HYPOGLYCEMIC SYMPTOMS PROVOKED BY REPEATED GLUCOSE INGESTION IN A CASE OF RENAL DIABETES R. B. Gibson, Ph.D., and R. N. Larimer, M.D., Iowa City 

One of us (R. B. G.), in November last, reviewed the chemical findings in a case from our diabetic clinic before the Iowa Clinical Medical Society. Interest in the case centered in the fact that a final diagnosis of what was otherwise a case of pronounced renal diabetes could not be made because the sugar curve indicated a deficient glycogenesis of the mildly diabetic type. A study of the effects of a repeated ingestion of glucose on the sugar curve by Hamman and Hirschman was recalled, and we predicted in our report that a decisive differentiation might be obtained if we employed the double sugar curve test in this case. The patient was requested to return for further observation, and promised to come to the clinic in January of this year. 

We have in the clinic, at the present time, a second patient with a fasting hypoglycemia and a glycosuria of long standing which does not respond to diabetic management. The data presented in this communication were obtained in this case. Glycogenesis is stimulated by glucose ingestion, as is indicated by the rapid fall of the blood sugar from the peak of the curve (usually forty-five minutes) to a figure at the end of two hours almost always less than the fasting control observation. A second administration of glucose brings about a yet more rapid removal of sugar from the blood stream and a consequent lowering of the sugar curve. The desugarized diabetic patient may show an effect similar to the normal person, but of much less degree (one case, Hamman and Hirschman). When tried in our case, the effect of the double sugar curve test was so great that hypoglycemic symptoms were observed in two out of three trials. 

REPORT OF CASE Mrs. B., aged 30, white, weight 110 pounds (50 kg.) (best weight 115 pounds [52 kg.] ten years ago) was admitted to the hospital with a history of glycosuria of ten years' standing. This had been discovered by a urine examination during the first of her two pregnancies. She had never had other symptoms of diabetes except for some pruritus seven years ago; she had dieted off and on since that time. The condition seemed to be familial, the patient stating that she had one sister surely and one probably glycosuric patients without other symptoms; however, she had no knowledge of glycosuria in either of her parents. The patient was placed on a diet of 50 gm. of protein, 50 gm. of carbohydrate, and 125 gm. of fat; on this, she excreted from 4.5 to 8.5 gm. of glucose daily. Her blood uric acid was 3 mg., and blood urea nitrogen, 18 mg. Fasting blood sugar determinations or figures obtained two hours after meals were always hypoglycemic. The results of our tests with the double sugar curve are given in the accompanying table. 

Definite hypoglycemic symptoms were obtained in the first and third trials; they were identical with the several mild insulin reactions which we have observed in our diabetic patients, consisting of burning and flushing of the face, weakness, tremor and sweating. The second shock was the more severe of the two; the patient was completely relieved in fifteen minutes when given 100 c.c. of orange juice. The lowering of the leyel of the entire curve in the third trial is in accord with the experience that glycogenic effects may become more pronounced if the ordinary procedure is repeated without a sufficient number of days elapsing between tests. When questioned as to the occurrence of similar attacks at home, the patient stated that she had experienced such of milder degree, but could not associate these with any definite circumstance. One sister had like attacks. It seems likely that hypoglycemic symptoms not artificially produced are a definite clinical entity.

In explanation of a diminished glycogenesis in pronounced renal diabetes, it was stated, in the paper referred to above, that "It is quite possible that glycogenesis in our case may be functionally diminished because of the rapid removal of glucose through the kidneys; if so, repeated administration of glucose might so stimulate the glycogenic power fhat a normal or subnormal sugar curve will result." Since this report was submitted for publication, threshold hypoglycemic symptoms with a blood sugar of 0.045 per cent, have been induced in our first patient; the maximum hypoglycemic effect is quite transient.