[MIM 188 580, 613 329, 614 834]

Association of a hypokalemic periodic paralysis to biological hyperthyroidism, commonest in male Asian patients. It is likely that the increase of membrane ATPase activity and the increase in sensitivity of beta-2 adrenergic receptors related to hyperthyroidism are responsible for the attacks of paralysis. It is likely that a genetic predisposition exists in those patients: association of mutations of the CACNA1S gene (1q32), of the GABRA3 gene (Xq28) and mostly of the KCNJ18 gene (17p11.2) coding for the potassium channel Kir2.6.

The treatment of hyperthyroidism causes the disappearance of symptoms.

Anesthetic implications: 

attack of flaccid paralysis. A treatment with beta-blockers improves the symptoms while waiting for the disappearance of hyperthyroidism.

References : 

-        Wong GWK, Leung TF, LO AFC, Ahuja AT, Cheng PS. 
Thyrotoxic periodic paralysis in a 14-year-old boy. 
Eur J Pediatr 2000; 159: 935.

-        Eve O, Soubirou J-L, Crevon L, Martinez J-Y, Escarment J. 
Paralysie hypokaliémique révélant une hyperthyroïdie. 
Ann Fr Anesth Réanim 2004 ; 23 : 745-7.

-         Diderich DA, Wedel DJ.  
Thyrotoxic periodic paralysis and anesthesia: report of a case and literature review. 
J Clin Anesth 2006; 18: 286-92.

-        Bandschapp O, Iaizzo PA. 
Pathophysiologic and anesthetic considerations for patients with myotonia congenital or periodic paralyses. 
Pediatr Anesth 2013; 23: 23:824-33

Updated: July 2021