SD was seen in 40 (7.8%) out of the 511 Patients who had been treated with glucocorticoid hormon (GCH); most frequently in the patients with leukemia (13 cases) followed by aplastic anemia (12 cases). Incidence of SD was 29.3% in aplastic anemia, 25.0% in hemolytic jaundice, 22.2% in other blood dyscrasias, 11.8% in bronchial asthma and 11.3% in leukemia.
The following factors were apparently related to elicit high incidence of SD; the age ranged from 51 to 60 years old, an averaged total dose given corticosteroids was 1666.7mg, an averaged period during which GCH has been given was 83.5 days and an averaged total amout of blood transfusion was 4138.8mg
In the cases manifestign SD, 50g glucose tolerance test (GTT) has shown always diabetic type and (immuno-reactive insulin (IRI) has displayed usually hyperresponse and delayed type of response curves. Concerning the serum lipids, level of the cholesterol was often elevated and an increase of palmitic and a decrease of linoleic acid were revealed in percentage composition of total fatty acids.

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It is well known that adrenal corticosteroids have many biological effects on the carbohydrate metabolism.
However, the mechanism of corticosteroids on carbohydrate metabolism has not been completely clarified and remains to be studied.
In the present investigation, it was intended to study the effects of dietary carbohydrates on the experimental steroid diabetes induced by Ingles method in which 10 mg of cortisone was administered to rats daily. Furthermore, the effect of anabolic steroid (Oxymetholone-HMD) on steroid diabetes was studied.
In this experiment, rats were divided into two groups, namely 1) rats fed with customary diet 2) rats forcedly fed with high carbohydrate diet. In the case of customary feeding, the rats were fed with 18.0 g of commerical diet (Oriental Co. LTD.) daily containing 9.47 g of carbohydrate, 0.99 g of fat and 4.36 g of protein. In the second group, they were forcedly fed by a gastric tube with the solution containing 17.08 g of carbohydrate, 2.76 g of fat and 5.94 g of protein.
During the experimental period, fasting blood sugar level, urinary glucose excretion and body weight were determined. The glucose tolerance test was performed using 10 cc of 20% glucose solution just before, one week and two weeks after cortisone administration.
The results of this experiment are summarized as follows :
1) In both customary and high carbohydrate diet groups, it was ascertained that the fasting blood sugar level increased late in the experimental period (10 to 14 days after cortisone administration). The rise of blood sugar level was slight in the customary diet group, but in the high carbohydrate diet group a marked rise in the blood sugar level was noticed.
The group fed with the high carbohydrate diet alone, showed a rise of fasting blood sugar level early in the experimental period (2 to 4 days) and then returned to normal late in the experimental period.
2) Urinary glucose was not shown in the customary diet group during the whole experimtal period in spite of the cortisone administration. In the group fed with high carbohydrate diet alone, urinary glucose was temporarily seen early in the experimental period. When cortisone was administered to the group fed with high carbohydrate diet, glucose excretion in the urine increased more remarkably late in the experimental period than in the rats fed with high cardohydrate diet alone.
3) The hyperglycemic effect of cortisone in the high carbohydrate diet group was inhibited completely by simultaneous administration with anabolic steroid. Urinary glucose excretion was inhibited also completely by simultaneous administration of two agents. In the high carbohydrate diet group treated with anabolic steroid, fasting blood sugar level decreased, but a little glucosuria was seen in some animals.
4) A remarkable dercrease in body weight was observed in both groups fed with high carbohydrate diet and customary diet after cortisone administration. However, the decrease in body weight was inhibited by the combined administration of anabolic steroid steroid and cortisone. On the other hand, the boy weight increased considerably in the high carbohydrate diet group after anabolic steroid administion.
5) The glucose tolerance of rats fed with the customary diet lowered considerably after administration of cortisone and in the animals administered with cortisone and anabolic steroid simultaneously, glucose tolerance lowered one week but returned to normal two weeks later.

