The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Mechanism of Thyrotoxic Periodic Paralysis
Open accessAbstract
The pathogenesis of thyrotoxic periodic paralysis has long been thought related to increased Na(+)-K(+) ATPase activity stimulated by thyroid hormone and/or hyperadrenergic activity and hyperinsulinemia. This mechanism alone, however, cannot adequately explain how hypokalemia occurs during acute attacks or the associated paradoxical depolarization of the resting membrane potential. Recent findings that loss of function mutations of the skeletal muscle-specific inward rectifying K(+) (Kir) channel, Kir2.6, associate with thyrotoxic periodic paralysis provide new insights into how reduced outward K(+) efflux in skeletal muscle, from either channel mutations or inhibition by hormones (adrenalin or insulin), can lead to a vicious cycle of hypokalemia and paradoxical depolarization, which in turn, inactivates Na(+) channels and causes muscle unexcitability and paralysis.
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“Recent studies have supported the genetic loss of function mutations in inward rectifying potassium channels associated with TPP.”
From A Case of Thyrotoxic Periodic Paralysis: "I Can't Move!" (2023) · cites this paper as [8]
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“The dual hits of increased intracellular K+ influx from activated Na+, K+-ATPase and decreased K+ efflux from defective Kir channels potentiates the serum hypokalemia that upsets membrane polarization and muscle excitability in TPP (46).”
From A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants (2013) · cites this paper as [46]
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“These findings also suggest that reduced basal muscular Kir current may also be an important mechanism of TPP (46).”
From A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants (2013) · cites this paper as [46]
In the citing paper
“Thyrotoxic periodic paralysis is characterized by a thyroid hormone-induced intracellular shift of potassium, leading to muscle weakness and paralysis.”
From A Case of Thyrotoxic Periodic Paralysis: "I Can't Move!" (2023) · cites this paper as [8]
In the citing paper
“This, coupled with increased Na-K ATPase activity, can lead to a cycle of extreme hypokalemia, as seen in periodic paralysis [8].”
From A Case of Thyrotoxic Periodic Paralysis: "I Can't Move!" (2023) · cites this paper as [8]
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Ryan, D. P., Dias da Silva, M. R., Soong, T. W., Fontaine, B., Donaldson, M. R., Kung, A. W. C., Jongjaroenprasert, W., Liang, M. C., Khoo, D. H. C., Cheah, J. S., et al. (2010) · Cell · doi:10.1016/j.cell.2009.12.024 · Cited by 311
Lin, S.-H. (2005) · Mayo Clinic Proceedings · doi:10.4065/80.1.99 · Cited by 254
Self-citationAronson, P. S., & Giebisch, G. (2011) · Journal of the American Society of Nephrology · doi:10.1681/asn.2011040414 · Cited by 235
Voltage sensor charge loss accounts for most cases of hypokalemic periodic paralysis
Matthews, E., Labrum, R., Sweeney, M. G., Sud, R., Haworth, A., Chinnery, P. F., Meola, G., Schorge, S., Kullmann, D. M., Davis, M. B., et al. (2009) · Neurology · doi:10.1212/01.wnl.0000342387.65477.46 · Cited by 201
Laboratory Tests to Determine the Cause of Hypokalemia and Paralysis
Lin, S.-H., Lin, Y.-F., Chen, D.-T., Chu, P., Hsu, C.-W., & Halperin, M. L. (2004) · Archives of Internal Medicine · doi:10.1001/archinte.164.14.1561 · Cited by 167
Self-citationIn vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis.
