{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T23:48:04Z","timestamp":1791848884457,"version":"4.3.4"},"reference-count":26,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Acute hypokalemic paralysis, characterized by acute flaccid paralysis is primarily a calcium channelopathy, but secondary causes like renal tubular acidosis (RTA), thyrotoxic periodic paralysis (TPP), primary hyperaldosteronism, Gitelman\u2019s syndrome are also frequent.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To study the etiology, varied presentations, and outcome after therapy of patients with hypokalemic paralysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials And Methods:<\/jats:title>\n                    <jats:p>All patients who presented with acute flaccid paralysis with hypokalemia from October 2009 to September 2011 were included in the study. A detailed physical examination and laboratory tests including serum electrolytes, serum creatine phosphokinase (CPK), urine analysis, arterial blood gas analysis, thyroid hormones estimation, and electrocardiogram were carried out. Patients were further investigated for any secondary causes and treated with potassium supplementation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Result:<\/jats:title>\n                    <jats:p>The study included 56 patients aged 15-92 years (mean 36.76 \u00b1 13.72), including 15 female patients. Twenty-four patients had hypokalemic paralysis due to secondary cause, which included 4 with distal RTA, 4 with Gitelman syndrome, 3 with TPP, 2 each with hypothyroidism, gastroenteritis, and Liddle\u2019s syndrome, 1 primary hyperaldosteronism, 3 with alcoholism, and 1 with dengue fever. Two female patients were antinuclear antibody-positive. Eleven patient had atypical presentation (neck muscle weakness in 4, bladder involvement in 3, 1 each with finger drop and foot drop, tetany in 1, and calf hypertrophy in 1), and 2 patient had respiratory paralysis. Five patients had positive family history of similar illness. All patients improved dramatically with potassium supplementation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>A high percentage (42.9%) of secondary cause for hypokalemic paralysis warrants that the underlying cause must be adequately addressed to prevent the persistence or recurrence of paralysis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.4103\/0972-2327.112469","type":"journal-article","created":{"date-parts":[[2013,5,24]],"date-time":"2013-05-24T04:37:35Z","timestamp":1369370255000},"page":"211-217","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":22,"title":["Clinical and biochemical spectrum of hypokalemic paralysis in North"],"prefix":"10.4103","volume":"16","author":[{"given":"Ashok K.","family":"Kayal","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Munindra","family":"Goswami","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marami","family":"Das","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rahul","family":"Jain","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-18-20260109","doi-asserted-by":"crossref","first-page":"193","DOI":"10.1136\/pgmj.75.882.193","article-title":"Hypokalemic paralysis","volume":"75","author":"Ahlawat","year":"1999","journal-title":"Postgrad Med J"},{"key":"R2-18-20260109","doi-asserted-by":"crossref","first-page":"143","DOI":"10.1016\/0735-6757(92)90048-3","article-title":"Hypokalemic paralyses: A review of the etiologies, pathophysiology, presentation, and therapy","volume":"10","author":"Stedwell","year":"1992","journal-title":"Am J Emerg Med"},{"key":"R3-18-20260109","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1093\/qjmed\/94.3.133","article-title":"Hypokalemia and paralysis","volume":"94","author":"Lin","year":"2001","journal-title":"QJM"},{"key":"R4-18-20260109","doi-asserted-by":"crossref","first-page":"389","DOI":"10.1038\/ki.1981.151","article-title":"Clinical and pathophysiologic spectrum of acquired distal renal tubular acidosis","volume":"20","author":"Batlle","year":"1981","journal-title":"Kidney Int"},{"key":"R5-18-20260109","first-page":"92","article-title":"A new familial disorder characterized by hypokalemia and hypomagnesemia","volume":"79","author":"Gitelman","year":"1966","journal-title":"Trans Assoc Am Physicians"},{"key":"R6-18-20260109","doi-asserted-by":"crossref","first-page":"1177","DOI":"10.1056\/NEJM199904153401507","article-title":"Genetic disorder of renal electrolyte transport","volume":"340","author":"Scheinman","year":"1999","journal-title":"N Engl J Med"},{"key":"R8-18-20260109","first-page":"33","article-title":"A periodic palsy. 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