In 116 patients with esophageal varix due to liver cirrhosis who received the endoscopic sclerotherapy, the following complications were observed after the sclerotherapy: 38 ulcer formation; 19 chest pain; 16 hypotension; 15 fever; 12 pleural effusion; 6 esophageal stenosis and so on. Furthermore, two cases with marked changes of portal circulation were experienced after the sclerotherapy. The first case had severe bleeding out of duodenal varix four months after the sclerotherapy and died because of massive bleeding. The second case had hepatic encephalopathy six months after the sclerotherapy. In both cases, angiography revealed the development of collateral veins after the sclerotherapy. Because the abrupt intercept of the esophageal varix by the successful sclerotherapy causes the increase of the other collateral blood flow, the changes of portal circulation must be watched carefully afterward.
In isolated guinea pig gastric chief cells, gatrin-I and cholecystokinin-hexapeptide (CCK-4) stimulated pepsinogen release. However, the efficacies of these two peptide were 51% of that observed with CCK-octapeptide (CCK8). CR1409 and L-364718, both of which are new CCK receptor antagonists in pancreatic acinar cells, also inhibited 10-8M CCK8-stimulated pepsinogen release with a half-maximal inhibitory concentration (IC50) observed at 3×10-9M, respectively. The dose response curve to CCK8 for pepsinogen release shifted to the right in the presence of CR1409 or, L-364718. The IC50 of these two antagonists for the CCK8-stimulated increase in cytosolic Ca2+ concentration monitored by Fura-2 were equal to those for CCK8-stimulated pepsinogen release. By contrast, the IC50 of dibutyryl cyclic GMP, a well-known CCK receptor antagonist, for CCK8-stimulated pepsinogen release was less than that for CCK8-stimulated increase in cytosolic Ca2+ concentration. Results suggested that CCK receptors in gastric chief cells are unique and may be different from CCK receptors in other tissues previously repoted.
Rates of detection roentgenological and endoscopic examinations were investigated in 87 patients with 93 lesions of early gastric cancer measuring 1cm or less. In the depressed type, the minimum size for detection was 5mm roentgenologically and 3mm endoscopically. Depressed lesions with ulcer scars could be detected roentgenologically, but depressed lesions without ulcer scars could not be detected, unless the depressions were more than 0.5mm and were accompanied by mucosal elevations surrounding the lesions. The detection of undifferentiated cancer without ulcer scars was poor, because mucosal elevations surrounding the lesions were rare in such histological types. In the elevated type, the minimum size detectable roentgenologically was 7mm in width, 0.9mm in height, compared to 4mm in width, 0.3mm in height endoscopically. On diagnosis of the depth of invasion, the depressed type of cancers without ulcer scars and with granular depressions were mostly limited to the mucosa, on the other hand, clear depression and plateau like elevation were highly indicative of submucosal invasion. In cases of elevated cancers, a central depression was highly indicative of submucosal invasion.
AOM was administered subcutaneously once a week for 11 consecutive weeks to the rat. On the 15th and 30th week after starting of AOM injection, PGE2 content of the colonic mucosa, tumor and blood of portal vein and NK activity of the spleen and mesenteric lymph node (MLN) were evaluated. On the 15th week, a significant high value of the PGE2 content of colonic mucosa was shown when compared with that of the AOM non-administered group (control group). However, no significant difference was observed in the PGE2 content of blood of portal vein and NK activity of the spleen and MLN. On the 30th week, significant high values of the PGE2 content of AOM-induced tumor and blood of portal vein and low values of NK activity of the spleen and MLN were shown when compared with that of the control group. When indomethacin (IND) was administered intrarectally twice a week for 19 consecutive weeks after completion of AOM injection, induced-colon tumors was significantly suppressed. For this reason, it is important to administer IND at the point when the PGE2 content of colonic mucosa begins to augment.
We attempted to clarify the association between HLA and Crohn's disease. HLA-A, -B, -C, -DR and -DQ locus antigens in 108 Japanese patients with Crohn's disease were analyzed and the results were compared with findings of 472 healthy Japanese. In patients with Crohn's disease there was a strong positive association with HLA-DR4 (χ2=14.086, Pc<0.005, RR=2.231), and a weak positive association with HLA-B51, -Bw54, -DRw12, -DRw13 and -DRw52. While there was a strong negative association with HLA-DR2 (χ2=10.194, Pc<0.025, RR=0.435), DQw1 (χ2=14.680, Pc<0.001 RR=0.442) and DQw3 (χ2=7.760 Pc<0.025 RR=0.549), and a weak negative association with HLA-B7. In conclusion, susceptibility to Crohn's disease may relate to HLA-DR4, especially HLA-DR4.1, in Japanese patients.
