^ RELATlOy OF ACIDO.SIS TO iJlAJiiyi/C COMA 553 



coma of diabetes. Fiirtliermore, coma may occur in diabetics who are 

 producing- no such ((uantity of oriianic aeids as would seem tlieoreti- 

 cally to be necessarj^ to cause enough acid intoxication to result in 

 acidosis, and coma develops in diabetics who are being supplied with 

 sufficient bases for all requirements. Hence it must be concluded 

 that only a part of the symptomatology of diabetic coma depends on 

 acids as such, but as yet we do not know what other agents are 

 acting.^" 



/8-ox3'butyric and diacetic acid, according to many authorities, 

 seem to have no specific poisonous effects, but act simply as acids 

 in the blood. Acetone does not have this effect, not being an acid, 

 and seems not to be toxic to any considerable degree ; doses of 4 grams 

 per kilo cause effects similar to ethyl alcohol in dogs, 8 grams per 

 kilo being fatal, which corresponds to a dose of 500 grams for an adult 

 man. According to Rhann' ^" acetone is more toxic (for guinea pigs) 

 than methyl alcohol, while for rabbits Desgrez and Saggio ^* found 

 acetone the least toxic of the acetone bodies, diacetic acid next, and 

 ^-oxybutyric acid most. Ehrmann ^^ also claims that he has pro- 

 duced typical coma with the sodium salts of butyric and of /?-oxybuty- 

 ric acid, but as high as 40 grams of ^S-oxybutyric acid have been 

 found in the day's urine of a non-diabetic without any evidence of 

 intoxication. Ewing suggests that the acetone bodies may cause renal 

 injury, which is usually evident in acidosis, and M. H. Fischer's 

 views on the relation of acids to nephritis accord wdth this fact. 

 The withdrawal of the inorganic bases, especially Ca and Mg, may 

 also be responsible for symptoms, as it is well established that a proper 

 balancing of these ions is necessary for normal cell activity, especially 

 in the nervous system. *° 



Hurtley -^ sums up the evidence on the toxicity of the acetone 

 bodies by saying that aceto-acetic acid seems to be highly toxic only 

 in depancreatized animals, while oxybutyric acid is practically non- 

 toxic. He favors the view that aceto-acetic acid poisoning is respon- 

 sible for diabetic coma, for it increases in the urine on the approach 

 of coma, and the ratio of aceto-acetic to butyric acid in the urine in- 

 creases with the severity of the intoxication. The increased propor- 

 tion of aceto-acetic acid presumably means that it is being produced 

 in such quantities throughout the body that the liver cannot reduce 

 as large a proportion to oxj^butyric acid as it normally does. In con- 

 sidering the possibility that the acetone bodies may be responsible for 

 at least part of the intoxication of diabetic coma we must bear in 



36 Pribram and Loewy (Zeit. klin. Med., 101.3 (77). .384) siisifrost that ab- 

 normal products of protein cleavage are responsible, and Rosenblonm (X. Y. ^led. 

 Jour., Aug. 7, 1915) reports cases of typical dialietic coma witlioiit acetone bodies 

 in the urine. 



3 T .Tour. Amer. :\red. Assoc, 1012 (.58). 628. 



ssCompt. Rend. Soc. Biol., 1007 (63), 288. 



soBerl. klin. Woch., 1013 (50), 11. 



40 See Cammidge, Amer. Med., lOlG (11), 363. 