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In this report the influence of several glucocorticoids on fasting blood sugar level, urinary glucose excretion, body weight and glucose tolerance were studied in rats with experimental steroid diabetes.
Steroids used in this experiment were cortisone, prednisolone, dexamethasone, and betamethasone. The doses were 10 mg, 2.0 mg, 0.4 mg, and 0.4 mg, respectively.
The experimental period was two weeks. The rats were fed with high carbohyrate diet for 6 days the experiment began and then corticosteroids were administered.
The glucose tolerance was measured just before and on the last day of the experiment.
The results are summarized as folllows :
1) Fasting blood sugar level was highest in rats administered with prednisolone, and was followed by rats treated with cortisone, dexamethasone, betamethasone, respectively.
2) Urinary glucose excretion was most remarkable in rats administered with dexamethasone, and was followed by those given prednisolone, betamethasone, cortisone, respectively.
3). The rats treated with prednisolone showed the lowest glucose tolerance, and were followed by those given dexamethasone, cortisone and betamethasone in that order.
4) The decrease in body weight of rats treated with dexamethasone was most remarkale, and was followed in those treated with betamethasone, cortisone, prednisolone in lesser degrees, sespectively.
5) Parallel relationship between urinary glucose excretion and glucose tolerance was seen. However, inverse relationship was seen between rise of fasting blood sugar level and decrease of body weight.

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末梢性顔面神経麻痺または突発性難聴に対しハイドロコーチゾンを750 mg, 500 mg, 250 mg, 100 mg各3日間計12日間投与するという治療を行う際，糖尿病症例で高血糖を来した場合に適用する血糖管理プロトコールの有用性を3例について検討した．各食前のインスリンは超速効型インスリンアナログを用い，量の調節としては1日4回（朝食前と各食後）の血糖測定を行って前日の食後血糖値で当日の責任インスリン量を決定した．血糖値とインスリン量の関係は，130∼139 mg/dl→2単位減，140∼220 mg/dl→変更なし，221∼250 mg/dl→2単位増，251∼320 mg/dl→4単位増とした．これらの値をはずれるときのみ医師が決定した．本プロトコールを用いることにより比較的少ない血糖測定回数のもと，低血糖を起こすことは稀で，著明な高血糖を来さず，容易に血糖管理を行うことができた．以上，大量ステロイド療法中の血糖管理に際し，各食前の超速効型インスリンの使用法に関する，有用かつ安全と考えられるプロトコールを提唱した．

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Radioreceptorassay using particulate membrane of human placenta, liver and kidney of guinea pigs were carried out to investigate the effect of insulin antibodies on insulin receptors.
¹²⁵I-insulin binding to insulin receptors at 24°C increased slowly, binding in an apparent steady-state was reached within 1 h and continued for 3 h. ¹²⁵I-insulin binding to insulin antibodies at 24°C increased rapidly, binding in an apparent steady-state was reached within 0.5 h and continued for 3 h. ¹²⁵I-insulin incubated with buffer at 24°C was not degraded until 2.5 h, but ¹²⁵I-insulin incubated with 300μg of particulate membrane of human placenta at 24°C was degraded and its degradation rate was 37.5% at 1 h, 50.9% at 2 h, 60.4% at 3 h. The degradation rate of particulate membrane of human placenta in the same condition was 4.3% at 0.5 h, 1.8% at 1 h, 19.6% at 2 h. After these studies, the following four experiments were performed.
Group 1: ¹²⁵I-insulin was preincubated with insulin antibodies for 90 min., then insulin receptor was added to the incubation material. The mixture was incubated for 120 min..
Group 2: ¹²⁵I-insulin, insulin antibodies and insulin receptor were incubated together for 120 min..
Group 3: ¹²⁵I-insulin was preincubated with insulin receptor for 120 min., and insulin antibodies were added to the incubation material. The mixture was incubated for 90 min..
Group 4: Insulin antibodies were preincubated with insulin receptor for 30 min., then the mixture was washed once, ¹²⁵I-insulin was added, and the mixture was incubated for 120 min..
¹²⁵I-insulin binding to insulin receptor was inhibited in group 1, group 2, and group 4, but was not inhibited in group 3. The inhibition rate correlated positively with the titers of insulin antibodies. Different insulin target organs: human placental insulin receptor, and hepatic and renal insulin receptors of guinea pigs showed different inhibition rates. Insulin antibodies obtained in the insulin resistant period showed the most inhibition, but insulin antibodies from a patient with insulin resistant diabetes in the remissive state and from a patient with steroid induced diabetes showed decreased inhibition. The dissociation rate of ¹²⁵I-insluin from the insulin receptor was increased by insulin antibodies. Scatchard analysis showed that affinity constants of insulin antibodies (high affinity-low capacity component (K₁), low affinity-high capacity component (K₂) and average affinity constant (K_e) in the insulin resistant period) were 1.810×10⁹M^-1 (K₁), 0.046×10⁹ M^-1 (K₂), 0.083×10⁹ M^-1 (K_e), respectively, and K₁, K₂ and K_e of insulin antibodies in the remissive state of the insulin resistant diabetic were 0.542×10⁹ M^-1, 0.025×10⁹ M^-1, 0.060×10⁹ M^-1, respectively. K₁, K₂ and K_e of insulin receptor in the presence of insulin antibodies were 0.600×10⁹ M^-1, 0.132×10⁹ M^-1, 0.176×10⁹ M^-1, respectively. The numbers of insulin receptors decreased in the presence of insulin antibodies.
The inhibition rate is thought to be influenced by affinity constants as well as titers of insulin antibodies. Comparing the affinity constants of insulin receptors and insulin antibodies in the insulin resistant period, the ratio of K₂ of insulin receptor to K₁ of insulin antibodies was 1:8.30 and the ratio of K₁ of insulin receptor to K₂ of insulin antibodies was 1:0.058.