The reticuloendothelial system is important as one of the self defense mechanisms. We performed two investigations to confirm the reliability of the lipid emulsion test for determining the reticuloendothelial system function. 1) The lipid emulsion serum clearance was contrasted with the counts of lipid emulsions phagocyted by Kupffer cells in liver. 2) Lipid emulsion clearance was contrasted with the hepatic uptake rate of 99mTc-phytate. The result demonstrated a positive correlation among lipid emulsion clearance, the counts of lipid emulsions phagocyted by Kupffer cells and the hepatic uptake rate of 99mTc-phytate. These results confirm that the lipid emulsion test is sufficient to reflect Reticuloendothelial system function.
G30TBA is the total serum bile acid concentration obtained thirty minutes after injection of glucagon in the UDCA.GLUCAGON tolerance test. We have previously reported the usefulness of G30TBA in evaluating liver function. In this paper, changes in the portal blood flow in response to glucaon administration are measured and the relationship betwen those changes and G30TBA studied. We used an ultrasonic duplex system composed of a B-mode scanner and doppler flow meter of measure portal blood flow after injection of glucagon in thirty seven patients with chronic liver diseases. The results are as follows: The increase in portal blood flow by exogenous glucagon in liver cirrhosis is statistically significantly lower than that in chronic hepatitis. G30TBA in the good-response-to-glucagon group is statistically significantly lower than that in the poor-response group. These results suggest that the effect of glucagon on portal blood flow significantly influences the srum bile acid concentration in the UDCA.GLUCAGON tolerance test.
We investigated the expression of Pre-S2 antigen (Ag) and antibody (Ab) in sera quantitatively using ELISA. Four patients with acute hepatitis B and 87 chronic HBV carriers were included in this study. We also investigated the expression of Pre-S2Ag in the liver tissues obtained from 26 chronic HBV carriers by direct fluorescent antibody method. There was a significant correlation between Pre-S2Ag titers and HBsAg titers in sera. Pre-S2Ag titers were higher in sera positive for HBeAg, HBV-related DNA polymerase or HBV-DNA than in sera negative for those markers. The ratio of Pre-S2Ag titers to HBsAg titers, however, was constant irrespective of virus replicative markers. Pre-S2Ag in the liver had almost same intracellular localization with HBsAg in the liver. It was suggested that Pre-S2Ag was expressed with an intimate relation to the expression of HBsAg and was not useful as a virus replicative marker. Pre-S2Ag titers/HBsAg titers tended to be high in patients with chronic active hepatitis and high serum GPT levels compared to patients with chronic inactive hepatitis. This may be explained by the release of Pre-S2Ag in the liver. In addition, all patients positive for Pre-S2Ag on the membrane of hepatocytes had chronic active hepatitis. The overproduction of Pre-S2-containing surface proteins in the liver may have some implication related to cell injury via the immune response to Pre-S2Ag etc. Pre-S2Ab was detected only in few cases of chronic HBV infected patients. The lack of immune response to Pre-S2 region may play a role in the persistence of HBV infection.
Owing to the recent advancement of ultrasonographic instruments, we can now easily detect variously sized hypoechoic nodules as well as coarse echo pattern in cirrhotic liver. Based on the size and distribution of such hypoechoic nodules, we classified echo patterns of liver parenchyma into four types as follows. Type 0: Homogeneous echo pattern. Type I: Coarse echo pattern with no distinct hypoechoic nodules. Type II: Echo pattern showing scattered hypoechoic nodules sized 3-5mm. Type III: Echo pattern showing scattered hypoechoic nodules sized more than 5mm. In the present study, all the 25 patients of normal liver showed type 0, 29 of 42 patients with chronic hepatitis showed type 0 and the remained 13 type I. In 65 patients with liver cirrhosis, 54 (83.1%) were classified as type I, II, or III. The grade of parenchymal echo pattern was significantly correlated with the severity of liver cirrhosis. In addition, the parenchymal patterns proved to be very useful in diagnosis of liver cirrhosis, presenting overall accuracy value of 81.8%. The value was the highest compared with those of other diagnostic factors on ultrasonograms. Immersion experiment with autopsied liver specimens evidenced that hypoechoic nodules on ultrasonogram represent regenerative nodules of cirrhotic liver. It was also revealed that the parenchymal echo patterns closely corresponded to gross or histologoic findings of the liver.
