Among 1247 patients undergoing distal gastrectomy for gastric carcinoma during 1961 to 1977 at The Center for Adult Diseases, Osaka, 20 patients developed gastric carcinoma in the remnant stomach by the end of 1981. To determine whether patients after gastrectomy for gastric carcinoma have an increased risk of developing gastric remnant carcinoma or not, our 1247 patients were compared with general population through the person-year method. The frequency of gastric carcinoma in those who had received gastrectomy was lower than the expected rate of all gastric carcinoma in the general population, while it was higher than that of gastric carcinoma in the upper third of the stomach in the general population.
The numbers of G-cells, D-ccells and EC-cells per unit area were investigated by the specific immunoperoxidase staining technique in canine antral and corporal mucosa after selective proximal vagotomy (SPV). The G-cell density became significantly higher three months after SPV than that of pre-SPV, and the higher density of G-cell persisted during two years after SPY. On the other hand, the D-cell density increased later, reaching a peak at one year after SPV in the antrum and two years after in the corpus. The EC-cell density in the antrum became significantly higher one year after SPY and decreased significantly lower two years after SPY than that of control. On the other hand, the EC-cell density in the corpus increased significantly higher one year after SPY, and the higher density of EC-cell persisted during two years after SPY. In conclusion, it is suggested that the endocrine status of gastric G-, D- and EC-cells is altered by SPV.
The gastric secretory responses with graded doses of tetragastrin were investigated in patients with duodenal ulcer (recurrent group and non-recurrent group). There were no significant differences in basal and maximal secretion between recurrent group and non-recurrent group. But the sensitivity to submaximal stimulation was significantly increased in recurrent group. These results strongly suggest that the increased sensitivity to submaximal stimulation cause the recurrence of duodenal ulcer.
We have established an experimental model of chronic gastric ulcer, in which the rats were operated to produce regurgitation of entire duodenal juice into the stomach by transecting the lower horizontal division of the duodenum and anastomosing the forestomach to upper part of jejunum. After 12 weeks, all 8 rats so treated have developed an ulcer with average diameter of 6mm and range from 2 to 10mm in the pre-pyloric region on the lesser curvature of the glandular stomach. Histological studies revealed chronic peptic ulcers quite similar in many respects to human gastric ulcer. As a control series, transection at the pylorus instead of the lower horizontal division of the duodenum failed to develop an ulcer. Although a considerable number of literatures have appeared regarding the experimental production of chronic gastric ulcer, most of them have applied of chemical drugs or mechanical injuries on the gastric mucosa. Our present model, on the other hand, applied chronic regurgitation of duodenal juice as a more natural phenomenon, and obtained highly uniform result of ulcer formation. Further studies using this model are warranted on pathogenesis and mechanism of chronic peptic ulceration.
Four cases of Zollinger-Ellison syndrome were investigated from the perspective of gut hormones, with special emphasis on various kinds of provocation tests. None of these cases was diagnosed as Zollinger-Ellison syndrome at the time of the first operation for peptic ulcer. In all cases, peptic ulcer recurred and so, then, various kinds of provocation tests were performed. Thereafter, they were all diagnosed as Zollinger-Ellison syndrome. Fasting levels of plasma gastrin were not always high in these cases, however, they showed positive responses to the secretin, glucagon and calcium provocation tests. Moreover, plasma gastrin levels increased remarkably after test-meal loading. In regard to the method of the secretin provocation test, an initial bolus injection of secretin (3u/kg) followed by a continuous infusion of the same dose for one hour is a recommendable one. In those cases with both Zollinger-Ellison syndrome and duodenal ulcer, plasma motilin levels increased markedly in the secretin provocation test.
Absorption of bile acid in patients with bowel diseases, especially with ileocaecal lesion or resection, was studied by oral bile acid tolerance test. From the study of 10 normal controls by enzymatic method, it was found that oral administration of 600mg of unconjugated ursodeoxycholic acid (U.D.C.A.) was most useful for the tolerance test and the peak of total serum bile acid level was 20.9±3.4μM/L at 120 minutes after U.D.C.A. administration. In 7 patients of ileocaecal lesion and 5 patients of resection, 600mg U.D.C.A. tolerance test revealed a flat pattern of total serum bile acid curve, and it showed 9.5±2.0μM/L and 7.6±0.6μM/L at 120 minutes, respectively. These values were significantly lower than 20.9±3.4μM/L of normal controls. Peak values in all the patients were also significantly lower than those of normal controls. Consequently, it is suggested that the tolerance test by 600mg of unconjugated ursodeoxycholic acid is of great use to evaluate the impaired absorption of bile acid in patients with ileocaecal disorders.
