Novel etiopathophysiological aspects of thyrotoxic periodic paralysis
Abstract
Thyrotoxicosis can lead to thyrotoxic periodic paralysis (TPP), an endocrine channelopathy, and is the most common cause of acquired periodic paralysis. Typically, paralytic attacks cease when hyperthyroidism is abolished, and recur if hyperthyroidism returns. TPP is often underdiagnosed, as it has diverse periodicity, duration and intensity. The age at which patients develop TPP closely follows the age at which thyrotoxicosis occurs. All ethnicities can be affected, but TPP is most prevalent in people of Asian and, secondly, Latin American descent. TPP is characterized by hypokalemia, suppressed TSH levels and increased levels of thyroid hormones. Nonselective β adrenergic blockers, such as propranolol, are an efficient adjuvant to antithyroid drugs to prevent paralysis; however, an early and definitive treatment should always be pursued. Evidence indicates that TPP results from the combination of genetic susceptibility, thyrotoxicosis and environmental factors (such as a high-carbohydrate diet). We believe that excess T(3) modifies the insulin sensitivity of skeletal muscle and pancreatic β cells and thus alters potassium homeostasis, but only leads to a depolarization-induced acute loss of muscle excitability in patients with inherited ion channel mutations. An integrated etiopathophysiological model is proposed based on molecular findings and knowledge gained from long-term follow-up of patients with TPP.
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The underlying pathophysiological mechanism of TPP is excessive Na+/K+-ATPase pump activity in skeletal muscle.
“The underlying pathophysiological mechanism of TPP is excessive Na⁺/K⁺-ATPase pump activity in skeletal muscle [3].”
From Iatrogenic Thyrotoxicosis and Corticosteroid-Triggered Hypokalemic Periodic Paralysis in a Patient With Treated Hypothyroidism (2026) · cites this paper as [3]
Loss-of-function mutations in the skeletal muscle-specific Kir channel Kir2.6 and loci on 17q involved in Kir2.1 gene expression confer susceptibility to TPP.
“Recent studies have shown that susceptibility to TPP can be conferred by loss-of-function mutations in the skeletal muscle-specific Kir channel, Kir2.6 (40, 41, 42), and loci on 17q involved in Kir2.1 gene expression (43, 44, 45).”
From A 10-year analysis of thyrotoxic periodic paralysis in 135 patients: focus on symptomatology and precipitants (2013) · cites this paper as [42]
Thyroid hormone stimulates Na+/K+-ATPase gene transcription and increases beta-adrenergic receptor sensitivity in TPP.
“The mechanism of clinical paralysis involves thyroid hormone stimulating Na⁺/K⁺-ATPase gene transcription and increasing beta-adrenergic receptor sensitivity [3].”
From Iatrogenic Thyrotoxicosis and Corticosteroid-Triggered Hypokalemic Periodic Paralysis in a Patient With Treated Hypothyroidism (2026) · cites this paper as [3]
The resulting intracellular potassium shift causes hyperpolarization of muscle cell membranes, leading to clinical weakness or paralysis.
“This leads to an intracellular shift of potassium, causing hyperpolarization of the muscle cell membranes, ultimately resulting in clinical weakness or paralysis depending on the severity [3].”
From Iatrogenic Thyrotoxicosis and Corticosteroid-Triggered Hypokalemic Periodic Paralysis in a Patient With Treated Hypothyroidism (2026) · cites this paper as [3]
The overall incidence of THPP in Asian thyrotoxic patients is about 2% compared with 0.1-0.2% in North America.
“The overall incidence of THPP in Asian thyrotoxic patients is about 2% comparing with 0.1-0.2% in North America (3).”
From Thyrotoxic hypokalemic periodic paralysis triggered by dexamethasone administration (2020) · cites this paper as [3]
THPP occurs more commonly among young Asian men with underlying Graves' disease.
“It occurs more commonly amongst young Asian men with underlying Graves' disease.”
From Thyrotoxic hypokalemic periodic paralysis triggered by dexamethasone administration (2020) · cites this paper as [3]
THPP attacks are commonly precipitated by ingestion of carbohydrate-rich meals or alcohol, stress, or strenuous exercise.
“Attacks are commonly precipitated by ingestion of carbohydrate-rich meals or alcohols, stress or strenuous exercise.”
From Thyrotoxic hypokalemic periodic paralysis triggered by dexamethasone administration (2020) · cites this paper as [3]
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The Case | A patient with acute tetraparesis
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- Authors
- Maciel, R. M. B., Lindsey, S. C., & Dias da Silva, M. R.
- Affiliations
- Universidade Federal de São Paulo (BR)
- Venue
- Nature Reviews Endocrinology
- Published
- 2011-05-10
- Volume
- 7
- Issue
- 11
- Pages
- 657-667
- ISSN
- 1759-5029 (ISSN-L)
- 1759-5037
- OpenAlex
- W1986025238
- Cited by
- 86
- References
- 130
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 4 · 2023: 5 · 2022: 8 · 2021: 6 · 2020: 9 · 2019: 3 · 2018: 4 · 2017: 2 · 2016: 5 · 2015: 6 · 2014: 7 · 2013: 6 · 2012: 8
- FWCI
- 0.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- UNIFESP Institutional Repository (Universidade Federal de São Paulo) (submittedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Keywords
- thyrotoxic periodic paralysis, thyrotoxicosis, hyperthyroidism, hypokalemia, potassium homeostasis, skeletal muscle excitability, beta-cell function, ion channel mutations, genetic susceptibility, high-carbohydrate diet, propranolol, antithyroid drugs
- MeSH terms
- Animals, Humans, Hypokalemia, Thyrotoxicosis, Hypokalemic Periodic Paralysis
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