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Cited by 20Thyroid Disorders and TreatmentsPotassium and Related DisordersOphthalmology and Eye Disorders

Thyrotoxic periodic paralysis: case report and review of the literature

Open access
Vardhan Garla, Vishnu, Gunturu, Manasa, Reddy Kovvuru, Karthik, Abdul Salim, Sohail·2018·Electronic Physician
DOI 10.19082/7174PMC PMC6122872
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Abstract

INTRODUCTION: Thyrotoxic periodic paralysis (TPP) is a rare and potentially lethal complication of hyperthyroidism. It is characterized by sudden onset paralysis associated with hypokalemia. Management includes prompt normalization of potassium, which results in resolution of the paralysis. Definitive treatment of hyperthyroidism resolves TPP completely. CASE PRESENTATION: A 23-year-old African American male patient presented to the emergency room at the University of Mississippi Medical Center, USA in November 2016 with sudden onset quadriplegia. He also endorsed a history of weight loss, palpitations, heat intolerance and tremors. The patient reported similar episodes of quadriplegia in the past, which were associated with hypokalemia and resolved with normalization of potassium levels. Physical examination was significant for exophthalmos, smooth goiter with bruit consistent with the diagnosis of Graves' disease. Laboratory assessment showed severe hypokalemia, hypomagnesemia, suppressed thyroid stimulating hormone (TSH) and high free thyroxine (T4). Urine potassium creatinine ratio was less than one, indicating transcellular shift as the cause of hypokalemia. After normalization of potassium and magnesium, the paralysis resolved in 12 hours. He was started on methimazole. On follow up, the patient was clinically and biochemically euthyroid with no further episodes of paralysis. TAKE-AWAY LESSON: TPP is a rare and reversible cause of paralysis. Physicians need to be aware of the diagnostic and treatment modalities as delayed recognition in treatment could result in potential harm or unnecessary interventions.

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  • Pharmacologic β2-adrenergic agonists such as salbutamol and terbutaline can precipitate THPP by mimicking catecholamine action, activating β2 receptors and stimulating Na+/K+-ATPase expression and activity.

    “Pharmacologic β2-adrenergic agonists such as salbutamol and terbutaline can precipitate THPP by mimicking catecholamine action. These agents activate β2 receptors, stimulating Na+/K+-ATPase expression and activity [36].”

    From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [36]

    The Discussion (page not provided) says catecholamines stimulate Na-K-ATPase activity through beta-adrenergic receptors, and that blocking beta-adrenergic activity can alleviate TPP. It does not identify salbutamol or terbutaline as precipitants, specify β2 receptors, or attribute increased pump expression to β2 agonists; its discussion of transcriptional effects concerns thyroid hormones. (LLM, conf=0.86)

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  • Other electrolyte imbalances-hypophosphatemia, hypomagnesemia, and hypocalcemia-may occur in some patients with THPP, potentially due to transcellular electrolyte shifts, and often resolve spontaneously.

    “Other electrolyte imbalances—such as hypophosphatemia, hypomagnesemia, and hypocalcemia—may occur in some patients with THPP, potentially due to transcellular electrolyte shifts [36]. These disturbances often resolve spontaneously [3].”

    From Thyrotoxic Hypokalemic Periodic Paralysis: Pathophysiological Mechanisms (2025) · cites this paper as [36]

    The Discussion says hypomagnesemia and hypophosphatemia occur in TPP due to transcellular shifts, but it does not identify hypocalcemia as one of these disorders. The spontaneous-resolution statement has a separate citation in the citing sentence, so it is not judged against this source. (LLM, conf=0.87)

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Authors
Vardhan Garla, V., Gunturu, M., Reddy Kovvuru, K., & Abdul Salim, S.
Affiliations
University of Mississippi Medical Center (US)
Venue
Electronic Physician
Publisher
Knowledge Kingdom Publishing
Published
2018-08-25
Volume
10
Issue
8
Pages
7174-7179
ISSN
2008-5842 (ISSN-L)
DOI
10.19082/7174
PMC
PMC6122872
OpenAlex
W2888069582
Cited by
20
References
38
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 5 · 2019: 1
FWCI
1.99
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Electronic physician (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
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 › Pathology and Forensic Medicine › Ophthalmology and Eye Disorders
Keywords
thyrotoxic periodic paralysis, hyperthyroidism, hypokalemia, tetraplegia, Graves' disease, hypomagnesemia, potassium supplementation, methimazole, TSH suppression, goiter

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