scholarly journals Thyrotoxic Periodic Paralysis with Hypokalemia in an Adult Male from Nepal: A Case Report

2019 ◽  
Vol 57 (220) ◽  
Author(s):  
Sabina Khadka ◽  
Indu K.C. ◽  
Rabindra Jang Rayamajhi ◽  
Pravakar Dawadi ◽  
Pravash Budhathoki

Thyrotoxic periodic paralysis is rare complication of hyperthyroidism characterized by the sudden onset of hypokalemia and muscle paralysis. It is typically present in young Asian males. There are very few literatures regarding the occurrence of thyrotoxic hypokalemic periodic paralysis in Nepal. We reported a case of a 35-year-old male presented with the chief complaints of weakness of all four limbs of 1 day duration. He was diagnosed as a case of hyperthyroidism in the past, received treatment for 6 months and left medications on his own 6 months ago. Evaluation during admission revealed severe hypokalemia with serum potassium level 1.3mEq/l and high serum Triiodothyronine (>20.00µg/L) and low serum Thyroid Stimulating Hormone (<0.01µg/L). Potassium supplements resolved muscle weakness and the patient was restarted with anti-thyroid drugs. Hence, hypokalemic paralysis is a reversible cause of paralysis and high index of suspicion as well as timely interventions are required to prevent potential harm.

2018 ◽  
Vol 11 (1) ◽  
pp. e227946 ◽  
Author(s):  
Muhammad Arslan Cheema ◽  
Muhammad Abdullah Zain ◽  
Khadija Cheema ◽  
Waqas Ullah

The consumption of daily nutritional supplements has risen dramatically all over the world. Many people believe that dietary supplements, if not useful, are at least safe to fulfil small dietary gaps. Many nutritional supplements have not been approved by Federal Drug Administration due to their unregulated active ingredients, but they are available as over the counter. One of the active ingredients, exogenous triiodothyronine (T3), has been reported in dietary supplements. We present a case of sudden onset of tetraparesis. Laboratory workup showed hypokalaemia, low thyroid-stimulating hormone and thyroxine (T4) but normal T3 and thyroglobulin levels. The radioiodine uptake scan also showed reduced uptake. After aggressive serum potassium correction and stopping supplements, his condition got improved. So the suspicion of exogenous T3-induced thyrotoxic periodic paralysis was confirmed.


2019 ◽  
Vol 27 (1) ◽  
pp. 89-92
Author(s):  
Malinda Rasith Ileperuma ◽  
Badra Hewavithana

A case of post-traumatic proximal peroneal artery pseudoaneurysm following a proximal tibial shaft fracture, complicated by acute compartment syndrome, fixed using an external fixator, in a 22-year-old female is presented. She was investigated for sudden-onset bleeding from the external fixator pin site, 6 weeks after the initial injury, was anaemic and diagnosed with a pseudoaneurysm at lower limb angiography. Contrast leak from the site of pseudoaneurysm was noted and open surgery with ligation of the pseudoaneurysm was performed. This rare complication of a proximal tibial shaft fracture has to be considered in patients presenting with acute bleeding from the surgical site or from pin sites after a significant lag period and requires a high index of suspicion.


Author(s):  
E Rasheed ◽  
J Seheult ◽  
J Gibney ◽  
G Boran

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.


CJEM ◽  
2014 ◽  
Vol 16 (03) ◽  
pp. 247-251 ◽  
Author(s):  
Fu-Chiang Yeh ◽  
Wen-Fang Chiang ◽  
Chih-Chiang Wang ◽  
Shih-Hua Lin

ABSTRACT Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by β2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled β2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP.


2018 ◽  
Author(s):  
Modesta Petraviciute ◽  
Gintare Naskauskiene ◽  
Vigantas Dunauskas ◽  
Zydrune Visockiene

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Yicheng K. Bao ◽  
Vishwanath C. Ganesan ◽  
Richard Rapp ◽  
Shunzhong S. Bao

Reported is a case of a 39-year-old Caucasian man who presented to the emergency department with sudden onset bilateral lower extremity paralysis after consuming a large amount of carbohydrates and alcohol. A CT, MRI, and lumbar puncture were performed with negative results; lab results showed hyperthyroidism and hypokalemia. The patient was diagnosed with thyrotoxic periodic paralysis. In a patient presenting with sudden onset paralysis and hypokalemia, the emergency physician should include thyrotoxic periodic paralysis in the differential diagnosis and focus on treating and working up the hypokalemia instead of the paralysis.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A972-A973
Author(s):  
Anand Gandhi ◽  
Ahmad Al-Maradni ◽  
Karyne Lima Vinales ◽  
Ricardo Rafael Correa

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 &lt;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.


CHEST Journal ◽  
2020 ◽  
Vol 158 (4) ◽  
pp. A925
Author(s):  
Moeez Qureshi ◽  
Dharam Patel ◽  
Purnadeo Persaud

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. A909-A909
Author(s):  
Justin Do ◽  
Hoveda Mufti

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 &lt;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.


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