Thyrotoxic Periodic Paralysis in Mexican Mestizo Patients

Nellen, Haiko; Mercado, Moisés; Mendoza, Victoria; Villanueva, Salvador; Pérez, Martha Edith Macías; Hernandez, A. Ornelas; Arellano, Jorge

doi:10.1016/s0188-0128(98)00014-1

Cited by 11 publications

(6 citation statements)

References 16 publications

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“… 45 However, associations with HLA-B46/B40 or HLA-DRw8 were not seen in another study of Mexican patients. 11 In this study, patients with Graves' disease without TPP had a higher frequency of HLA-DR3 than those having TPP, 11 although the association between Graves' disease and HLA-DR3 was relatively strong in Caucasians. 46 Thus, available data cannot establish a definite causal relation between the lack of HLA-DR3 and the development of TPP in patients with Graves' disease.…”

Section: Geneticsmentioning

confidence: 54%

“… 8 Instead, the abnormality is secondary to an intracellular shift of potassium. 9 The severity of the hypokalemia usually parallels the extent of muscle weakness, 1 , 10 although this correlation is not absolute, 11 and TPP may occur when the serum potassium concentration is within normal limits. 1 , 5 , 12 – 15 Under these conditions, paralysis may result directly from abnormal thyroid hormone levels.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

“…17 , 18 Several reports describe patients who have had recurrent episodes of periodic paralysis for months or years before the hyperthyroidism was recognized. 11 , 20 , 30 , 31 A series reported from the Mayo Clinic observed that nearly half of the affected patients had only subtle signs and symptoms of hyperthyroidism in spite of clear-cut biochemical evidence. 18 …”

Section: Relation To Thyroid Statusmentioning

confidence: 99%

“…The severity of paralysis may not correlate with the degree of hyperthyroidism. 2 , 11 Some reports suggest that the level of zinc in red blood cells reflects the integrated functional state of the thyroid over the preceding 2 to 3 months, which signifies recent onset of thyrotoxicosis. 32 , 33 Therefore, it may be a useful indicator in patients presented with periodic paralysis without clinical symptoms of thyrotoxicosis.…”

Section: Relation To Thyroid Statusmentioning

confidence: 99%

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Thyrotoxic periodic paralysis: an overview

Hsieh

Kuo

Pei

et al. 2004

Annals of Saudi Medicine

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SUMMARYThyrotoxic periodic paralysis (TPP) is a fairly common manifestation of hyperthyroidism in Asian populations, with an incidence of about 1.9% in thyrotoxic patients, but it is rarely diagnosed among Caucasians and blacks in the Western world. The diagnosis often can be made on the basis of the clinical manifestations alone. Sometimes, periodic paralysis precedes hyperthyroidism or occurs in silent hyperthyroidism. As a result, physicians may easily overlook it even when life-threatening hypokalemia is present. The pathophysiology of this disorder is still not well understood. Correction of the thyrotoxic state is the definitive treatment. Potassium supplementation, propranolol, and spironolactone may be helpful both in the acute state and in preventing attacks.

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Section: Geneticsmentioning

confidence: 54%

Section: Clinical Manifestationsmentioning

confidence: 99%

Section: Relation To Thyroid Statusmentioning

confidence: 99%

Section: Relation To Thyroid Statusmentioning

confidence: 99%

See 2 more Smart Citations

Thyrotoxic periodic paralysis: an overview

Hsieh

Kuo

Pei

et al. 2004

Annals of Saudi Medicine

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“…TPP occurs in the hyperthyroid state and thyroid studies show a high thyroxine (T4) and suppressed TSH. However, the severity of the paralysis is not directly related to the degree of severity of hyperthyroidism (31). Electrocardiograms (EKG) are abnormal in 83–100% of patients with TPP (29, 32).…”

Section: Discussionmentioning

confidence: 99%

Thyrotoxic periodic paralysis: case report and review of the literature

Garla¹,

Gunturu²,

Kovvuru³

et al. 2018

Electron Physician

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IntroductionThyrotoxic 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 presentationA 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 lessonTPP 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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Thyrotoxic periodic paralysis: clinical and molecular aspects

2012

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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.

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Thyrotoxic Periodic Paralysis in Mexican Mestizo Patients

Cited by 11 publications

References 16 publications

Thyrotoxic periodic paralysis: an overview

Thyrotoxic periodic paralysis: an overview

Thyrotoxic periodic paralysis: case report and review of the literature

Thyrotoxic periodic paralysis: clinical and molecular aspects

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