scholarly journals SUN-519 Hypokalemic Periodic Paralysis

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sean Godfrey ◽  
Victoria Hudspeth ◽  
Patricia Amoako ◽  
Michael Drewno
Keyword(s):  
Thyroid Hormone ◽  
Normal Sinus Rhythm ◽  
Genetic Defect ◽  
Periodic Paralysis ◽  
Muscle Membrane ◽  
Conduction Delay ◽  
Extracellular Potassium ◽  
Free T4 ◽  
Rare Presentation ◽  
Thyrotoxic Periodic Paralysis

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 <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.

scholarly journals SUN-LB88 Thyrotoxic Periodic Paralysis in Hispanic Patients

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Tahira Sarwar ◽  
Jose Martinez ◽  
Johnathan Kirupakaran ◽  
Giovanna Rodriguez ◽  
Gül Bahtiyar
Keyword(s):  
Early Recognition ◽  
Case Reports ◽  
Laboratory Data ◽  
Periodic Paralysis ◽  
Graves Disease ◽  
Free T4 ◽  
Rare Presentation ◽  
Thyrotoxic Periodic Paralysis ◽  
Lower Extremity Weakness ◽  
Abnormal Gait

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.

scholarly journals Does thyrotoxic periodic paralysis have a genetic predisposition? A case report

2018 ◽  
Vol 55 (6) ◽  
pp. 713-716 ◽  
Author(s):  
E Rasheed ◽  
J Seheult ◽  
J Gibney ◽  
G Boran
Keyword(s):  
Thyroid Hormone ◽  
Clinical Presentation ◽  
Normal Population ◽  
Rare Complication ◽  
Gene Mutations ◽  
Periodic Paralysis ◽  
Acute Onset ◽  
Nucleotide Polymorphisms ◽  
Thyrotoxic Periodic Paralysis ◽  
Inwardly Rectifying Potassium Channel

Thyrotoxic periodic paralysis is a rare complication of hyperthyroidism where increased influx of potassium into skeletal muscle cells leads to profound hypokalaemia and paralysis. Most cases arise sporadically in Asians; however, it is being increasingly reported in Caucasians. It is regarded as a channelopathy where a genetic and/or acquired defect in the sodium-potassium (Na/K-ATPase) pump renders it more sensitive to excess thyroid hormone in susceptible individuals. Because the clinical presentation is similar to familial hypokalaemic periodic paralysis, genes implicated in this autosomal-dominant condition became candidates for thyrotoxic periodic paralysis, particularly if they were known to have thyroid hormone-responsive elements. These include the voltage-gated calcium (CACNA1S) and sodium (SCN4A) channel genes, KCNJ18 which encodes the inwardly rectifying potassium channel Kir2.6, and subunits of the Na/K-ATPase genes. Although no single pathogenetic mutation has been identified in thyrotoxic periodic paralysis, several single-nucleotide polymorphisms in these genes have been associated with it. We describe a 27-year-old Caucasian Irish male who presented with acute onset limb paralysis and severe hypokalaemia. He was diagnosed as having thyrotoxic periodic paralysis secondary to Graves’ disease based on clinical presentation, biochemical findings and rapid response to intravenous potassium. Genetic analysis identified heterozygous variants in three candidate genes: KCNJ18 (c.576G>C), SCN4A (c.2341G>A) and CACNA1S (c.1817G>A). Since these variants are not disease causing and occur at high prevalences of 50%, 2–3% and 1%, respectively, in the normal population, they do not explain the clinical phenotype in our patient suggesting that acquired environmental triggers or as-yet unidentified gene mutations remain as leading pathogenetic co-factors in thyrotoxic periodic paralysis.

scholarly journals When Your Thyroid Causes Muscle Paralysis

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A972-A973
Author(s):  
Anand Gandhi ◽  
Ahmad Al-Maradni ◽  
Karyne Lima Vinales ◽  
Ricardo Rafael Correa
Keyword(s):  
Muscle Weakness ◽  
Young Male ◽  
Sudden Onset ◽  
Periodic Paralysis ◽  
Adrenergic Stimulation ◽  
Free T4 ◽  
Thyrotoxic Periodic Paralysis ◽  
Beta Adrenergic ◽  
Thyroid State ◽  
Altered Thyroid