Chan, A., Shinde, R., Chow, C. C., Cockram, C. S., & Swaminathan, R. (1991) · BMJ · doi:10.1136/bmj.303.6810.1096 · Cited by 160
Hormonal and pharmacological modification of plasma potassium homeostasis
Clausen, T. (2010) · Fundamental and Clinical Pharmacology · doi:10.1111/j.1472-8206.2010.00859.x · Cited by 116
Insulin acts in hypokalemic periodic paralysis by reducing inward rectifier K current
Ruff, R. L. (1999) · Neurology · doi:10.1212/wnl.53.7.1556 · Cited by 112
Novel etiopathophysiological aspects of thyrotoxic periodic paralysis
Maciel, R. M. B., Lindsey, S. C., & Dias da Silva, M. R. (2011) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2011.58 · Cited by 86
Androgens stimulate preoptic area Na+,K+-ATPase activity in male rats
Guerra, M., Rodriguez Del Castillo, A., Battaner, E., & Mas, M. (1987) · Neuroscience Letters · doi:10.1016/0304-3940(87)90568-4 · Cited by 80
Binder, M. D., Hirokawa, N., & Windhorst, U. (2008) · Springer eBooks · doi:10.1007/978-3-540-29678-2_6003 · Cited by 78
Hyperinsulinaemia in thyrotoxic hypokalaemic periodic paralysis
Lee, K. O., Taylor, E. A., Oh, V. M. S., Cheah, J. S., & Aw, S. E. (1991) · The Lancet · doi:10.1016/0140-6736(91)91710-c · Cited by 69
Kjeldsen, K., Everts, M. E., & Clausen, T. (1986) · Pfl�gers Archiv European Journal of Physiology · doi:10.1007/bf00583377 · Cited by 56
Therapeutic analysis in Chinese patients with thyrotoxic periodic paralysis over 6 years
Shiang, J.-C., Cheng, C.-J., Tsai, M.-K., Hung, Y.-J., Hsu, Y.-J., Yang, S.-S., Chu, S.-J., & Lin, S.-H. (2009) · European Journal of Endocrinology · doi:10.1530/eje-09-0553 · Cited by 56
Self-citationEarly diagnosis of thyrotoxic periodic paralysis: Spot urine calcium to phosphate ratio*
Lin, S.-H., Chu, P., Cheng, C.-J., Chu, S.-J., Hung, Y.-J., & Lin, Y.-F. (2006) · Critical Care Medicine · doi:10.1097/01.ccm.0000242249.10856.49 · Cited by 47
Self-citationINa and IKir are reduced in Type 1 hypokalemic and thyrotoxic periodic paralysis
Puwanant, A., & Ruff, R. L. (2010) · Muscle & Nerve · doi:10.1002/mus.21693 · Cited by 32
Cheng, C.-J., Lin, S.-H., Lo, Y.-F., Yang, S.-S., Hsu, Y.-J., Cannon, S. C., & Huang, C.-L. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.a111.249656 · Cited by 6
Self-citation
Cited by
Sorted by citations
An Integrated View of Potassium Homeostasis
Gumz, M. L., Rabinowitz, L., & Wingo, C. S. (2015) · New England Journal of Medicine · doi:10.1056/nejmra1313341 · Cited by 299
Hyperthyroidism: aetiology, pathogenesis, diagnosis, management, complications, and prognosis
Wiersinga, W. M., Poppe, K. G., & Effraimidis, G. (2023) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(23)00005-0 · Cited by 254
Chang, C.-C., Cheng, C.-J., Sung, C.-C., Chiueh, T.-S., Lee, C.-H., Chau, T., & Lin, S.-H. (2013) · European Journal of Endocrinology · doi:10.1530/eje-13-0381 · Cited by 114
Self-citationExtracellular Potassium Homeostasis: Insights from Hypokalemic Periodic Paralysis
Cheng, C.-J., Kuo, E., & Huang, C.-L. (2013) · Seminars in Nephrology · doi:10.1016/j.semnephrol.2013.04.004 · Cited by 107
Self-citationThyrotoxic periodic paralysis: clinical and molecular aspects
Falhammar, H., Thorén, M., & Calissendorff, J. (2012) · Endocrine · doi:10.1007/s12020-012-9777-x · Cited by 74
Metadata
- Authors
- Lin, S.-H., & Huang, C.-L.
- Affiliations
- Tri-Service General Hospital (TW)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Lin, Shih-Hua
- ORCID
- Lin, Shih-Hua
- Venue
- Journal of the American Society of Nephrology
- Published
- 2012-06
- Volume
- 23
- Issue
- 6
- Pages
- 985-988
- ISSN
- 1046-6673 (ISSN-L)
- PMC
- PMC3358768
- OpenAlex
- W2097464324
- Cited by
- 174
- References
- 17
- Citations by year
- 2026: 11 · 2025: 14 · 2024: 20 · 2023: 18 · 2022: 18 · 2021: 12 · 2020: 14 · 2019: 5 · 2018: 9 · 2017: 11 · 2016: 8 · 2015: 9 · 2014: 13 · 2013: 10 · 2012: 2
- FWCI
- 4.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of the American Society of Nephrology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fondation pour la Recherche Médicale
- Tri-Service General Hospital
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Nephrology › Potassium and Related Disorders
- Keywords
- thyrotoxic periodic paralysis, hypokalemia, inwardly rectifying potassium channels, skeletal muscle, Na+/K+-ATPase, hyperinsulinemia, resting membrane potential, thyroid hormones
- MeSH terms
- Kcnj10 Channel, Sodium-Potassium-Exchanging ATPase, Female, Humans, Male, Membrane Potentials, Potassium, Prognosis, Severity of Illness Index, Thyroid Function Tests, Thyroid Hormones, Thyrotoxicosis, Treatment Outcome, Risk Assessment, Hypokalemic Periodic Paralysis, Potassium Channels, Inwardly Rectifying
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