In order to investigate the role of immunogenetic controls in hepatocellular carcinoma (HCC), HLA antigens were examined in 103 patients with HCC. The patients were classified into four groups: HB-sAg-positive group, anti-HBs-positive group, and HBsAg•anti-HBs-negative non-heavy drinker and heavy drinker groups. Haplotype Bw54-Cw1-DR4-MT3, which represents a linkage of disequilibrium in healthy Japanese, was frequent in all patients with HCC and in all the groups, indicating a relationship to this haplotype. This tendency was pronounced in the HB virus marker-negative groups. The frequency of DRw9 in the HBsAg-positive group was found to be significantly higher than that in normal controls (52.4% vs 27.8% in controls). Bw55 (18.2% vs 2.4% in controls) in the anti-HBs-positive group and Bw35 (41.2% vs 13.3% in controls) in the HBsAg•anti-HBs-negative non-heavy drinker group were statistically significant in frequency (Pc<0.01 and Pc<0.004, respectively).
When immunoreactive glucagon (IRG) in plasma was measured by use of two different antisera against pancreatic glucagon, 30K and OAL-123, discrepancy was seen between the two values, IRG with 30K antiserum (30K-IRG) and OAL-123 antiserum (OAL-IRG), in eight cases out of eleven with liver cirrhosis, but not seen in all three healthy controls tested. In order to investigate the causes of this discrepancy observed, we examined the heterogeneity of plasma IRG by gel filtration on a column of Bio Gel P-10. The two kinds of antisera gave similar IRG values in fractions with molecular weight of about 3500 (IRG3500) in each case of all the patients with liver cirrhosis and controls. The correlation coefficient (r) between the two values measured with the two antisera was 0.978 (p<0.001) and the regression curve was calculated to be Y=1.07X-17.8, where X and Y were 30K-IRG3500 and OAL-IRG3500, respectively. On the other hand, great differences were observed between the two IRG values in fractions of the so called "big plasma glucagon" (BPG) from plasma of the eight patients, IRG values in which showed discrepancy, and these differences were not observed in BPG fractions from other patients and controls. Glycocholic acid has been shown to increase in plasma of patients with liver cirrhosis and to disturb the accuracy of 30K-IRG. On gel filtration of plasma containing glycocholic acid, however, only small amount of glycocholic acid was eluted with BPG and most of the bile acid was eluted in the fractions corresponding to the molecular weight of the bile acid itself. These results indicate that the discrepancy observed between 30K-IRG and OAL-IRG in plasma from the cirrhotic patients is due solely to the differences in IRGs in BPG fractions and that glycocholic acid does not contribute to this discrepancy.
In 152 patients with liver diseases induced by virus, alcohol, drugs and obesity, levels of 3, 5, 3'-triiodothyronine (T3), thyroxine (T4) and 3, 3', 5'-triiodothyronine (rT3) were determined to study the relationships between these levels and the activity of arylamidase, a non-specific carboxylesterase, located in hepatic microsomes. There was a significant positive correlationship between the serum T3/T4 ratio and microsomal arylamidase activity in liver tissue (r=0.71, p<0.001, n=56), suggesting that the T3/T4 ratio reflected the microsomal function most markedly. The serum T3/T4 ratios in patients with acute hepatitis (acute stage), drug-induced liver injury (cytotoxic type), alcoholic liver cirrhosis and posthepatitic liver cirrhosis were significantly lower than that in the control (p<0.01), but the ratios in asymptmatic HBsAg carriers and in patients with druginduced liver injury (cholestatic type) were relatively high. These results suggested that the serum T3/T4 ratio reflected the mobility of liver diseases characteristically and can be one marker for hepatic microsomal function.
