Cited by 160Thyroid Disorders and TreatmentsIon Transport and Channel RegulationCardiac electrophysiology and arrhythmias

In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis.

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Chan, A, Shinde, R, Chow, C C, Cockram, C S, Swaminathan, R·1991·BMJ

Abstract

OBJECTIVE: To examine whether sodium pump activity plays a part in the pathogenesis of thyrotoxic periodic paralysis. DESIGN: Measurement of platelet sodium-potassium ATPase and in vivo sodium pump activities in healthy subjects and thyrotoxic subjects with and without paralysis. SETTING: University hospital in Hong Kong. SUBJECTS: 21 healthy subjects, 23 untreated thyrotoxic subjects, 13 untreated men with periodic paralysis, seven treated thyrotoxic subjects, and six treated men with periodic paralysis. MAIN OUTCOME MEASURES: Platelet Na+, K(+)-ATPase activity and plasma rubidium concentration after oral loading. RESULTS: Median (range) platelet Na+, K(+)-ATPase activity in thyrotoxic subjects was 253 (169-821) mumol inorganic phosphate/h/g protein--significantly higher than that in healthy subjects (134 (81-180) mumol/h/g protein; p less than 0.001). Na+, K(+)-ATPase activity in those with periodic paralysis was 374 (195-1196) mumol/h/g protein, again significantly higher than that in healthy subjects (p less than 0.001) and that in other thyrotoxic subjects (p less than 0.01) despite similar degrees of hyperthyroidism. Activities in treated thyrotoxic subjects with and without periodic paralysis were 148 (110-234) and 131 (86-173) mumol/h/g protein respectively. Mean (95% confidence interval) plasma rubidium concentration five hours after oral administration in thyrotoxic subjects (7.0 (6.6 to 7.5) mumol/l) was significantly lower than in healthy subjects (10.2 (9.5 to 10.9) mumol/l; p less than 0.001) and higher than in those with periodic paralysis (6.0 (5.7 to 6.3) mumol/l; p less than 0.01). CONCLUSIONS: Sodium pump activity in untreated subjects with periodic paralysis is higher than in other thyrotoxic subjects, and this may be responsible for the hypokalaemia.

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  • The activity of Na+-K+ ATPase pumps in skeletal muscle is significantly increased in TPP.

    “The important role of Na+-K+ ATPase pumps in the pathogenesis of TPP is supported by the finding that their activity in the skeletal muscle is significantly increased.”

    From Thyrotoxic Periodic Paralysis: Clinical Challenges (2014) · cites this paper as [7]

  • Thyrotoxic patients with periodic paralysis have higher sodium pump activity than those without paralytic episodes.

    “Thyrotoxic patients with PP have been found to have higher sodium pump activity than those without paralytic episodes [7].”

    From Thyrotoxic Periodic Paralysis: Clinical Challenges (2014) · cites this paper as [7]

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Authors
Chan, A., Shinde, R., Chow, C. C., Cockram, C. S., & Swaminathan, R.
Affiliations
Chinese University of Hong Kong (HK)
Venue
BMJ
Publisher
BMJ
Published
1991-11-02
Volume
303
Issue
6810
Pages
1096-1099
ISSN
  • 0007-1447 (ISSN-L)
  • 0959-8138
  • 1468-5833
OpenAlex
W2036976592
Cited by
160
References
30
Citations by year
2026: 2 · 2025: 1 · 2024: 4 · 2023: 3 · 2022: 7 · 2021: 4 · 2020: 5 · 2018: 6 · 2017: 4 · 2016: 3 · 2015: 8 · 2014: 12 · 2013: 9 · 2012: 9
FWCI
1.50
Type
journal article
Language
en
Open access
Locations
  • BMJ (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed (publishedVersion)
Funders
Chinese University of Hong Kong
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
thyrotoxic periodic paralysis, sodium pump activity, Na+/K+-ATPase, platelets, hyperthyroidism, hypokalemia, pathogenesis
MeSH terms
Sodium-Potassium-Exchanging ATPase, Adult, Blood Platelets, Humans, Male, Paralysis, Periodicity, Rubidium, Thyrotoxicosis, Thyrotropin, Thyroxine, Triiodothyronine

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