In the course of recent years, as already indicated, a number of so-called pathological acetonurias have been described that properly occupy an independent position. A number of causes have been incriminated with producing the acetone in all of the different forms. A number of these acetonurias were soon recognized to be purely symptomatic, so that they were soon excluded from the number of independent disease pictures that were grouped under the general heading of acetonuria. Some of the symptom complexes, however, in which acetone bodies were excreted are still considered to be independent clinical entities, as, for instance, experimental acetonuria in phlorizin and pancreas diabetes, the acidosis occurring in diabetes in human subjects, the febrile form of acid intoxication and the cryptogenetic form of these intoxications. The primary factors that determine the formation of acetone bodies in these cases are presumably certain poisons that are formed in the intestinal canal and that directly or indirectly lead to the formation of acetone bodies (Kraus). So far no one has succeeded in demonstrating that such primary intestinal toxins exist. As a matter of fact, it does not seem to us necessary to postulate their existence, especially in diseases in which B-oxybutyric acid and its derivatives are excreted. For if we study the connection between the acetone bodies and the decomposition and utilization of the carbohydrates in the organism it becomes clear that all acetonurias are due to some one-sided perversion of nutrition. From this standpoint the attempt will be made in the following to describe a connected conception of the large series of acetonurias that have been referred to.

The first of this group of acetonurias that was discovered by Lustig, after extirpation of the coeliac plexus in rabbits, and that was considered to be an essential acetonuria by this investigator, does not stand the light of critical illumination. Thus Peiper repeated some of the experiments of Lustig and could not completely corroborate them. The animals after the operation suffered serious disturbances of general nutrition, so that the acetonuria might well have been the result of malnutrition. In addition, moreover, acetonuria was not a constant result of the operation. We believe that these cases are instances of so-called "hunger acetonuria." At the same time we call attention to the fact that in these animals it is less the "under feeding" than the lack of carbohydrates that is the most important factor (see above). At all events the experiments of Lustig are in no way fundamental, as far as deciding anything in regard to the acetone question is concerned. The experiments of ClaudeBernard are more important. This investigator discovered acetone in addition to dextrose in the urine after performing piqûre. In this case, however, the connection between insufficient utilization of carbohydrates and excretion of acetone is apparent. In phlorizin diabetes acetone, oxybutyric acid and an increased quantity of ammonia are also found in the urine in addition to dextrose. In one case of Von Mering's a comatose condition even developed. The particular animal was allowed to starve for four days before the phlorizin was administered; in this way Von Mering made the animal carbohydrate-free; as soon as the phlorizin was stopped and the sugar excretion ceased, both the symptoms of coma and the acetonuria also disappeared. Kraus interprets the connection between glycosuria and the formation of acids in these cases as follows: He imagines that phlorizin interferes with the chemical interchange of the different substances in the organism and that B-oxybutyric acid is formed from abnormal splitting of N-free remnants of the proteids - that are undergoing rapid disintegration. On the other hand, we think that the acid intoxication in phlorizin diabetes can be explained very much more simply by assuming that the utilization of the carbohydrates is reduced. This view is borne out by the fact that the ferric chloride reaction appears soon after the operation and that B-oxybutyric acid (in small quantities, it is true) also appears sometime afterwards (Minkowski).