Acta Medica Okayama 16巻 3号

The liver glucuronyl transferase (GT) activity and uridine diphosphate glucuronic acid (UDPGA) content in the patients with viral hepatitis were determined using 4-methyl umbelliferone (4-MU) as a glucuronide receptor. The results were as follows: 1. In acute viral hepatitis, the decrease in the GT activity was more remarkable in the later stage of the recovery. In chronic viral hepatitis, the GT activity was decreased in accordance with the increase in the degree of liver injury. Liver UDPGA content was significantly reduced only in postnecrotic cirrhosis. 2. The decrease or injury in the parenchymal liver cells caused a decrease in the liver GT activity. These quantitative reductions in the liver parenchyme were not the only factor for the alteration in the GT activity of the liver. The results of the present study suggested an involvement of a qualitative change in the liver GT activity in human liver injuries, especially in the early stage of acute viral hepatitis; namely, there might be even an activation of the liver GT other than the reduction resulting from the decrease in the liver parenchyme. 3. The decrease in the liver GT activity correlated significantly with the decrease in the salicylamide glucuronide formation in vivo, while the alteration in the liver UDPGA content failed to correlate with that in the glucuronide formation in vivo. It was suggested that the velocity of in vivo UDPGA production rather than the UDPGA content of the liver was as important a rate-limiting factor for the glucuronide formation in vivo as the liver GT activity.

1. An attempt has been made to find the diagnostic criteria for early gastric cancer. It is most important to detect the evidences or suspected features of the malignant growth in incipient stage in order to attain the radical cure by surgical operation. 2. Twelve patients with early gastric cancer (groups A and B) were selected out of 476 patients who had undergone gastrectomy during the past three years in the Okayama Saiseikai General Hospital. The other 6 patients in the "precancerous group" (group C) were also studied, who had abnormal epithelial proliferation in the resected stomach membrane during the same period. 3. The processes of discovery of early cancer have been described. Fairly precise diagnosis can be made in the mucosal carcinoma, but it is not in the ulcer-carcinoma. It was generally difficult to estimate the degree of the malignancy and the extension of the growth preoperatively. 4. The details of the diagnostic aids are as follows. i. Negative occult blood of stool does not always mean the definite diagnostic aid. ii. The malignant gastric change may occur even in non-anacidity. Further investigations should be followed up on gastric ulcer patients if malignant alteration is under the consideration. iii. Minor roentgenological findings, such as the absence or irregularity of mucosal folds, rigid and/or overlapped contour, localized absence or decrease of the peristaltic waves and absence or bow-shaped deformity of the angulus, are of important significance. Such changes should be minutely sought for by X-ray film examination. iv. On gastroscopy and gastrocamera photography, such changes as erosion or irregular granular thickening of the membrane with abnormal reddening and edematous appearance, irregularity of ulcer edge, uneven swelling on ulcer margin with reddening and unsharpness of the edge of adherent coat on ulcer floor, must be noted in the early gastric cancer. v. It is not safe to leave a patient having stomach ulceration under a mere conservative management because it is often quite difficult to dissolve the question of malignancy of the lesion with all sorts of examinations. vi. So far as clinical examinations have indicated malignancy, histological examination must be carried out immediately at the time of operation, even when malignant lesion is absent in inspection and palpation on the exposure of the stomach. vii. On the gross observation of the resected stomach, a particular attention must be paid to erosion, depression or atrophy, irregular granular thickening and abnormal reddening on the restricted areas of the mucosal surface.

An attempt was made to establish the method for the estimation of glucuronide formation in vivo using salicylamide and further to study the alteration in the glucuronide formation in liver disease. The results were as follows: 1. The method for the determination of free salicylamide separately from other conjugates of salicylamide in urine, without involving any hydrolysis of the other conjugates, was presented. When 1 g. of salicylamide was administered to the subjects with or without liver injuries, no free salicylamide was detected by the present method in the urine following the salicylamide administration. 2. The analytical method for the determination of salicylamide glucuronide was also devised by employing a hydrolysis with β-glucuronidase. The ratio of the salicylamide liberated by the enzymatic hydrolysis of the 10-hour urine following the administration of 1 g. of salicylamide to the total salicylamide excreted in the same urine was neither affected by the total recovery of the salicylamide nor by the urine volume. This ratio was thus used as a means of estimating the capacity of the glucuronide formation in vivo, although it was considered that the ratio might be affected to some extent by the competition between the glucuronide and other conjugate formations in vivo. 3. As a result of this salicylamide glucuronide excretion test, it was indicated that the in vivo formation of salicylamide glucuronide in the patients with postnecrotic cirrhosis was slightly decreased compared with that in normal controls.