title: In vivo and in vitro sodium pump activity in subjects with thyrotoxic periodic paralysis.
abstract: OBJECTIVE
  To examine whether sodium pump activity plays a part in the pathogenesis of thyrotoxic periodic paralysis.
  
  
  METHODS
  Measurement of platelet sodium-potassium ATPase and in vivo sodium pump activities in healthy subjects and thyrotoxic subjects with and without paralysis.
  
  
  METHODS
  University hospital in Hong Kong.
  
  
  METHODS
  21 healthy subjects, 23 untreated thyrotoxic subjects, 13 untreated men with periodic paralysis, seven treated thyrotoxic subjects, and six treated men with periodic paralysis.
  
  
  METHODS
  Platelet Na+, K(+)-ATPase activity and plasma rubidium concentration after oral loading.
  
  
  RESULTS
  Median (range) platelet Na+, K(+)-ATPase activity in thyrotoxic subjects was 253 (169-821) mumol inorganic phosphate/h/g protein--significantly higher than that in healthy subjects (134 (81-180) mumol/h/g protein; p less than 0.001). Na+, K(+)-ATPase activity in those with periodic paralysis was 374 (195-1196) mumol/h/g protein, again significantly higher than that in healthy subjects (p less than 0.001) and that in other thyrotoxic subjects (p less than 0.01) despite similar degrees of hyperthyroidism. Activities in treated thyrotoxic subjects with and without periodic paralysis were 148 (110-234) and 131 (86-173) mumol/h/g protein respectively. Mean (95% confidence interval) plasma rubidium concentration five hours after oral administration in thyrotoxic subjects (7.0 (6.6 to 7.5) mumol/l) was significantly lower than in healthy subjects (10.2 (9.5 to 10.9) mumol/l; p less than 0.001) and higher than in those with periodic paralysis (6.0 (5.7 to 6.3) mumol/l; p less than 0.01).
  
  
  CONCLUSIONS
  Sodium pump activity in untreated subjects with periodic paralysis is higher than in other thyrotoxic subjects, and this may be responsible for the hypokalaemia.
authors.affiliation: Department of Chemical Pathology, Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT.
authors.forename: A
authors.initials: A
authors.lastname: Chan
authors.forename: R
authors.initials: R
authors.lastname: Shinde
authors.forename: C C
authors.initials: CC
authors.lastname: Chow
authors.forename: C S
authors.initials: CS
authors.lastname: Cockram
authors.forename: R
authors.initials: R
authors.lastname: Swaminathan
mesh_terms: D000328:Adult; D001792:Blood Platelets / Q000201:enzymology; D006801:Humans; D008297:Male; D010243:Paralysis / Q000097:blood / Q000201:enzymology*; D010507:Periodicity; D012413:Rubidium / Q000097:blood; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism* / Q000502:physiology*; D013971:Thyrotoxicosis / Q000097:blood / Q000201:enzymology*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D014284:Triiodothyronine / Q000097:blood
chemical_list: D014284:Triiodothyronine; D013972:Thyrotropin; D000254:Sodium-Potassium-Exchanging ATPase; D012413:Rubidium; D013974:Thyroxine