Abstract
The older literature on family periodic paralysis contains observations which might suggest a relationship of disturbed K metabolism to the attacks. K citrate was thought by Mitchell 1 to have a slightly beneficial effect on the seizures, and McCann 2 found descendants of Mitchell's patient still relying on the drug. Herrington 3 has recently stated that K citrate will prevent an oncoming seizure but will not cure an attack once developed. Furthermore, earlier Japanese investigators4,5 showed that certain substances (adrenalin, sugar, insulin) which are now known to lower serum K would induce a seizure.
We were thus led to examine the level of serum K in a patient with this disease and have found a definite lowering (25 to 30%) during severe attacks. Aitken and Allott 6 independently observed a similar fall during severe seizures, but in milder attacks they found that the decrease was less, and at times not even detectable.
The experiments which are here reported have been conducted on a 16-year-old boy over a period of 15 months. Our purpose has been to gain information concerning the mechanism of the changes in serum K and their relation to the periodic attacks of the disease.
We have found no excessive elimination of K by the kidney preceding the seizures and have, therefore, sought some other cause of the lowering of serum K during the attack. The seizures generally developed at 3 to 4 A. M., and urinary excretion studies showed that at this time the absorption of K from the gut was quite low. Furthermore, the K taken in with the day's diet had been largely eliminated before midnight. We have, therefore, concluded that such an individual has an unusual need for K salts to maintain contractility of certain of his muscles.
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