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Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis

Hypokalemic periodic paralysis (hypo KPP) is a rare form of autosomal dominant channelopathy characterized by muscular weakness and paralysis caused by decreased potassium levels. Precipitating factors are a diet rich in starches and sweets, and rest after an unusual degree of exercise. Paralytic at...

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Autores principales: Achakzai, Humaira, Khan, Sadia, Amin, Qazi Kamran, Ahmed, Naseer, Anwar, Safa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9094734/
https://www.ncbi.nlm.nih.gov/pubmed/35573575
http://dx.doi.org/10.7759/cureus.24046
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author Achakzai, Humaira
Khan, Sadia
Amin, Qazi Kamran
Ahmed, Naseer
Anwar, Safa
author_facet Achakzai, Humaira
Khan, Sadia
Amin, Qazi Kamran
Ahmed, Naseer
Anwar, Safa
author_sort Achakzai, Humaira
collection PubMed
description Hypokalemic periodic paralysis (hypo KPP) is a rare form of autosomal dominant channelopathy characterized by muscular weakness and paralysis caused by decreased potassium levels. Precipitating factors are a diet rich in starches and sweets, and rest after an unusual degree of exercise. Paralytic attacks are more common between the ages of 15 and 40 years. The presentation can be a total paralysis or severe quadriplegia or mild weakness in certain group of muscles. During the acute episode of weakness proximal muscles are involved initially with gradual spread to the distal muscles. Deep reflexes are decreased or absent but the cognitive functions and sensory systems are intact. The paralysis may last for few hours to several days, but recovery is usually sudden in most patients. Hypo KPP is usually associated with thyroid disorders and distal renal tubular acidosis (DRTA). Here we report a case of young female patient who presented in emergency with two days history of weakness of all four limbs. The patient also had two episodes of similar illness in the last two and half years. On examination she had decreased tone and power in all four limbs with absent deep tendon reflexes, and plantar reflexes were down going bilaterally. On initial laboratory workup, patient was diagnosed to have hypokalemic, hyperchloremic metabolic acidosis with alkaline urine secondary to hypothyroidism. Features of hypokalemia with metabolic acidosis and failure to acidify urine was consistent with DRTA. Intravenous potassium chloride and bicarbonate replacement resulted in biochemical and clinical improvement.
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spelling pubmed-90947342022-05-14 Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis Achakzai, Humaira Khan, Sadia Amin, Qazi Kamran Ahmed, Naseer Anwar, Safa Cureus Endocrinology/Diabetes/Metabolism Hypokalemic periodic paralysis (hypo KPP) is a rare form of autosomal dominant channelopathy characterized by muscular weakness and paralysis caused by decreased potassium levels. Precipitating factors are a diet rich in starches and sweets, and rest after an unusual degree of exercise. Paralytic attacks are more common between the ages of 15 and 40 years. The presentation can be a total paralysis or severe quadriplegia or mild weakness in certain group of muscles. During the acute episode of weakness proximal muscles are involved initially with gradual spread to the distal muscles. Deep reflexes are decreased or absent but the cognitive functions and sensory systems are intact. The paralysis may last for few hours to several days, but recovery is usually sudden in most patients. Hypo KPP is usually associated with thyroid disorders and distal renal tubular acidosis (DRTA). Here we report a case of young female patient who presented in emergency with two days history of weakness of all four limbs. The patient also had two episodes of similar illness in the last two and half years. On examination she had decreased tone and power in all four limbs with absent deep tendon reflexes, and plantar reflexes were down going bilaterally. On initial laboratory workup, patient was diagnosed to have hypokalemic, hyperchloremic metabolic acidosis with alkaline urine secondary to hypothyroidism. Features of hypokalemia with metabolic acidosis and failure to acidify urine was consistent with DRTA. Intravenous potassium chloride and bicarbonate replacement resulted in biochemical and clinical improvement. Cureus 2022-04-11 /pmc/articles/PMC9094734/ /pubmed/35573575 http://dx.doi.org/10.7759/cureus.24046 Text en Copyright © 2022, Achakzai et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Endocrinology/Diabetes/Metabolism
Achakzai, Humaira
Khan, Sadia
Amin, Qazi Kamran
Ahmed, Naseer
Anwar, Safa
Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis
title Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis
title_full Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis
title_fullStr Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis
title_full_unstemmed Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis
title_short Hypokalemic Periodic Paralysis: An Atypical Presentation of Non-autoimmune Hypothyroidism With Distal Renal Tubular Acidosis
title_sort hypokalemic periodic paralysis: an atypical presentation of non-autoimmune hypothyroidism with distal renal tubular acidosis
topic Endocrinology/Diabetes/Metabolism
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9094734/
https://www.ncbi.nlm.nih.gov/pubmed/35573575
http://dx.doi.org/10.7759/cureus.24046
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