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Of 180 cases with acute and chronic hepatitis and liver cirrhosis treated with glucocorticoids, 33 cases of steroid diabetets were selected for this study. Atmpts were done on the relation of a mode of occurrence and the clinical feature of steroid diabetes to pathologic changes of the liver.
The results were as follows:
1) Steroid diabetes was found in seven cases of 39 acute hepatitis (17.9%), nine of 65 chronic hepatitis (13.0%) and 17 of 72 liver cirrhosis.
2) The incidence of steroid diabetes was slightly high in the obese cases and patients with serum hepatitis, and significantly high in patients with diabetic desposition.
3) There was no significant difference among Prednisolone, Dexamethasone and Paramethasone in the incidence of steroid diabetes. Although the cases treated with both Norandrostenolone phenylpropionate and Androstanolone showed no differece from those with glucocorticoid alone, the cases treated with the combination of Oxymetholone showed extremely high incidence of steroid diabetes. (eight of 17 cases; 47.1%)
4) Steroid diabetes could be classified into two types; early developed and lately developed type, according to the time of developmnt and the clinical feature The former showed clinical findings of diabetes. On the contrally, no diabetic findings were shown in the latter.
5) In liver cirrhosis, more early developed types of steroid diabetes were fouud and in acute and chronic hepatitis, no difference was seen in the incidence of the two types.
6) In the early developed type, a considerable number of cases showed heredity of diabetes, obesity, fatty degeneation of the liver cells and vacuole degeneration of nuclei at a punch biopsy, and abnormal glucose tolerance test (not diabetic) before the treatment of glucocorticoids. On the other hand, the lately developed type did not show those above mentioned.
7) Diabetic desposition or latent diabetes and abnormal glucose metabolism caused by a original disease were found in many of the early developed type, and few in the lately developed tvpe. It is presumed that these differences played a important role in the time of the development and the clinical feature of steroid diabetes.
8) The incidence and the clinical feature of steroid diabetes, and the time of onset and disappearance of glycosuria were not always closely related to the degree of the disturbance of liverfunctions. However, they were closely related to the fatty degeneration of the liver cells and vacuole degeneration of the nuclei.
9) In many cases of steroid diabetes, the fatty degeneration of the liver cells and vacuole degeneration of the nuclei appeared or progressed after the glucocorticoids treatment. However, no tendency was seen in distribution of fat in acini of the liver.

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