Abstract Background: Periodic paralysis represents a spectrum of disorders characterized by ion channel dysfunction, mainly Na-K-ATPase channels. Thyrotoxic periodic paralysis (TTP) is defined by the presence of hypokalemia and diffuse muscular paralysis in a pre-existing hyperthyroid state. Diagnosis can be challenging, especially in cases of undiagnosed hyperthyroidism due to the non-specific presentation of this illness. We present a case of a young male who presented with recurrent, spontaneous paralysis found to have Graves’ disease. Clinical Case: A 38-year-old Asian male presented with sudden onset diffuse weakness, numbness, and tingling. The weakness was so severe that he could barely walk more than a few steps. However, his symptoms resolved in less than 24 hours without any intervention. Five months later, the patient experienced a recurrent episode of this similar constellation of diffuse muscle weakness and paresthesia. The patient was taken to a nearby hospital, where he was provided with intravenous fluid resuscitation. Initial laboratory workup was notable for hypokalemia to 1.4 mmol/L (n: 3.6 - 5.3 mmol/L), hypophosphatemia to 0.6 mmol/L (n: 2.4 – 4.8 mmol/L), and elevated creatinine kinase to 807 U/L (n: 22 – 198 U/L). Additionally, TSH was <0.001 mU/L (n: 0.45 – 4.5 mU/L) along with free T4 3.4 ng/dL (n: 0.80 – 1.70 ng/dL. The patient denied any other symptoms or a family history of similar symptoms. Lumbar puncture and brain/spine MRIs were unremarkable. Symptoms gradually improved throughout hospitalization with fluid and electrolyte repletion. Hyperthyroidism was treated with methimazole 5mg twice daily, later changed to PTU 50mg every eight hours due to recurrent headaches. Thyroid uptake scan showed diffuse bilateral uptake to 39.11% at 4 hours and 61.8% at 24 hours. Follow up labs revealed: TSH 0.3 mU/L, free T4 1.44 ng/dL, free T3 3.5 pg/mL (n: 2.3 – 4.1 pg/mL). Patient denied recurrent episodes of weakness or paresthesia. Definitive hyperthyroidism treatment with RAI was planned. Conclusions: The prevalence of TPP is higher in Asian males compared to other ethnic groups. TPP manifests as a sporadic onset of muscle weakness ranging from mild weakness to flaccid paralysis. It has been described that thyroid hormone itself augments the activity of the Na-K-ATPase channel and increases its responsiveness to beta-adrenergic stimulation. In addition, hyperthyroidism is associated with insulin resistance leading to hyperinsulinemia. Both beta-agonism and insulin promote potassium to be driven into cells resulting in hypokalemia. As such, activities which increase beta adrenergic stimulation, like stress and exercise, and promote the secretion of insulin, such as heavy carbohydrate intake, are well described triggers of TPP. Treatment revolves around acutely treating hypokalemia followed by preventing subsequent attacks via regulation of the altered thyroid state.

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.

scholarly journals Thyrotoxic Periodic Paralysis in Young Caucasian Male

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A966-A966
Author(s):  
Sujata Panthi ◽  
Rajib Kumar Bhattacharya
Keyword(s):  
Muscle Weakness ◽  
Past History ◽  
Lower Extremities ◽  
Asian Population ◽  
Periodic Paralysis ◽  
Medical Emergency ◽  
Graves Disease ◽  
Free T4 ◽  
Thyrotoxic Periodic Paralysis ◽  
Caucasian Male

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.

scholarly journals A Case of Recurrent Paralysis and Low Potassium: Is It the Thyroid?

