ACUTE HYPOKALEMIC PARALYSIS AND HASHIMOTO’S THYROIDITIS
Keywords:Acute hypokalemic paralysis, , Distral renal tubular acidosis, , paralysis, dRTA, Hypothyroidism
AbstractAcute hypokalemic paralysis (AHP) is a life-threatening emergency. It is exceptionally unusual for hypothyroidism to present with AHP. This association can be either primary or secondary through distal renal tubular acidosis. We report two cases who presented with acute quadriplegia. The succeeding investigations revealed severe hypokalemia and autoimmune hypothyroidism. The second case was found to have Sjogren’s syndrome additionally. The underlying etiology of hypokalemia in both cases was found to be dRTA. The combination of such conditions is reported sporadically. Here we also discuss the potential association of AHP with autoimmune conditions by proxy through dRTA.
Velarde-Mejía Y, Gamboa-Cárdenas R, Ugarte-Gil M, Asurza CP. Hypokalemic Paralysis: A Hidden Card of Several Autoimmune Diseases. Clin Med Insights Arthritis Musculoskelet Disord 2017;10:1179544117722763.
Arambewela MH, Sumanathilaka MR, Pathirana KD, Bodinayaka CK. A possible association of hypokalaemic periodic paralysis, autoimmune thyroiditis and neuromyotonia. Ceylon Med J 2013;58(4):175–6.
Bandhakavi M. Periodic paralysis as an unusual presentation of autoimmune hypothyroidism with goiter. Clin Pediatr (Phila) 2009;48(6):677–8.
Sinha U, Sengupta N, Sinharay K, Sahana PK. Recurrent hypokalemic paralysis: An atypical presentation of hypothyroidism. Indian J Endocrinol Metab 2013;17(1):174–6.
Meregildo-Rodríguez ED, Failoc-Rojas VE. Case Report: Recurrent hypokalemic periodic paralysis associated with distal renal tubular acidosis (type 1) and hypothyroidism secondary to Hashimoto's thyroiditis. F1000Res 2018;7:1154.
Koul PA, Wahid A. Distal renal tubular acidosis and hypokalemic paralysis in a patient with hypothyroidism. Saudi J Kidney Dis Transpl 2011;22(5):1014–6.
Lim S. Approach to hypokalemia. Acta Med Indones 2007;39(1):56–64.
Mustaqeem R, Arif A. Renal Tubular Acidosis. In: StatPearls. Treasure Island (FL): StatPearls Publishing Copyright © 2021, StatPearls Publishing LLC.; 2021.
Sedhain A, Acharya K, Sharma A, Khan A, Adhikari S. Renal Tubular Acidosis and Hypokalemic Paralysis as a First Presentation of Primary Sjögren's Syndrome. Case Rep Nephrol 2018;2018:9847826.
Kadeeja N, Senthilnathan N, Viswanathan S, Aghoram R. Sporadic hypothyroidism-related hypokalemic paralysis: Diagnosis in a resource-poor setting. J Family Med Prim Care 2017;6(4):862–4.
Yılmaz H, Kaya M, Özbek M, ÜUreten K, Safa Yıldırım İ. Hypokalemic periodic paralysis in Sjogren's syndrome secondary to distal renal tubular acidosis. Rheumatol Int 2013;33(7):1879–82.
Inagaki K, Otsuka F, Otani H, Sato C, Miyoshi T, Ogura T, et al. Apparent mineralocorticoid excess manifested in an elderly patient with hypothyroidism. Am J Hypertens 2007;20(1):104–7.
Talal N, Zisman E, Schur PH. Renal tubular acidosis, glomerulonephritis and immunologic factors in Sjögren's syndrome. Arthritis Rheum 1968;11(6):774–86.
Journal of Ayub Medical College, Abbottabad is an OPEN ACCESS JOURNAL which means that all content is FREELY available without charge to all users whether registered with the journal or not. The work published by J Ayub Med Coll Abbottabad is licensed and distributed under the creative commons License CC BY ND Attribution-NoDerivs. Material printed in this journal is OPEN to access, and are FREE for use in academic and research work with proper citation. J Ayub Med Coll Abbottabad accepts only original material for publication with the understanding that except for abstracts, no part of the data has been published or will be submitted for publication elsewhere before appearing in J Ayub Med Coll Abbottabad. The Editorial Board of J Ayub Med Coll Abbottabad makes every effort to ensure the accuracy and authenticity of material printed in J Ayub Med Coll Abbottabad. However, conclusions and statements expressed are views of the authors and do not reflect the opinion/policy of J Ayub Med Coll Abbottabad or the Editorial Board.
USERS are allowed to read, download, copy, distribute, print, search, or link to the full texts of the articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This is in accordance with the BOAI definition of open access.
AUTHORS retain the rights of free downloading/unlimited e-print of full text and sharing/disseminating the article without any restriction, by any means including twitter, scholarly collaboration networks such as ResearchGate, Academia.eu, and social media sites such as Twitter, LinkedIn, Google Scholar and any other professional or academic networking site.