Abstract
For the object of elucidating the pathophysiology of diabetic coma, patients in this state were placed on continuous low-dose insulin therapy, and changes in blood levels of insulin-antagonistic hormones-glucagon (IRG), growth hormone (h-GH) and cortisol-were pursued in the course of therapy. The subjects for study were complized 9 cases of diabetic ketoacidosis (4 males and 5 females), aged 30 on the average (12-51 years) and 3 patients with non-ketotic hyperosmolar coma (2 males and 1 female), aged 56 on the average (46-67 years). Consciousness disturbance was observed in 7 of the 9 ketotic patients (7/9) and in one of the 3 patients with hyperosmolar coma (1/3). MC-actrapid insulin (0.1 U/kg/hr) was given by continuous intravenous infusion.
For rephydration, saline was chiefly used, being added with glucose and potassium in adequate amounts for prevention of hypoglycemia and hypopotassemia. All clinical symptoms accompanying the coma were abolished in a mean of 16.5 hr, and all the patients recovered the normal state with only one exception, who died, being complicated by DIC.
The duration of intravenous insulin infusion was 18±2 hr (Mean±SEM) for ketoacidosis and 11±4 hr for hyperosmolar coma; the total insulin dose, 94.8±16.5 U/24 hrs for the former and 69.3±12.2 U/24 hrs for the latter; and the total fluid infusion volume, 5.8±0.51/24 hrs for the former and 4.5±1.21/24 hr for the latter.
Plasma-IRG level was 352.9±81.7 pg/ml before the therapy, but 92±33.1 pg/ml at 6 hr of the therapy, thus showing abrupt fall. On admission, however, only 4 cases showed level higher than 500 pg/ml.
Serum h-GH level, which was 6.4±1.6 ng/ml before the therapy was transiently elevated to 13.0±3.1 ng/ml at 2 hr after the start of insulin infusion, but there after it gradually fell, though it was again increased slightly at 24 hr.
Serum cortisol level, which was as high as 461.8±74.4 ng/ml before the therapy, slowly fell after its start, but at 24 hr, it still remained as high as 173.4±18.6 ng/ml. These results suggest the following: 1) The effect of glucagon on diabetic coma may be slight.
2) The effect of cortisol and h-GH may rather be greater.
3) The low-dose insulin therapy was effective for the improvement of abnormal levels of insulin-antagonistic hormons in diabetic coma.
