The changes of cardiopulmonary function after endoscopic injection sclerotherapy for esophageal varices were studied. Endoscopic injection sclerotherapy was performed by intravariceal injection of 5% ethanolamine oleate. Immediately after injection, pulmonary arterial resistance and pulmonary arterial pressure increased (p<0.01). At the same time, arterial oxygen pressure decreased (p<0.01), and physiological pulmonary shunt ratio and alveolar-arterial oxygen tension difference increased (p<0.01). They recovered within 3 days after injection. These changes suggest the presence of a transient pulmonary diffusion disorder. They were not observed after esophagoscopy without injection of the sclerosing agent. Therefore, these results were considered to be due to injection of the sclerosing agent.
The purpose of this study is to investigate some factors that influence the process of gastric carcinogenesis. We used rats, which N-[methyl-3H]-N'-nitro-N-nitrosoguanidine ([methyl-3H] MNNG) was given orally. The amount of imcorporated [methyl-3H] MNNG with gastric mucosal DNA was measured by a liquid scintillation counter. In control, the amount of imcorporated [methyl-3H] MNNG was 25.4± 5.9pmole/mgDNA. When prostaglandine E2 or pirenzepine, which increased gastric mucus, was administered orally prior to [methyl-3H] MNNG, the imcorporated amount was 11.7±3.8pmole/mgDNA and 6.2±5.6pmole/mgDNA respectively. On the contrary, in the administration of indomethacin, which decreased gastric mucus, the increase of incorporation up to 42.9±14.4pmole/mgDNA was measured. From these results, the negative correlation was found between the amount of gastric mucus and incorporated carcinogen. Accordingly, gastric mucus has a protective effect not only against ulcergenic agents but also carcinogens. So it is suggested that gastric mucus plays an important role in the defensive mechanism against carcinogenesis.
Plasma secretin concentration and bicarbonate concentration in duodenal juice were simultaneously measured in response to intraduodenal infusion of hydrocloric acid in 14 gastric ulcer patients and 26 duodenal ulcer patients. Analysis of gastric juice output was also performed on the same subjects. The results obtained herein were as follows; 1) The mean value of BAO and MAO was significantly higher in douodenal ulcer patients than that of gastric ulcer patients (p<0.01). 2) The mean value of total bicarbonate output was lower in duodenal ulcer patients than that of gastric ulcer patients, although the difference was not significant. 3) The total bicarbonate output/MAO ratio was significantly lower in duodenal ulcer patients than that of gastric ulcer patients (p<0.01). 4) A significant correlation between the total bicarbonate output and amylase output was observed in all peptic ulcer patients (p<0.005). 5) The peak increment of secretin value (peak secretin value-basal secretin value) and total bicarbonate output was significantly correlated in gastric ulcer patients (p<0.05), but not in duodenal ulcer patients. 6) The plasma secretin response in duodenal ulcer patients was similar to that of gastric ulcer patients. These data suggest that there is an impairment in the mechanism by secretin of pancreatic juice secretion in some of the patients with duodenal ulcer.
The characteristics of anticolon antibody and lymphocytophilic antibody in sera from 41 patients with ulcerative colitis (UC) were examined by flow cytometry using a fluorescence activated cell sorter (FACS). The higher prevalence of both antibodies in the patients' sera was demonstrated than those previously reported. Anticolon antibody in sera was revealed to be IgG which had specificity for colon cells. This antibody bound to colon cell antigens in the form of monomer antibody via Fab' portion. These findings imply that anticolon antibody may participate in the mechanism of antibody dependent cell-mediated cytotoxicity (ADCC) in colon cell injury of UC patients. Lymphocytophilic antibody in UC sera was demonstrated to be mainly reactive with suppressor T cells, but also reactive with the other T cell subsets by two-color staining method. This antibody was not cytotoxic against peripheral T cells in the complement-dependent cytotoxicity assay. It was also shown that the antibody was heterogenous and might include anticolon antibody in part. All these results suggest that anticolon antibody and lymphocytophilic antibody may play an important role in the immunological pathogenesis of tissue injury in UC.
Measurement of serum zinc concentration on admission, zinc balance study and zinc loading test (oral administration of 40mg of zinc) performed during ED therapy using naso-duodenal feeding tube were carried out in 18 patients with Crohn's disease of non-operated cases and 8 normal controls. In the patients with Crohn's disease, a positive correlation between zinc and albumin levels of the serum, and a negative correlation between serum zinc level and activity index (CDAI, Dutch AI) were observed. These correlations were significant. A significant positive correlation was observed between AUC (area under the curve) and srum zinc level, howerver correlation was not observed between AUC and serum albumin level just before zinc loading test in the patients with Crohn's disease. These results suggest that disturbance of zinc absorption from intestinal tract is the main cause of the low level of serum zinc in Crohn's disease and it is effected by the activity of this disease.
