scholarly journals Thyrotoxic Periodic Paralysis and Polymorphisms of the ADRB2, AR, and GABRA3 Genes in Men with Graves Disease

2016 ◽  
Vol 31 (1) ◽  
pp. 142 ◽  
Author(s):  
Suyeon Park ◽  
Tae Yong Kim ◽  
Soyoung Sim ◽  
Seonhee Lim ◽  
Mijin Kim ◽  
...  
Keyword(s):  
Periodic Paralysis ◽  
Graves Disease ◽  
Thyrotoxic Periodic Paralysis

scholarly journals Rhabdomyolysis Induced by Nonstrenuous Exercise in a Patient with Graves’ Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-3 ◽  
Author(s):  
Sarawut Summachiwakij ◽  
Issac Sachmechi
Keyword(s):  
Differential Diagnosis ◽  
Periodic Paralysis ◽  
Graves Disease ◽  
Past Medical History ◽  
Thyrotoxic Periodic Paralysis ◽  
Radioiodine Uptake ◽  
Thyroid Stimulating Immunoglobulins ◽  
History Of ◽  
Brown Urine ◽  
Thyroid Ophthalmopathy

Hyperthyroidism can result in several musculoskeletal conditions such as thyrotoxic periodic paralysis, thyrotoxic myopathy, and thyroid ophthalmopathy. Rhabdomyolysis has been rarely reported to be associated with hyperthyroidism. We describe a 33-year-old man who presented with bilateral thigh pain and dark brown urine after regular squatting. He had a past medical history of hyperthyroidism but stopped taking it 2 months prior to admission. He was found to have rhabdomyolysis, myoglobinuria, and thyrotoxicosis. Presence of thyroid-stimulating immunoglobulins (TSI) and high radioiodine uptake confirmed a diagnosis of Graves' disease. He received aggressive fluid resuscitation and sodium bicarbonate intravenously along with monitoring fluid and electrolyte. Methimazole was also resumed. The patient responded to treatment and rhabdomyolysis gradually resolved. Therefore, nonstrenuous exercise can potentially induce rhabdomyolysis in patients with hyperthyroidism. Although hyperthyroidism is not widely recognized as a cause of rhabdomyolysis, it should be considered in the differential diagnosis of rhabdomyolysis.

scholarly journals Thyrotoxic Periodic Paralysis and Cardiomyopathy in a Patient with Graves’ Disease

Cureus ◽  
2018 ◽  
Author(s):  
Anna A Abbasi ◽  
Prarthna Chandar ◽  
Shyam Shankar ◽  
Sushilkumar S Gupta ◽  
Yizhak Kupfer
Keyword(s):  
Periodic Paralysis ◽  
Graves Disease ◽  
Thyrotoxic Periodic Paralysis

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
Keyword(s):  
Muscle Weakness ◽  
Early Recognition ◽  
Periodic Paralysis ◽  
Graves Disease ◽  
Thyrotoxic Periodic Paralysis ◽  
Asian Populations ◽  
Definitive Therapy ◽  
Life Threatening ◽  
Acute Paraparesis ◽  
Saudi Male

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.

scholarly journals Contribution of Asian Haplotype of KCNJ18 to Susceptibility to and Ethnic Differences in Thyrotoxic Periodic Paralysis

2019 ◽  
Vol 104 (12) ◽  
pp. 6338-6344
Author(s):  
Shinsuke Noso ◽  
Naru Babaya ◽  
Yoshihisa Hiromine ◽  
Hiroyuki Ito ◽  
Yasunori Taketomo ◽  
...  
Keyword(s):  
Direct Sequencing ◽  
East Asian ◽  
Japanese Patients ◽  
Periodic Paralysis ◽  
Graves Disease ◽  
Strong Linkage Disequilibrium ◽  
Single Nucleotide Variants ◽  
Thyrotoxic Periodic Paralysis ◽  
Asian Populations ◽  
Haplotype 1

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.

scholarly journals Thyrotoxic Periodic Paralysis: A Rare Presentation of Graves’ Disease

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A966-A967
Author(s):  
Bishow Chandra Shrestha ◽  
Chheki Sherpa ◽  
Swarup sharma Rijal ◽  
Vasudev Magaji ◽  
Vinita Singh
Keyword(s):  
Asian Population ◽  
Periodic Paralysis ◽  
Flaccid Paralysis ◽  
Definitive Treatment ◽  
Muscle Membrane ◽  
Graves Disease ◽  
Low Grade ◽  
Thyrotoxic Periodic Paralysis ◽  
Potassium Replacement ◽  
Hyperthyroid Patients

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 <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.

scholarly journals SUN-514 Thyrotoxic Periodic Paralysis in Adolescence Patient a Case Report and Literature Review

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Luke He ◽  
Veronica Lawrence ◽  
Wayne V Moore ◽  
Yun Yan
Keyword(s):  
Emergency Department ◽  
Muscle Weakness ◽  
Periodic Paralysis ◽  
Adolescent Male ◽  
Conduction Delay ◽  
Graves Disease ◽  
Adult Males ◽  
Thyrotoxic Periodic Paralysis ◽  
Intraventricular Conduction ◽  
Potassium Replacement

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.

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