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1/4. amiodarone-induced thyrotoxicosis presenting as hypokalemic periodic paralysis.

    Thyroid disorder is a well-recognized side effect of amiodarone therapy. thyrotoxicosis is less common than hypothyroidism. hypokalemic periodic paralysis is one manifestation of thyrotoxicosis, and is more often seen in Oriental and Latin American men than in other demographic groups. This phenomenon, however, has not been previously described in thyrotoxicosis due to amiodarone usage. We describe a case of amiodarone-induced thyrotoxicosis in a 34-year-old man who presented with sudden lower extremity weakness, heat intolerance, and weight loss. physical examination demonstrated fine tremors. serum potassium level was 2.2 mEq/L on admission. Gastrointestinal and renal causes of potassium loss were excluded by history and physical examination. Further biochemical testing demonstrated abnormal thyroid function. The urinary potassium and serum bicarbonate, magnesium, and calcium levels were within normal limits. lower extremity weakness resolved immediately after potassium replacement therapy. methimazole therapy was initiated, and the patient was clinically euthyroid on discharge. ( info)

2/4. Severe infantile hyperkalaemic periodic paralysis and paramyotonia congenita: broadening the clinical spectrum associated with the T704M mutation in SCN4A.

    The authors describe an Italian kindred with nine individuals affected by hyperkalaemic periodic paralysis associated with paramyotonia congenita (hyperPP/PMC). Periodic paralysis was particularly severe, with several episodes a day lasting for hours. The onset of episodes was unusually early, beginning in the first year of life and persisting into adult life. The paralytic episodes were refractory to treatment. patients described minimal paramyotonia, mainly of the eyelids and hands. All affected family members carried the threonine to methionine substitution at codon 704 (T704M) in exon 13 of the skeletal muscle voltage gated sodium channel gene (SCN4A). The association between T704M and the hyperPP/PMC phenotype has been only recently revealed. Nevertheless, such a severe phenotype has never been reported so far in families with either hyperPP or hyperPP/PMC. These data further broaden the clinical spectrum of T704M and support the evidence that this mutation is a common cause of hyperPP/PMC. ( info)

3/4. Anaesthetic management of labour and caesarean delivery of a patient with hyperkalaemic periodic paralysis.

    We describe a parturient with hyperkalaemic periodic paralysis who presented for induction of labour and subsequently, caesarean section. Epidural analgesia and anaesthesia were used successfully in a multidisciplinary plan aimed at avoiding a peripartum attack and providing safe delivery. Management of this rare condition is discussed along with a review of the available literature. ( info)

4/4. Paralysis periodica paramyotonica caused by SCN4A Arg1448Cys mutation.

    Paralysis periodica paramyotonica is an overlapping disease that shares the features of paramyotonia characteristic of paramyotonia congenita (PC) and periodic paralysis characteristic of hyperkalemic periodic paralysis. We report the case of a 23-year-old man with paralysis periodica paramyotonica. His father and a younger brother also exhibited a similar phenotype. A SCN4A Arg1448Cys mutation was detected in this family. The affected family members exhibited marked shifts in compound muscle action potential amplitudes on exercise test, and muscle weakness could be induced by potassium loading and cold exposure. This case demonstrates that SCN4A Arg1448Cys can produce paralysis periodica paramyotonica. Other genetic or environmental factors may modulate the manifestation of SCN4A Arg1448Cys mutation. ( info)

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