658 FREDERICK S. HAMMETT 



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placenta of albuminous material foreign to the host, and an inadequate 

 elaboration of a destructive protective substance "syncytiolysin." Ascoli, 

 Weichardt ()(&), Shenk (a.) (6), and Liepmann had varying success 

 in supporting this hypothesis, which was finally and successfully repu- 

 diated by the work of Lichtenstein (a)(&)(c), Dryfuss, Freund, Mathes, 

 Wormser, Pollak, and others. In view of his extensive studies on pla- 

 cental enzymes, Hofbauer (c) felt justified in advocating the belief that 

 the cause of eclampsia lay in an escape of these enzymes in excess into 

 the maternal blood with subsequent development of toxic products. This 

 hypothesis was supported by Dryfuss, Freund, Mathes, Wormser, Pollak, 

 and others. In view of his extensive studies on placental enzymes, Hof- 

 bauer (c) felt justified in advocating the belief that the cause of eclampsia 

 lay in an escape of these enzymes in excess into the maternal blood with 

 subsequent development of toxic products. This hypothesis was supported 

 by Dryfuss, Freund, and also by Savare, who found that autolysis 

 has already commenced in the placenta from eclamptic pregnancies, and 

 that the activity of the desamidases was greater in these placentas 

 than in those obtained from normal pregnancies. It is thus evident that 

 the question of this disease is inherently bound up in the con- 

 ception of its being an intoxication process, but that the seat of the dis- 

 turbance, as well as its mechanism, is a matter of speculation and 

 uncertainty. A careful study of all available data was made by Lichten- 

 stein, who, enlarging the idea of Czempin, came to the conclusion 

 that the origin of eclampsia does not lie in the production by the pla- 

 centa of toxic material per se, but that in all probability through 

 a perversion or diminution, or both, of placental function, the fetal meta- 

 bolic by-products are allowed to escape in quantity into the maternal 

 system, and these being present, in addition to those produced by the 

 maternal organism as the result of its own metabolism, put such 

 additional burden upon the excretory and detoxicating organs that they 

 cannot deal with it and toxemia results. Now Czempin had noted that 

 there was an increased nitrogen in eclamptics, and Farr and Williams, 

 and Slemmons and Morris had also found indications that the urea 

 nitrogen in such cases was increased over the normal, while Hammett (e) 

 has demonstrated that not only has the placenta a high urea-forming abil- 

 ity, but that the placentas from pregnancies accompanied by toxemia are 

 much higher in urea content than are those from normal cases. The first 

 group of findings demonstrate clearly that in eclampsia there is an accumu- 

 lation of unexcreted nitrogenous metabolic by-products, and the latter that 

 the placenta is capable of converting the intermediary nitrogenous products 

 of metabolism into a form normal for excretion. Moreover, unpublished 

 studies of J. L. Brenner on the histological structure of placentas from 

 eclamptic patients seem to indicate that in some placentas at least there 

 has occurred such changes in the syncytium and underlying tissues as 



