CoChat
Sign Up
Cited by 74Thyroid Disorders and TreatmentsPotassium and Related DisordersCardiac electrophysiology and arrhythmias

Thyrotoxic periodic paralysis: clinical and molecular aspects

Falhammar, Henrik, Thorén, Marja, Calissendorff, Jan·2012·Endocrine
DOI 10.1007/s12020-012-9777-x
Open this paper in CoChat — free account

Abstract

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism that most often affects young East Asian males but increasingly also in other ethnic groups. The typical presentation is acute attacks varying from mild weakness to total paralysis starting at night or in the early morning a few hours after a heavy meal, alcohol abuse or strenuous exercise with complete recovery within 72 h. Signs and symptoms of hyperthyroidism may not be obvious. The hallmark is hypokalemia from increased cellular sodium/potassium-ATPase pump activity with transport of potassium from the extracellular to the intracellular space in combination with reduced potassium output. Recently, KCNJ18 gene mutations which alter the function of an inwardly rectifying potassium channel named Kir2.6 have been detected in 0-33 % of cases. Hence, the pathophysiology in TPP includes a genetic predisposition, thyrotoxicosis and environmental influences and the relative impact from each of these factors may vary. The initial treatment, which is potassium supplementation, should be given with caution due to a high risk of hyperkalemia. Propranolol is an alternative first-line therapeutic option based on the assumption that hyperadrenergic activity is involved in the pathogenesis. If thyroid function tests are unobtainable in the acute situation the diagnosis is supported by the findings of hypokalemia, low spot urine potassium excretion, hypophosphatemia with hypophosphaturia, high spot urine calcium/phosphate ratio, and electrocardiographic abnormalities as tachycardia, atrial fibrillation, high QRS voltage, and atrioventricular block. Definitive treatment is cure of the hyperthyroidism. The underlying mechanisms of TPP remain, however, incompletely understood awaiting further studies.

Integrity signals

Registry

Crossref · 10.1007/s12020-012-9777-x

Cites

109 of 109 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The pathophysiology of TPP involves intracellular potassium shifting caused by increased Na+/K+-ATPase activity, enhanced by both thyroid hormone and corticosteroids.

    “The pathophysiology involves intracellular potassium shifting caused by increased Na⁺/K⁺-ATPase activity, enhanced by both thyroid hormone and corticosteroids (Figure 1) [7].”

    From Iatrogenic Thyrotoxicosis and Corticosteroid-Triggered Hypokalemic Periodic Paralysis in a Patient With Treated Hypothyroidism (2026) · cites this paper as [7]

  • The recurrence of identical episodes following the same corticosteroid agent and dose further supports the dual-trigger interaction and raises the possibility of underlying genetic susceptibility, such as channelopathies involving CACNA1S or SCN4A variants, which may lower the threshold for paralysis in the setting of thyroid hormone excess.

    “The recurrence of identical episodes following the same corticosteroid agent and dose further supports this interaction and raises the possibility of an underlying genetic susceptibility, such as channelopathies involving CACNA1S or SCN4A variants, which may lower the threshold for paralysis in the setting of thyroid hormone excess [4,7].”

    From Iatrogenic Thyrotoxicosis and Corticosteroid-Triggered Hypokalemic Periodic Paralysis in a Patient With Treated Hypothyroidism (2026) · cites this paper as [7]

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Falhammar, H., Thorén, M., & Calissendorff, J.
Affiliations
  • Karolinska University Hospital (SE)
  • Karolinska Institutet (SE)
Corresponding author
Falhammar, Henrik
ORCID
Venue
Endocrine
Publisher
Springer Science and Business Media LLC
Published
2012-08-24
Volume
43
Issue
2
Pages
274-84
ISSN
  • 0969-711X (ISSN-L)
  • 1355-008X
  • 1559-0100
DOI
10.1007/s12020-012-9777-x
OpenAlex
W2081639414
Cited by
74
References
109
Citations by year
2026: 4 · 2025: 5 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 10 · 2019: 6 · 2018: 9 · 2017: 5 · 2016: 3 · 2015: 6 · 2014: 6 · 2013: 5
FWCI
0.75
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Endocrine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Potassium and Related Disorders
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
Keywords
thyrotoxic periodic paralysis, hyperthyroidism, hypokalemia, potassium supplementation, propranolol, hypophosphatemia, hypophosphaturia, electrocardiographic abnormalities, hyperthyroidism treatment
MeSH terms
Female, Humans, Hyperthyroidism, Hypokalemia, Male, Mutation, Paralyses, Familial Periodic, Sex Factors, Thyrotoxicosis, Disease Management, Potassium Channels, Inwardly Rectifying

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review