Thyrotoxic Periodic Paralysis

Alam, Nimat; Esteban, Linda; Tobias, Enrique; George, Jenet

doi:10.4172/2165-7920.1000839

Cited by 2 publications

(7 citation statements)

References 7 publications

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“…More frequently seen in patients of Asian or Hispanic origin; this shared predisposition has been linked to genetic variation in Kir2.6, a muscle-specific, thyroid hormone-responsive K+ channel [1,2]. More common in males than females suggests of differential action of androgen on Na + /K + ATPase activity.…”

Section: Epidemologymentioning

confidence: 99%

“…Hyperthyroidism results in a hyper adrenergic state. β-Adrenergic stimulation in muscle cells may directly induce cellular potassium uptake by increasing intracellular cyclic adenosine monophos-phate leading to activation of the Na+, K+-ATPase pump [1]. Moreover, thyroid hormone per se directly stimulates Na+, K+-ATPase pump and increases the number and sensitivity of β-receptors, which further increase catechol-aminemediated potassium uptake.The chemical structure of thyroxine is similar to that of catecholamines, exerting its cellular effect via catecholamine receptors.…”

Section: Etiology and Pathophysiologymentioning

confidence: 99%

“…Hypokalemia is the most consistently found electrolyte abnormality in TPP and is believed to be a primary source of paralysis [1,2]. In recent reports, hypophosphatemia another cause of muscle weakness was seen commonly in patients with TPP [8,9].…”

Section: Blood Electrolyte Findingsmentioning

confidence: 99%

“…Thyrotoxic periodic paralysis (TPP) is not a uncommon condition with an incidence of approximately 2% in patients with thyrotoxicosis of any cause [1].…”

Section: Introductionmentioning

confidence: 99%

“…TPP is commonly misdiagnosed in because its presentation has similarities with familial periodic paralysis. Familial periodic paralysis is an autosomal dominant disorder in which defect is in the gene coding for L-type calcium channel 1-subunit (CACNA1S) on chromosome 1q31-32 [1]. The neuromuscular presentations of both are similar, but presence of subtle features of hyperthyroidism in the presence of hypokalemic periodic paralysis favours the diagnosis of TPP.…”

Section: Introductionmentioning

confidence: 99%

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Thyrotoxic Periodic Paralysis- A Clinical Review

Khare¹

2018

OAJE

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Thyrotoxic periodic paralysis (TPP) is not a uncommon condition often seen in Asian males characterized by sudden onset hyperthyroidism-related hypokalemia and paralysis. Intracellular shift of potassium due to activation of thyroid hormone sensitive Na + /K + ATPase is the possible pathological mechanism of hypokalemia, rather than depletion of potassium from the body, thus redistributive hypokalemia. Treatment involves correction of underlying hyperthyroidism, prevention of intracellular shift of potassium with non selective beta blockers and potassium replacement in emergency condition. Early identification of TPP is important for appropriate treatment and prevention of further episodes of hypokalemia or rebound hyperkalemia.

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Section: Epidemologymentioning

confidence: 99%

Section: Etiology and Pathophysiologymentioning

confidence: 99%

Section: Blood Electrolyte Findingsmentioning

confidence: 99%

“…Thyrotoxic periodic paralysis (TPP) is not a uncommon condition with an incidence of approximately 2% in patients with thyrotoxicosis of any cause [1].…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Thyrotoxic Periodic Paralysis- A Clinical Review

Khare¹

2018

OAJE

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Hypertensive Crisis: The Causative Effects of Nonsteroidal Anti- Inflammatory Drugs

Landefeld¹,

Gonzales²,

Sander³

2016

J Clin Case Rep

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62-year-old female presents with hypertensive urgency while taking daily NSAIDs. This case demonstrates the effect of NSAIDs on BP, an often over-looked etiology of secondary hypertension. The detrimental effects of NSAIDs upon blood pressure have been well documented. The report reiterates and reviews the severity of the problem. We will review the existing literature and discuss the importance of small increases in blood pressure. This paper has not been submitted elsewhere, is not under review, or published previously and all of the authorship are aware of and approve the manuscript being submitted to this journal. Keywords: Hypertension; NSAID-induced hypertension; Chronic pain Case ReportHigh pressure situation A 62 year-old white female with no documented past medical history of hypertension or any other chronic disease state presented to the Emergency department with severe occipital headache and was found to have hypertensive urgency, with initial blood pressure (BP) of 225/110 mmHg ( Figure 1). She had started taking OTC ibuprofen 3200 mg to 4000 mg daily for three weeks due to cervical-spine radicular pain. Her clinical course is outlined in detail in Table 1. Physical exam revealed flushing and mild non-pitting edema of the digits. Ophthalmologic and cardiac exams were normal as was the ECG. Initial work-up revealed a normal renal function with 2+ proteinuria on urinalysis, mild hypokalaemia that resolved spontaneously, and a CT head that was negative for haemorrhage. She initially received 0.2 mg of clonidine and the ibuprofen was discontinued. When she saw her primary care physician the following day, BP was 170/100 mmHg; she was started on 100/25 mg of losartan/HCT, an angiotensin-receptor blocker/thiazide combination and 5 mg of amlodipine, a calcium channel blocker, for Stage II hypertension. The patient was then seen by a hypertension specialist; 5 mg nebivolol, a β1 cardioselective vasodilating β-blocker, was added and home BP measurements were initiated. Home BP documented that BPs soon decreased to <120/80 mmHg, after which amlodipine and losartan/HCT were tapered off and nebivolol alone continued. The patient was noted to have a white-coat hypertension pattern, but on continued follow up has done very well as again indicated in Table 1. It does appear that she had pre-existing hypertension prior to her acute episode. DiscussionNSAID-induced hypertension nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most frequently used medications in the USA; more than 29 million adults are reported to be regular users of NSAIDs [1]. Often thought of as benign medications, NSAIDs have been shown to have a number of serious side effects including hypertension, renal failure, gastrointestinal bleeding, bronchospasm, and severe cardiovascular complications such as myocardial infarction, stroke, and congestive heart failure. This case demonstrates the effect of NSAIDs on BP, an often over-looked etiology of secondary hypertension. We will review the existing literature and discuss the impo...

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Thyrotoxic Periodic Paralysis

Cited by 2 publications

References 7 publications

Thyrotoxic Periodic Paralysis- A Clinical Review

Thyrotoxic Periodic Paralysis- A Clinical Review

Hypertensive Crisis: The Causative Effects of Nonsteroidal Anti- Inflammatory Drugs

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