PARATHYEOID GLANDS 663 



ectomy the tetany is more violent than when it is also removed, and, 

 further, that subsequent removal of the thyroid lessens the violence of the 

 tetany. Still, as Biedl has pointed out, the disease picture of postoperative 

 tetany, as regards intensity of symptoms, course and duration, is so ex- 

 tremely variable that it would be dangerous, from a consideration of their 

 behavior alone, to draw direct conclusions regarding the kind of functional 

 connection tkat exists between the thyroid gland and the parathyroids. 

 Moreover, numerous experiments made by Biedl himself, and others made 

 by Wiener, have failed to confirm the observations of a more violent tetany 

 after thyroparathyroidectomy than after a pure parathyroidectomy. And 

 many good clinical observers assert that the administration of thyroid sub- 

 stance exerts a definitely ameliorative effect upon the symptoms of tetania 

 strumipriva. There does not seem, therefore, to be sufficient support for 

 the detoxication hypothesis, at least in its original form, in which the 

 thyroid was looked upon as the poison making organ. 



Accordingly, investigators at present assume in general a toxic sub- 

 stance arising somewhere in the organism, and speak of it as the "tetany 

 poison of unknown origin." Uhlenhuth's studies point to its origin in the 

 thymus gland. 



Some evidence has been brought forward to show that the tetany poison 

 is present in the circulating blood (MacCallum and Voegtlin, Fano and 

 Zanda, Baldi, Biedl), for severe attacks of tetany can be quickly amelio- 

 rated by copious bleeding, the improvement lasting for twenty-four hours 

 if some fresh normal blood be transfused after the venesection. 



The attempts of Wiener to prove that the tetany poison, whatever it is, 

 possesses the character of an antigen, to which the normal organism builds 

 an antitoxin (self-immunization), seems improbable and certainly lacks 

 sufficient experimental support. 



When discussing the metabolism of tetany, we pointed to the multiple 

 observations of an increased ammonia output in tetany. On account of this 

 finding, the theory of ammonia poisoning and of carbaminic acid poisoning 

 as an explanation of the intoxication in tetany was early put forward. 

 Frouin (1910) asserted that he could produce typical tetany within twenty- 

 four or forty-eight hours after removal of the thyroid apparatus by injec- 

 tion of three or four grams of carbaminate of soda, though when the 

 injection of this substance was combined with that of a soluble calcium salt 

 no signs of tetany appeared. But the theory that tetany might be due to 

 disturbance of liver function with loss of power to destroy ammonia or 

 diminution of that power, also developed by Carlson and Jacobson in 1910, 

 has been given up, these latter authors themselves having shown in a later 

 publication that there are essential differences between the muscle spasms 

 due to tetany and those due to ammonia poisoning. 



Since an increased ammonia output in the urine is usually a sign of 



