he had a pulse of 100/min, BP of 157/85 mmHg with rest of vitals signs normal. Motor strength on bilateral lower extremities were 2/5. Upper extremity strength was normal. No thyromegaly or thyroid bruit was noted in the exam. The rest of the physical exam was normal. Labs showed Potassium 1.9 with a normal reference range (RR) of 3.5 - 5.1 mmol/l. His TSH was < 0.01 (RR 0.35 - 5.00 MCU/ML), Free T4 was 5.0 (RR 0.6- 1.6 NG/DL), Total T3 was 425 (RR 87 - 180 NG/DL) and CK was 70 (RR 35- 232 U/L). EKG showed sinus rhythm at 90 bpm with no PR, T/ST, or QT abnormalities. He was given IV potassium and was also started on methimazole 10mg TID and metoprolol. His weakness and tachycardia were improved the next day. We discussed with him the options of medical management vs. surgery. He underwent a total thyroidectomy. Biopsy showed nodular hyperplasia consistent with graves’ disease. Discussion: Thyrotoxic periodic paralysis (TPP) is characterized by hypokalemia and episode of acute muscle weakness in lower extremities in the setting of hyperthyroidism. The pathophysiology of TPP remains uncertain. Hyperthyroidism is a hyperadrenergic state in which beta-2-adrenergic stimulation in muscle cells directly induces cellular K+ uptake by increasing cAMP, leading to activation of Na/K ATPase. The increase in the influx of intracellular K+ leads to hypokalemia and skeletal muscle weakness. Some studies show pathophysiology can be different in Caucasians compared to the Asian population that there could be abnormalities in Na and K channels other than Na/K ATPase. Potassium replacement should be done with caution as hypokalemia is due to intracellular shift and rebound hyperkalemia is common during the management. Beta-blocker may reverse adrenergic overstimulation of Na/K ATPase. It can help rapidly improve paralytic symptoms.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Tahira Sarwar ◽  
Jose Martinez ◽  
Johnathan Kirupakaran ◽  
Giovanna Rodriguez ◽  
Gül Bahtiyar

Abstract BACKGROUND: Thyrotoxic periodic paralysis (TPP) presents as acute intermittent attacks of weakness related to hypokalemia, commonly reported in Asians and rare in Hispanics(1). Patients with TPP will have triiodothyronine (T3) triggered increased Na+/K+ ATPase pump activity and transcription of the KCNJ18 gene that encodes for the Kir2.6 channel(2). This permits insulin, catecholamines, stress and alcohol(3) to increase cellular intake of potassium, which causes depolarization and leads to weakness and paralysis. We report a case of TPP in a young Hispanic man who presented with lower extremity weakness and falls. CASE PRESENTATION: A 34-year-old Hispanic man with Graves’ disease, non-adherent to medications presented with generalized weakness, more pronounced in legs, and recurrent falls. Physical examination was unremarkable except for mild enlargement of thyroid gland and abnormal gait due to weakness. Laboratory data showed hypokalemia of 1.8 mmol/L (3.7-5.1 mmol/L) and a TSH level of <0.004 mIU/L (0.34-5.6 mIU/L). Free T4 3.74 ng/dL (0.6-1.6 ng/dL), free T3 597 pg/dL (230-420 Pg/dL), thyroid stimulating Ig 148 (<130). Electrocardiogram did not show U waves. Radio iodine 123 scan of thyroid revealed diffusely increased 24-hour radioactive uptake of 66.5% (10-30%). The patient was diagnosed with TPP and supplemented with three doses of potassium 40 mEq IV infusion. Methimazole and metoprolol were started. He made a good clinical recovery within days. After discharge, he was treated with I-131 (13 mci) and developed postablative hypothyroidism on long term. He was euthyroid on levothyroxine. He did not have any recurrence of weakness at 7-year follow-up. CONCLUSION: TPP is uncommonly seen in Hispanics patients as opposed to Asians(3). Physicians should consider TPP as part of the differential diagnosis in young hyperthyroid Hispanic men presenting with weakness or paralysis, as early recognition and treatment can reduce recovery time and potentially prevent tachyarrhythmia or death. REFERENCES: 1. Matta A, Koppala J, Gossman W. Thyrotoxic hypokalaemic periodic paralysis: a rare presentation of Graves’ disease in a Hispanic patient. BMJ Case Rep. 2014;2014. 2. Ryan DP, Ptacek LJ. Mutations in Potassium Channel Kir2.6 Cause Susceptibility to Thyrotoxic Hypokalemic Periodic Paralysis. Cell, 140(1), pp.88-98. 3. Amblee, A. and Gulati, S. (2016). Thyrotoxic Periodic Paralysis: Eight Cases in Males of Hispanic Origin from a Single Hospital. AACE Clinical Case Reports, 2(1), pp.e58-e64.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Rita Yuk-Kwan Chang ◽  
Brian Hung-Hin Lang ◽  
Ai Chen Chan ◽  
Kai Pun Wong

Objective. Thyrotoxic periodic paralysis (TPP) is a potentially life-threatening complication of Graves’ disease (GD). The present study compared the long-term efficacy of antithyroid drugs (ATD), radioactive iodine (RAI), and surgery in GD/TPP.Methods. Sixteen patients with GD/TPP were followed over a 14-year period. ATD was generally prescribed upfront for 12–18 months before RAI or surgery was considered. Outcomes such as thyrotoxic or TPP relapses were compared between the three modalities.Results. Eight (50.0%) patients had ATD alone, 4 (25.0%) had RAI, and 4 (25.0%) had surgery as primary treatment. Despite being able to withdraw ATD in all 8 patients for 37.5 (22–247) months, all subsequently developed thyrotoxic relapses and 4 (50.0%) had ≥1 TPP relapses. Of the four patients who had RAI, two (50%) developed thyrotoxic relapse after 12 and 29 months, respectively, and two (50.0%) became hypothyroid. The median required RAI dose to render hypothyroidism was 550 (350–700) MBq. Of the 4 patients who underwent surgery, none developed relapses but all became hypothyroid.Conclusion. To minimize future relapses, more definitive primary treatment such as RAI or surgery is preferred over ATD alone. If RAI is chosen over surgery, a higher dose (>550 MBq) is recommended.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A911-A911
Author(s):  
Lakshmi Priyanka Mahali ◽  
Amanda Pechman

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.


Author(s):  
Annie W.C. Kung

The association of thyrotoxicosis and periodic paralysis was first described in 1902 in a white patient. However, it soon became evident that thyrotoxic periodic paralysis (TPP) affects mainly Asian populations, in particular Chinese and Japanese, although isolated cases have also been reported in other ethnic groups such as white, Hispanic, African-American, and American Indian populations. The incidence of TPP in non-Asian thyrotoxic patients is around 0.1%, whereas in Chinese and Japanese thyrotoxic patients, TPP affects 1.8% and 1.9%, respectively (1–3). Despite a higher incidence of thyrotoxicosis in women, TPP affects mainly men, with a male to female ratio ranging from 17:1 to 70:1, according to different series. In the Chinese population, TPP affects 13% of male and 0.17% of female thyrotoxic patients. In the Japanese population, TPP was reported to occur in 8.2% of male and 0.4% of female thyrotoxic patients in the 1970s, but in 1991 the reported incidence had decreased to 4.3% and 0.04%, respectively (4).


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