The correlation between serum HBV-DNA polymerase (DNA-P) activity and HBe antigen/anti-HBe system was examined in 216 samples, and relationship between DNA-P activity and transaminase (GPT) value was also investigated in 17 untreated patients with HBs antigen positive liver diseases. DNA-P activity correlated significantly with the concentration of HBe antigen detected by micro-Ouchterlony method. On the contrary, this activity showed almost negative in the anti-HBe positive samples, and the correlation between DNA-P activity and the titer of HBe antigen by radioimmunoassay or the titer of HBs antigen was respectively low. In addition, two cases of chronic active hepatitis which were anti-HBe positive were persistently high in DNA-P activity. These facts suggest that some essential difference might be exist in these two HBV markers. Twelve cases of chronic active hepatitis were separated into two groups in relation to DNA-P activity and transaminase. One of them showed the rapid elevation of DNA-P activity followed by acute exacerbation of transaminase, and the other revealed no relation between them.
Digital subtraction angiography (DSA) was performed on 56 patients with hepatic diseases and evaluated for its imaging quality. Intra-venous DSA (IVDSA) was useful for diagnosing of hypervascular tumor lesions as hepatocellular carcinoma or liver hemangioma, especially of hepatocellular carcinoma larger than 5.0cm in diameter. IVDSA is a relatively noninvasive procedure and effective method as examination for outpatients or observation after transcatheter arterial embolization therapy. On the other hand, intra-arterial DSA (IADSA) was found to be available especially for diagnosis of lesions in portal venous system, because the same image quality as conventional angiography was obtained using small amount of contrast medium. DSA image was disturbed by respiratory movement, body motion or bowel gas, and restricted by sites or sizes of lesions and their vascularity.
In this study, we have described a simple and safe method of inserting a needle into the left hepatic duct and our experience of this method in 217 patients with obstructive and non-obstructive jaundice. Technique: The 7th or 8th intercostal space was used for the puncture site to avoid injuries of the diaphragmatic cornu and the height for the puncture site was midaxillar line under X-ray television control. The angle for insertion of the needle is 15 degrees to the anterior ventral wall towards horizontal line. The landmark was made on the midpoint between the just above the apex of the duodenal bulb being received 5 grams of effervesscent granules orally just before the procedure and intersection of the right diaphragm and vertebra on the right paravertebral line. The puncture needle was inserted towards the landmark untill the tip reached the depth of the vertebral center. Results: 217 cases of the left hepatic canulations were successful in 212 patients with obstructive and non-obstructive jaundice. A simple approach to left hepatic duct for percutaneous transhepatic cholangiography is described. The success canulation of left hepatic duct was 97.7 percent. The method described here is a simple and accurate procedure which can be used in any hospital.
Secretory component (SC) and immunoglobulins (Igs) in human duodenal juice obtained by PS test were measured and their significance in the pancreatic disease were studied. SC and Igs were determined by RIA method and single radial immunodiffusion method, respectively. Concentration of SC and IgA were elevated in pancreatic cancer and chronic pancreatitis when compared with the other pancreatic disease groups. Furthermore, IgA in S2 and S3 fractions (10 to 20 minutes and 20 to 40 minutes periods after secretin provocation) was significantly increased in pancreatic cancer comparing to chronic pancreatitis (p<0.02 and p<0.05, respectively). There were many fractions of PS test in which concentration and quantity of IgM were significantly increased in acute pancreatitis when compared with the other pancreatic diseases. Since, no correlation between pancreatic exocrine secretion and secretion of SC in the pancreatic juice could be found, they were regulated by different mechanisms. Furthermore, possibility of Igs secretion by simple inflammatory exsudation was excluded.
Elastase activity of duodenal aspirate in PS test was determined by three different methods, Succinyl -trialanyl-p-nitroanilide (Suc-(Ala)3-pNA) method, elastin diffusion plate method and radioimmunoassay for elastase-1. Statistically significant correlations were seen among elastase activities measured by these methods. Elastase activity was measured by Suc-(Ala)3-pNA method in duodenal aspirate, and elastase output in various diseases was determined in PS test as compared with the simultaneously measured amylase output. Elastase output was significantly lower in patients with chronic pancreatitis, arteriosclerosis and liver cirrhosis than in controls. The ratio of elastase output to amylase output definitely decreased in arteriosclerosis and liver cirrhosis, but not in chronic pancreatitis. These observations indicate that pancreatic elastase content decreases characteristically in arteriosclerosis and liver cirrhosis. Decreased pancreatic elastase may participate in progression of these diseases since it has been suggested that pancreatic elastase plays a role in elastin metabolism.