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• W2022988557 abstract "In reply: I appreciate Dr Tran's positive comments on my concise review of TPP, which is a hyperthyroidism-related hypokalemia with muscle weakness resulting from an acute shift of potassium into cells without a total potassium deficit. Two distinct findings in patients with TPP-low renal excretion of potassium and relatively normal acid-base status-support the shift mechanism, in contrast to the metabolic acidosis or alkalosis associated with high or low potassium excretion seen with gastrointestinal or renal potassium loss. Regarding Dr Tran's young patient with thyrotoxicosis and hypokalemia, it would be premature to diagnose TPP without first determining her renal potassium excretion and acid-base status, as well as the amount of potassium chloride required to correct her hypokalemia. The presence of thyrotoxicosis and hypokalemia does not always indicate TPP. The patient was using exogenous thyroid hormone for weight loss, and she also may have been taking other drugs that cause hypokalemia. Overzealous use of liothyronine sodium certainly causes thyrotoxicosis but not necessarily hypokalemia and episodic paralysis, especially in female patients. Without measurement of urinary electrolyte levels and a clinical course consistent with TPP, the patient could have hypokalemia due to potassium deficit and/or thyrotoxic myopathy. Although thyroxine challenge was shown to elicit paralytic attacks in patients with a history of periodic paralysis in 1925,1Shinosaki T Klinische studien uber die periodische extremitatenlahmung.Ztschr f d ges Neurol u Psychiat. 1925; 100: 564Crossref Scopus (7) Google Scholar subsequent studies have not substantiated the episodic paralytic effects of thyroxine.2Wolf A The effective use of thyroid in periodic paralysis.N Y State J Med. 1943; 43: 1951-1963Google Scholar, 3Engel AG Thyroid function and periodic paralysis.Am J Med. 1961; 30: 327-333Abstract Full Text PDF PubMed Scopus (56) Google Scholar Therefore, the susceptibility of some individuals to hypokalemia or periodic paralysis in the presence of hyperthyroidism may be genetically determined, yet unproved. It is impossible to induce hypokalemia or paralytic attacks in nonsusceptible subjects with use of sufficient exogenous thyroid hormone to produce severe thyrotoxicosis. However, exogenous thyroxine challenge may become useful in the assessment of phenotype-genotype expression once the genetic abnormality responsible for TPP has been defined. Despite the male preponderance in TPP, no clear inheritance pattern has been determined, unlike the autosomal dominant inheritance pattern identified in familial periodic paralysis. Sodium Oxybate (γ-Hydroxybutyrate): Anesthetic Agent or Source of Anesthetic Interactions?Mayo Clinic ProceedingsVol. 80Issue 7PreviewTo the Editor: Sodium oxybate (?-hydroxybutyrate [GHB]) has been used as a hypnotic, anxiolytic, and sedative agent and as an adjuvant to general anesthesia elsewhere, but experience with the drug is limited in the United States. Recent therapeutic applications include management of opioid and alcohol withdrawal and reduction of the number of cataplexic attacks in patients with narcolepsy.1 The Food and Drug Administration approved GHB for treatment of narcolepsy with cataplexy only recently. We describe a patient who experienced adverse anesthetic events associated with GHB. Full-Text PDF" @default.
• W2022988557 created "2016-06-24" @default.
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• W2022988557 date "2005-07-01" @default.
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• W2022988557 title "Thyrotoxic Periodic Paralysis–Reply–I" @default.
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• W2022988557 doi "https://doi.org/10.4065/80.7.961" @default.
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