Have also been attributed to autointoxication with acetone and the origin of the acetone has been laid in the intestine, according to Lorenz. Recently Stumpf and Stolz have gathered more casuistic material on acetonuria occurring in pregnant women and during labor and have advanced the theory that the relative frequency of acetonuria in such cases must be attributed to an increased destruction of fat in the maternal organism. No very convincing proofs, however, have been adduced in favor of this far-reaching theory, for the reason, chiefly, that the character of the nutrition in these cases has not been sufficiently considered, so that on these grounds alone one is hardly justified in assuming an increased destruction of fat. The same applies to acetonuria in pregnancy in cases in which the fetus is dead. These cases of acetonuria were interpreted to signify toxogenic destruction of fat resulting from the absorption of poisonous products from the uterus (Waldvogel.) This assumption is altogether unjustified, for this form of acetonuria is also directly influenced by carbohy drates. This may be illustrated by the following two cases observed by von Noorden; both were women with febrile tuberculosis of the lungs, and both were in the eighth month of pregnancy. For fourteen days neither of them had felt any fetal movements nor could any fetal heart sounds be heard. The nutrition of both of these cases was greatly reduced and the ingestion of food had been very small for a number of weeks, and consisted moreover, principally of meat broth, eggs and tea. Legal's test was very positive, also the ferric chloride reaction. In the course of the next few days the nutrition of these patients was improved by the addition of milk and bread to the diet, whereupon the ferric chloride reaction disappeared at once and Legal's test was only slightly positive for a little while and finally disappeared almost completely. No positive ferric chloride reaction could be obtained after this, because the nutrition in these patients was carefully maintained until the macerated fetus was born on the fifth day in one case and the seventh day in the other.

In poisoning with antipyrine, sulphuric acid, atropine, extractum filicis, morphine, lead, etc., and also after chloroform narcosis, another form of acetonuria has been described that is called toxic acetonuria. (Becker). A large number of these cases were thought to be due to toxic disintegration of albumen and lack of oxygen - the latter being attributed to the destruction of red blood corpuscles. According to Ebstein, there is a condition that he calls "insufficiency of intracellular respiration due to the action of these poisons. A priori one cannot deny that in poisoning with some of these bodies disturbances of oxidation may occur and that the excretion of acetone may be due to deficient catabolism of certain bodies that would ordinarily be oxidized further than the acetone stage. We call attention in this connection to the experiments of Araki on poisoning with carbon monoxide. On the other hand, one must never forget that in the most pronounced forms of toxic acetonuria the patients were in a condition of prolonged somnolence and took little food for long periods of time, and that, further, the acetone was rarely discovered until these patients had been fasting for several days. It is remarkable how naive and indiscriminate the interpretation of some of these cases is, for some of the authors pay no attention whatsoever to the nutrition of the patient. As far as acetonuria after narcosis in particular is concerned, one of us can state from personal experience that the excretion of acetone in these cases disappears after the administration of carbohydrates, or is at least greatly reduced by carbohydrates, so that the same conditions apparently exist here as in acetonuria from fasting.

We can conclude, therefore, from all that we have learned in regard to pathological acetonuria that this form behaves exactly like the experimental form that is brought on artificially by fasting or by feeding a diet that consists exclusively of meat and fat. If we are justified in the experimental forms in concluding that the absence of carbohydrates produces the acetonuria, then it would appear that we are also justified in concluding that pathological acetonuria may be due to the same cause. One might object that these two forms have merely this in common, that the addition of carbohydrates to the diet causes the acetonuria to disappear, but that in all these different cases the primary cause of the acetonuria is different. One could, therefore, assume, that there are a variety of forms of acetonuria of different etiology. We believe, however, that this assumption is false, particularly in regard to the forms of acetonuria that follow fasting or a onesided, carbohydrate free diet and in regard to diabetic acetonuria.