Identification and functional characterization of Kir2.6 mutations associated with non-familial hypokalemic periodic paralysis. (49/68)

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A sodium channel knockin mutant (NaV1.4-R669H) mouse model of hypokalemic periodic paralysis. (50/68)

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Expression patterns of two potassium channel genes in skeletal muscle cells of patients with familial hypokalemic periodic paralysis. (51/68)

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Distal renal tubular acidosis and hypokalemic paralysis in a patient with hypothyroidism. (52/68)

A 43- year- old woman on treatment for primary hypothyroidism presented with 1- day progressive weakness of all her limbs and history of similar episodes in the past. Clinical examination revealed grade 2 hyporeflexive weakness. Investigations revealed features of hypokalemia, metabolic acidosis, alkaline urine, and a fractional bicarbonate excretion of 3.5%, consistent with distal renal tubular acidosis. Antithyroid peroxidase and antithroglobulin antibodies were positive, suggesting an autoimmune basis for the pathogenesis of the functional tubular defect. Bicarbonate therapy resulted in a sustained clinical recovery.  (+info)

Acetazolamide efficacy in hypokalemic periodic paralysis and the predictive role of genotype. (53/68)

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Surgical treatment for thyrotoxic hypokalemic periodic paralysis: case report. (54/68)

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Hypokalemic paralysis following administration of intravenous methylprednisolone in a patient with Graves' thyrotoxicosis and ophthalmopathy. (55/68)

Glucocorticoids are commonly used in the treatment of patients with thyroid disorders, in particular Graves' ophthalmopathy. Thyrotoxic hypokalemic periodic paralysis (TPP) is an infrequent but potentially serious condition characterised by recurrent episodes of weakness associated with hypokalemia. We describe the development of acute hypokalemic paralysis in a middle-aged Caucasian man with recently diagnosed thyrotoxicosis and severe, active Graves' opthalmopathy who developed progressive flaccid paralysis 12 hours following intravenous administration of methylprednisolone. Rechallenge with the same dose after the patient had been rendered euthyroid did not provoke TPP. Clinicians should exercise caution when administering high-dose glucocorticoids during thyrotoxicosis as there is a risk of provoking hypokalemic paralysis in susceptible patients.  (+info)

Mechanism of thyrotoxic periodic paralysis. (56/68)

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