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A909-A909
Author(s):  
Justin Do ◽  
Hoveda Mufti
Keyword(s):  
Radioactive Iodine ◽  
Rare Complication ◽  
Periodic Paralysis ◽  
Definitive Treatment ◽  
Free T4 ◽  
Thyrotoxic Periodic Paralysis ◽  
Sodium Potassium ◽  
Potassium Atpase ◽  
Hispanic Male ◽  
Hyperthyroid Patients

Abstract Introduction: Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that is characterized by episodes of hypokalemia and acute weakness. Although hyperthyroidism is more common in females, over 95% of cases of TPP have been observed in males, especially in Asian males with an incidence of 2% among hyperthyroid patients. In non-Asian populations, the incidence in hyperthyroid patients is estimated to be around 0.1 to 0.2% [1]. We describe a case of TPP seen in a Hispanic male. Case Report: A 36-year-old Hispanic male with no past medical history presents with weakness in all extremities and difficulty breathing after consuming a carbohydrate heavy meal the night prior. He reports a recent, similar episode evaluated in another ER, which resolved after given potassium supplementation. He denied any vomiting, diarrhea, polyuria, diaphoresis, use of insulin or other medications, or any family history of paralysis. His labs were significant for hypokalemia of 1.9, TSH of <0.005 (0.358-3.740), free T4 of 2.22 (0.76-1.46), and total T3 of 2.7 (0.60-1.81). Thyroid stimulating immunoglobulin was 0.12 (0.0-0.55). His symptoms improved and potassium levels normalized following the administration of potassium chloride. He was discharged on propranolol and advised to follow up for further workup of his hyperthyroidism with radioactive iodine uptake scan. Discussion: Thyrotoxic periodic paralysis is a potentially life-threatening condition associated with cardiac arrhythmias and respiratory failure. Hyperthyroidism increases response to β-adrenergic stimulation, which increases activity of the sodium-potassium ATPase and causes hyperpolarization of skeletal muscle [2]. Hyperthyroid patients are prone to episodes of paralysis due to their increased susceptibility to the hypokalemic action of insulin, which activates the sodium-potassium ATPase pump, and epinephrine, which stimulates β-adrenoreceptors. Management of an acute attack of TPP includes potassium administration. In cases where paralysis and hypokalemia are not reversed, intravenous propranolol has been shown to resolve the attack by blocking the β-adrenergic receptors. Definitive treatment of TPP includes managing the hyperthyroid state with medical therapy, radioactive iodine therapy, or surgery. Until the euthyroid state is reached, a β-blocker can prevent episodes of acute paralysis. Avoidance of carbohydrate heavy meals, exercise, and stress are recommended as these factors can potentially exacerbate hypokalemia. In patient with acute paralysis, it is important to consider the diagnosis of TPP as this condition can be prevented once euthyroidism is achieved. Diagnosis and management will lead to prevention of morbidity and mortality associated with the hypokalemia. References: 1.Vijayakumar A, et al. J Thyroid Res. 2014;2014:649502. 2.Layzer RB. Annals of Neurology. 1982;11(6):547–552.

scholarly journals Skin Deep: A Rare Case of Thyrotoxic Periodic Paralysis in an African American Patient

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A954-A954
Author(s):  
Ela Banerjee
Keyword(s):  
African American ◽  
Asian Population ◽  
Periodic Paralysis ◽  
African American Patient ◽  
Free T4 ◽  
Thyrotoxic Periodic Paralysis ◽  
Grave’S Disease ◽  
American Patient ◽  
40Mg Daily ◽  
Grave's Disease

