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Arch Intern Med. 1999 Mar 22;159(6):601-6.

Clinical and metabolic features of thyrotoxic periodic paralysis in 24 episodes.

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Department of Medicine, Santa Clara Valley Medical Center, San Jose, Calif 95128, USA.



Hypokalemia is a well-known, consistent finding in thyrotoxic periodic paralysis (TPP). It is less well known that hypophosphatemia and mild hypomagnesemia are often present in TPP and that rebound hyperkalemia can occur as a result of potassium therapy.


To report the prevalence of these electrolyte abnormalities in 24 episodes of TPP in 19 patients admitted to a single university-affiliated public hospital during a 15-year period.


The medical records of all patients admitted to the Santa Clara Valley Medical Center in San Jose, Calif, between August 1, 1982, and June 1, 1997, with any type of hypokalemic periodic paralysis were reviewed. In patients with TPP, serum potassium, phosphorus, and magnesium levels were evaluated during and after episodes of paralysis. The administered dose of potassium chloride, recovery time from hypokalemia, and prevalence of rebound hyperkalemia after recovery were also ascertained. Data are presented as mean +/- SD.


Hypokalemia was present in all 24 initial episodes of TPP, with serum potassium levels ranging from 1.1 to 3.4 mmol/L (mean, 1.9+/-0.5 mmol/L). After recovery from hypokalemia, the maximum serum potassium level significantly increased, ranging from 4.0 to 6.6 mmol/L (mean, 4.9+/-0.5 mmol/L; P<.001). In 10 (42%) of 24 episodes, rebound hyperkalemia (serum potassium level >5.0 mmol/L) was present. Recovery time did not correlate with the potassium chloride dose administered (r = 0.17). Initial serum phosphorus levels ranged from 0.36 to 0.97 mmol/L (mean, 0.61+/-0.23 mmol/L) (1.1-3.0 mg/dL [mean, 1.9+/-0.7 mg/dL]), with hypophosphatemia present in 12 (80%) of 15 episodes. Serum phosphorus levels significantly increased (P<.01), to 1.26 to 1.74 mmol/L (mean, 1.48+/-0.16 mmol/L) (3.9-5.4 mg/dL [mean, 4.6+/-0.5 mg/dL]), with or without phosphorus replacement therapy. A slight increase in serum magnesium levels after paralysis resolved was observed in all patients (P<.07). No further episodes of paralysis occurred in any patients after they became euthyroid.


Hypokalemia, hypophosphatemia, and mild hypomagnesemia are characteristic features of TPP. Hypokalemia occurred in 100% and hypophosphatemia in 80% of the episodes in our study. Rebound hyperkalemia is a potential hazard of potassium administration and occurred in 42% of 24 episodes.

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