尿中アセトアルデハイド生成コルチコイド排泄に就いて
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概要
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Daily urinary excretion of total (free and conjugated) acetaldehydogenic corticoids (ACS) was measured by modified Cox's method in patients with various diseases as well as normal subjects, and the following results were obtained.<BR>1. The mean urinary excretion of ACS for normal men, with 95% confidence limit, was 3.0 ±0.5mg /day, and the mean for normal women was 2.0 ±0.5mg/day.<BR>2. Most of the diseases investigated were observed to affect the urinary excretion of ACS, 17-hydroxycorticosteroids (17-OH·CS) and formaldehydogenic corticosteroids in the same way, that is, the excretion of all the three groups of substances seemed to increase or decrease together according as the disease involved produced enhancement or suppression of the function of the pituitary-adrenal system. It was observed, however, that the ACS-forming activity of the adrenal gland did not always keep steps with its adrenocortical-hormone-forming activity, either of the two being sometimes very vigorous while the other remained low. Marked decrease of the ACS excretion was observed in one case each of liver cirrhosis, tetany, pituitary anorexia and Simond's disease as well as two cases of Addison's disease. On the other hand, striking increase was observed in a number of patients with high fever, another who had received transplantation of a bovine pituitary gland and two others who had been surgically operated. This is worthy of notice, as it is contrary to the generally accepted view that such elevated ACS excretion is characteristic of patients with certain adrenocortical tumours. In patients with Cushing's syndrome or Basedow's disease, it was observed that the urinary 17-OH-CS excretion increased while the ACS excretion remained normal or decreased. This may be explained by adopting the view that Cushing's syndrome accompanies elevated production of adrenocortical hormones alone and Basedow's disease belongs to the kind of disorder in which the reduction of hydrocortisone alone is accelerated.<BR>3. All the subjects except those with extremely disordered adrenal gland function, e.g., advanced Addison's disease, responded to administration of ACTH with increased ACS excretion. This suggests that ACS production is promoted by ACTH.<BR>4. Administration of adrenocortical hormones brought about hardly any increase of ACS excretion either in the normal subjects or the patients, but even some decrease in a few cases.<BR>5. Administration of Fowler's solution, adrenochrome-monosemicarbazon or pyrogen had almost no effect on the ACS excretion.<BR>From these results it may be reasonably concluded that the ACS appearing in the urine is directly derived from some substances produced in the adrenal gland such as 17,20-dihydroxy-20-methylsteroids and that the process of formation is promoted by ACTH, probably prior to their conversion to progesterone.<BR>Under conditions accompanying increased progesterone production, such as pregnancy, augmentation of the ACS excretion was observed. Can 17-hydroxylation take place in the placenta, ovaries etc. ? Nobody has produced conclusive evidence to decide this issuer either way. If 17-hydroxylation of progesterone takes place only in the adrenal gland, the amount of ACS excreted will indirectly indicate the level of the adrenocortical activity.
- 日本内分泌学会の論文