Abstract Background: Thyrotoxic Periodic Paralysis (PP) is a rare form of hypokalemic PP that occurs in association with hyperthyroidism, especially Grave’s disease. This disease is frequently seen in males and is particularly prevalent among Asians with an incidence rate of 2%. In non-Asian populations, the incidence among those with hyperthyroidism is even lower at 0.1 - 0.2% and therefore significantly rare in African populations. Inability to recognize this emergency in the non-Asian population can therefore result in potentially fatal outcomes. Case Presentation: A 27 year old African American male with a history of Grave’s disease presented to the emergency department (ED) with the inability to move his muscles. Patient was initially diagnosed with Grave’s disease in 2017 when he was found to have suppressed TSH with elevated TSI and started on methimazole 40mg daily. The patient ran out of methimazole about 2 weeks prior to presentation and woke up on the day of admission with extreme muscle weakness. At the outside hospital, he was found to have potassium of 1.5mEq/L,TSH of < 0.1uL/ml and Free T4 of 3.4 ng/dL. He was given 1000 mg Propylthiouracil, stress dose hydrocortisone, propranolol and potassium replacement and then transferred to our ED for Endocrine evaluation. On assessment, he complained of nausea, vomiting, full body muscle weakness, tingling in his extremities and irritability. He denied any recent illnesses. On physical exam, Temperature 97.4 F, Respiration 18, Pulse 84, BP 157/72, O2 saturation 99%. His thyroid gland was enlarged however non-tender and without bruit. He had normal respiratory and cardiac exam. He was lying flat in bed and unable to raise his limbs against gravity and also unable to hold up his limbs when raised. He lacked his patellar and ankle jerk reflexes bilaterally. He was otherwise alert and oriented x 3. On labs, TSH was 0.004 uL/ml, Total T3 was 294 ng/dL, Free T4 of 3.01 ng/dL, Potassium was 2.1 mEq/L. His potassium was cautiously replaced and improved to 4.7 mEq/L later in the day, at which time, the patient was able move and sit up in bed. He was restarted on Methimazole 40mg daily for his thyroid disease and arranged for outpatient follow up. Discussion: Thyrotoxic PP is seen in a male-to-female ratio ranging from 17:1 to 70:1 and occurs at an average age of 20-40 years. Thyrotoxic PP is especially rare in the non-Asian population at an incidence rate of 0.1 - 0.2%. Nevertheless, in setting of ever-growing diversity due to immigration and inter-race relationships, it is difficult to predict one’s genetics based on the color of their skin. It is possible that our African American patient may have an Asian ancestor unbeknownst to him. Therefore, we must keep a broad differential regardless of one’s race so as to not miss timely diagnosis of medical emergencies which can result in reduced muscle strength, flaccid paralysis, respiratory failure, cardiac arrhythmias and eventual death.

scholarly journals Hyperthyroidism With Atrial Fibrillation in Children: A Case Report and Review of the Literature

2021 ◽  
Vol 12 ◽  
Author(s):  
Deepa Subramonian ◽  
Yuwei Juliana Wu ◽  
Shazhan Amed ◽  
Shubhayan Sanatani
Keyword(s):  
Atrial Fibrillation ◽  
Case Report ◽  
Thyroid Hormone ◽  
Mitral Regurgitation ◽  
Normal Sinus Rhythm ◽  
Ventricular Rate ◽  
Review Of The Literature ◽  
Free T4 ◽  
Normal Sinus ◽  
Current Guidelines

Atrial fibrillation is exceedingly rare in children with structurally and functionally normal hearts. We present a novel case of a 15-year-old female with known hyperthyroidism who subsequently developed atrial fibrillation. She had been suffering from fatigue, heat intolerance and myalgias for 6 months. Her initial TSH was 0.01mU/L, and free T4 was 75.4 pmol/L, with a free T3 of >30.8 pmol/L. An electrocardiogram showed atrial fibrillation with a ventricular rate of 141 beats per minute. An echocardiogram demonstrated an enlarged left atrium and ventricle, with mild mitral regurgitation. She was treated with methimazole and underwent synchronized cardioversion. She subsequently returned to a euthyroid state and remained in normal sinus rhythm. In this case, we discuss the physiologic and arrhythmogenic properties of thyroid hormone, with a summary of the existing literature on atrial fibrillation in hyperthyroidism in children. Current guidelines for treatment of atrial fibrillation are also outlined.

Muscle membrane excitability after exercise in thyrotoxic periodic paralysis and thyrotoxicosis without periodic paralysis

2007 ◽  
Vol 36 (6) ◽  
pp. 784-788 ◽  
Author(s):  
Kimiyoshi Arimura ◽  
Yumiko Arimura ◽  
Arlene R. Ng ◽  
Shun-Ichi Sakoda ◽  
Itsuro Higuchi
Keyword(s):  
Periodic Paralysis ◽  
Muscle Membrane ◽  
Membrane Excitability ◽  
Thyrotoxic Periodic Paralysis
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