The intrahepatic distribution of HBcAg and evaluation of the histological outcome using a numerical scoring system of Histological Activity Index (HAI) by Knodell et al, were studied in paired liver biopsy specimens from 14 HBeAg-positivie patients with chronic active hepatitis B before and after interferon (IFN) treatment. Intrahepatic HBcAg was detected by immunoperoxidase technique and the pattern of HBcAg expression were present in the hepatocyte nucleus (nHBcAg) or cytoplasm (cHBcAg) or in both. Before treatment, intrahepatic HBcAg was distributed both in the nucleus and cytoplasm without significant differences. After treatment, nHBcAg expression however, decreased signigicantly (p<0.001), while cHBcAg remained unchanged or rather increased. These changes of nHBcAg and cHBcAg before and after IFN treatment were observed irrespective of disappearance or presence of DNA-P and/or HBeAg in serum after IFN treatment. The HIA scores decreased significantly (0.05<P<0.001) after treatment. These findings above suggest that the intrahepatic HBcAg may shift from nucleus to cytoplasm in chronic active hepatitis B during IFN treatment.
To clarify the immunological effects of transcatheter arterial embolization (TAE) therapy for hepatocellular carcinoma (HCC), various immunological parameters were measured before and after TAE respectively. In most effective group of which AFP levels at first week after TAE therapy had decreased more than 50% compared with those before TAE, the percentage of OKT-4 and IL-2R positive cells in the peripheral blood lymphocytes (PBL) had significantly increased in number. In addition, IL-1, TNF, IL-2 and LAK activity were also enhanced by it. These immunological enhancement after TAE therapy was suggested to be a favourite condition for transferring LAK cells to the patients with HCC. Therefore the combination therapy with TAE and LAK-adoptive immunotherapy was conducted in 12 patients iwth HCC. Partial response to it was obtained in one case and minor response in three. However no effectiveness was also found in eight (Progressive Disease: 1 case, No Change: 7 cases). Immunological response after combined TAE-LAK adoptive immunotherapy revealed that NK activity and LAK activity were markedly enhanced. Furthermore, the percentage of OKT-11+, IL-2R+ and Leu-7- 11c+ cells in the PBL had increased in number with statistically significant differences and OKT-8+ cells had increased in relative number. In conclusion, this study suggested that this combination therapy might be a well designed immunological and clinical therapy for HCC because it was done under the condition of well enhanced immunological parameters against tumors.
Using the cholangiofiberscope, electrohydraulic lithotripsy was performed in 20 patients with biliary tract stones. In all cases, stones were destroyed and removed without any serious complications. Since these treatments no recurrence of stones has been recognized (average 8.6 months, longest 16 months). The average period of PTCD needed for the treatments was 34.3±8.1 days, and the average number of treatments needed was 1.7±1.0. The average time taken was 91±26 minutes, and the peroid from PTCD until hospital discharge was 39.8±6.1 days for cases of common bile duct stone, and 46.3±8.8 days for common bile duct and gall bladder stone. This period for cases of common bile duct stone is equivalent to that taken by surgical procedures in our hospital. This treatment seems to be at least as good as EST or surgery for cases of common bile duct stone. It is especially appropriate for those patients who reject surgery, are elderly, poor risks, or recurrent cases.
Pancreatic enzymes in the bile of congenital choledochal cyst with anomalous pancreaticobiliary ductal union were analyzed. Almost all pancreatic proteases were already activated in the bile aspirated immeadiately after insertion of PTCD tube. However, inactive proteases gradually increased after continuation of drainage by PTCD. Pancreatic protease activities appeared again after clamping the PTCD tube. In vitro study of trypsin activities in the bile containing no initial trypsin activity, active type of trypsin did not appear throughout the experimental period. It is suggested that continuous reflux of pancreatic juice into the bile and certain incubation time are necessary for activation of pancreatic protease in the bile of congenital choledochal cyst.
The effects of oral and intraperitoneal administration of biotin in urease-induced hyperammonaemic rats, as well as the influence of biotin deficiency, have been studied. Biotin deficiency was produced by feeding standard diet MF (Oriental Yeast Co.) supplemented with dry egg-white (egg-white group). Egg-white+biotin group had free access to 0.0014% of biotin solution at all time. Following an intraperitoneal injection of urease, 25U/kg (B.W.), plasma ammonia levels in egg-white+biotin group were lower than in egg-white group, especially there was significance (p<0.05) at 8 hours after the urease injection. Similarly, plasma ammonia levels in biotin-injected rats, in which 1mg of biotin had been injected intraperitoneally prior to the experiment, were significantly low compared with saline-injected controls at 4 and 6 hours after urease administration. Results of plasma amino acid analysis, 9 hours after the urease injection indicated that Fischer's molar ratio (Leu+Ileu+Val/Tyr+Phe) was significantly higher in the biotin-injected rats than the saline-injected control. It suggests that biotin might decrease blood ammonia by facilitating the detoxification mechanism as follow: L-glutamate+NH3→L-glutamane.