This section is from the book "Part 4. The Acid Autointoxications. Clinical Treatises On the Pathology and Therapy of Disorders of Metabolism and Nutrition", by Prof. Carl von Noorden and Dr. Mohr. Also available from Amazon: Clinical Treatises On the Pathology and Therapy of Disorders of Metabolism and Nutrition, Part 4.
The patient O. K., age 55, suffered from diabetes that was recognized two months before his entrance into the hospital (Nov. 14th, 1902). On admission he excreted about 35 grm. of sugar and in addition 0.132 grm. of acetone on a strict diet plus 100 grm. of white bread. After this patient had been on a strict diet for several days, the sugar disappeared from the urine, but at the same time, as is usually the case, the excretion of acetone rose to 1.232 grm. a day and the ferric cloride reaction, that had been negative up to now, became positive. No oxybutyric acid was discovered. Soon after, the excretion of acetone gradually decreased. The patient during the last week of his sojourn in the hospital received in addition to the strict meat-vegetable-fat-diet, 45 grm. of graham bread, 25 grm. of oatmeal and 100 grm. of apple daily. The urine was free from sugar during this time, and from Dec. 2, to Dec. 8th he excreted an average of 0.405 grm. of acetone. Ferric cloride reaction negative. The patient, who was very conscientious, lived on exactly the same diet for three months longer at home and again received the same diet when he re-entered the hospital on the 12th of March, 1903, for the purpose of further observation. Again no sugar was found in the urine. The quantity of acetone, however, had fallen to 0.060 grm. from 0.4. grm. (average on three days).
As has been said, we have a number of observations on record of cases in which the diet remained the same and the excretion of sugar remained the same, but in which the excretion of acetone varied greatly at different times in the course of the disease.
We need not, therefore, be surprised to find that of 20 diabetics who are living on the same diet and who are excreting the same or approximately the same quantity of sugar, in whom, in other words, according to our conception, the carbohydrate metabolism is the same, hardly two or three excrete the same quantity of acetone bodies. This phenomenon is most striking in those cases who live on a rigid diet and receive a moderate quantity of albuminates so that the excretion of sugar becomes almost zero. We refer to observations of this kind that von Noorden published some time ago. We have a large number of observations of this kind ; in some of them all the acetone bodies were determined for weeks at a time. The following two observations may be quoted here to illustrate our meaning: Patient Adolph S., age 50, four days of strict diet and disappearance of sugar from the urine; and Miss Anna R., age 25, disappearance of the sugar after ten days of strict diet and two days in which some vegetables were allowed. After the urine was free from sugar for eight days, all the necessary urinary determinations were made as below, while the same strict diet was continued. The figures indicate the average values on ten days.
Adolph S. | Anna R. | |
Quantity of urine | 1530 grm. | 1980 grm. |
Nitrogen | 16.8 grm. | 13.5 grm. |
Sugar | 0 | 0 |
Acetone | 0.08 grm. | 1. 1 grm. |
Oxybutyric acid | 0. | 15.0 grm. |
Ferric chloride reaction | negative | positive |
Ammonia | 0.9 grm. | 1.9 grm. |
The two examples just quoted show us that two ex ceedingly important factors, that are independent of the character of the food, may determine the excretion of acetone bodies in diabetes. These two factors are the individuality of the patients and the fact that they become accustomed to a certain diet. We must remember, however, that both factors may also be operative to a certain extent in non-diabetic acetonuria. There are whole populations that exist exclusively on a diet consisting of albumen and fat, and only rarely, and that only at certain times of the year, ingest a little carbohydrate in the form of milk (Laplanders, Esquimaux). No facts have been reported in regard to the acetone excretion of these peoples and it is not known whether they excrete more acetone bodies than inhabitants of warmer climates who are accustomed to a mixed diet. Von Noorden in his Text Book on the Pathology of Metabolism, called attention to the fact ten years ago that obese subjects who are undernourished in the course of reduction cures, as a rule do not develop acetonuria. This observation was corroborated many times later and it was found that fat people who eat between 50 and 60 grm. of carbohydrates per diem and whose diet consisted otherwise exclusively of albumen and fat (including the fat of their own body which they disintegrate) never excreted more than a few centigrams of acetone except on the first few days of the new diet. Only one of these patients excreted as much as from 2 to 3 dgr. and this patient developed diabetes a year later. The reason why these subjects excrete so little acetone when they undergo a reduction cure is probably the fact that they have been accustomed for a long time to eating very little carbohydrate. In order to demonstrate the validity of this view, von Noorden recently undertook the following experiment: A fat subject during the first week of the reduction treatment, received in addition to 500 grm. of meat, green vegetables and salad, meat broth, tea and coffee, some 200 grm. of bread (about 130 grm. of carbohydrate). The urine contained only traces of acetone. As soon as the organism had in this way been accustomed to carbohydrate, the latter was suddenly withdrawn and replaced by 80 grm. of butter (about 63 grm. of fat). The excretion of acetone began immediately and on the third day as much as 0.2 grams were excreted. Soon, however, the acetone excretion became smaller, and at the end of a week hardly traces of this body could be detected in the urine. On general principles, therefore, an obese subject reacts exactly like a healthy person, with this difference, however, that habit causes certain variations.
The other phenomenon mentioned, namely the dependence of the acetonuria on the individuality of the patient (compare the last small table) which is so conspicuous and so easily verified in diabetics, is occasionally also observed in subjects who are not diabetic. One of us examined, for instance, the acetone-body excretion in two subjects, the one suffering from a polyneuritis of syphilitic origin, the other one from hysterical disturbances of the stomach. Both were eating the same diet, consisting of 200 grm. of meat and 300 grm. of butter. The former patient on the second day of this diet excreted 3 grm of oxybutyric acid and 2 1/2 grm. of acetone. At the same time, the ferric chloride reaction of the urine was very strong. The latter patient excreted no oxybutyric acid, only 0.9 grm. of acetone, while the ferric-chloride reaction was negative. I have records of a number of other such cases that are not so pronounced, however. Mention might also be made in this connection that certain differences can be observed in this respect among the mammalian species, for while it is an easy matter, for instance, to produce considerable degrees of acetonuria in human subjects by fasting, this is very difficult to accomplish in a dog. As soon, however, as a dog has once developed acetonuria, the excretion of acetone follows the same laws that we have discussed above, that is, to a great extent it is dependent on the amount of carbohydrate eaten.
The law that the excretion of acetone is due to insufficient metabolism of carbohydrates is not absolute, and while many of the peculiarities just enumerated (the influence of habit and individuality) constitute deviations from this law, we are nevertheless forced to the conclusion that in diabetes certain factors are operative that are not active in normal conditions or in any other pathological state; one of the most important factors is the quantitative difference existing between the acetonuria in diabetes and in other conditions. A diabetic frequently excretes very much more acetone than a healthy subject whose carbohydrate metabolism is the same or even much smaller. Or again, a diabetic may excrete considerable quantities of acetone under conditions in which a healthy subject would excrete only traces.
 
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