A follow-up study of 185 cases of liver cirrhosis admitted in our institution during a period of 1971-1980 was undertaken to determine survival rate of these patients and compared to the survival rate reported previously from our institution during a period of 1956-1966. The 1, 2, 3, 4, 5, 7 and 10 year cumulative survival rates were 83.2%, 77.3%, 69.0%, 61.9%, 55.2%, 38.0%, 35.7%, respectively. The 1, 2, 3 and 4 year survival rates were significantly improved as compared to the rates reported in the previous study. Much greater improvement was achieved in the cases with ascites or hypoalbuminemia. In regard to treatment, the use of more potent diuretics (spironolactone and furosemide), plasma protein preparations (albuminate, plasmanate or albumin) and lactulose increased significantly and cases treated with corticosteroids decreased as compared to the previous study. The causes of 93 deaths constituted liver failuar (44.1%), gastrointestinal bleeding (18.3%), hepatocellular carcinoma (24.7%) and other non-liver-related causes (12.9%). As compared to the previous study, frequencies of liver failuar and gastrointestinal bleeding decreased and frequencies of other causes including hepatocellular carcinoma increased.
To elucidate the immunopathogenesis of intrahepatic cholestasis in alcoholic liver disease, the authors investigated the possible participation of cholestatic factor. The peripheral lymphocytes from patients with intrahepatic cholestasis in alcoholic liver disease were stimulated with ethanol and liver specific lipoprotein in vitro and the cluture supernatant was fractionated by gel filtration using a Sephadex G-75 column. When a definitive fraction (fraction 4) was injected into the mesenteric vein of rats, a marked reduction of bile flow was observed. Similar results were obtained when blood serum of patients was fractionated in an identical manner and the same fraction was injected to rats via mesenteric vein. Histologically, a dilated bile canaliculus with the diminution of microvilli and increased vesicles around the dilated canaliculi were observed by an electron microscopy after injection of the active fraction into rats. These results strongly suggest that not only the sensitized lymphocytes produce the cholestatic factor(s) which caused the intrahepatic cholestasis by specific stimulation, but also this factor involves significantly in the pathogenesis of intrahepatic cholestasis which observed in the patients with intrahepatic cholestasis in alcoholic liver disease.
We studied plasma kallikrein-kinin system in various liver disease especially in alcoholic liver injury from the inflammatory standpoint of view. Plasma was collected from 21 cases with alcoholic liver injuries and 55 cases with non-alcoholic liver diseases. Plasma prekallikrein (PPK) and kallikrein (PK) activities were determined by the method of Nakamura's. Plasma high molecular weight kininogen (HMG-KN) concentration was determined by the method of Uchida and Katori's. PK activity was significantly elevated in aloholic liver injuries and decreased when absteining from alcohol. There was a significantly negative correlation between PK activity and HMG-KN concentration in alcoholic liver injuries. A single oral intake of 0.8g/kg ethanol was followed by the elevation of PK activity and gradual decrease in HMG-KN concentration in man. PPK activity and HMG-KN concentration were significantly decreased in relation to the severity of hepatoparencymal damage. Increase of PK activity in alcoholics might be related to a florid pathophysiological change in alcoholic liver injuries.
The therapeutic effect of transarterial embolization (TAE) on daughter nodules of hepatocellular carcinoma (HCC) was evaluated by examining the post-TAE changes of daughter nodules and prognosis of HCC with daughter nodules. One hundred and fifty-two daughter nodules were angiographically idenfified in 31 patients with HCC. They measured from 4 to 53mm in diameter. Ninety-six (98%) of 98 daughter nodules detected at the 1st angiography and 10 (53%) of 19 detected newly after the 2nd TAE either disappeared or reduced, confirming the effectiveness of TAE on daughter nodules that are angiographically visualized. The 2-year survival rate did not differ between HCC with daughter nodules and the total cases of HCC (21% and 27% respectively). Management by TAE was found to produce favorable prognostic results even in HCC with daughter nodules.
Hemodynamics of the spleen in patients with portal hypertension was studied with ultrasonic equipment in comparison with that of the spleen in normal controls and hematologic diseases with splenomegaly. In hematologic diseases, splenomegaly was prominent and the splenic blood flow showed a marked increase (960±538ml/min). In these cases, the cross-sectional area of the splenic vein increased (0.99±0.54cm2) but the maximal flow velocity of the splenic venous blood did not increase. In cirrhotic patients, splenomegaly was prominent and the splenic blood flow had a tendency to increase (507±224ml/min). In these patients, the cross-sectional area of the splenic vein increased (0.66± 0.27cm2) but the maximal flow velocity of the splenic venous blood dropped (23.0±7.1ml/min). In the patients with portal hypertension, there was a positive relationship between the cross-sectional area of the splenic vein and the portal pressure.Pressure index 1, which was the ratio between the major axis and the minor axis of the splenic vein, showed good postive relationship to the portal pressure in all patients. We feel that we will be able todeduce and confirm the portal pressure with these non-invasive measurements.
Ninety-two patients with gallbladder carcinoma in whom direct cholangiography clearly opacified the pancreatico-biliary ductal union, and 64 patients with an anomalous union of these two duct systems at a distance greater than 15mm from the papilla of Vater were analyzed in their relationship. It was found that this anomalous ductal union occurred in 16.3% of the patients with gallbladder carcinoma in comparison with an incidence of 2.8% among 641 consecutive patients with various hepatobiliary and pancreatic diseases studied by endoscopic retrograde cholangiopancreatography who did not have gallbladder carcinoma, and that gallbladder carcinoma occurred in 23.4% of the 64 cases of anomalous ductal union in comparison with a 1.9% incidence of this cancer among 635 consecutive patients similarly studied and found without anomalous ductal union (p<0.001). Thus a close etiologic association was suggested between this anomaly and gallbladder carcinoma. Of the 64 cases of anomalous ductal union, 50 had congenital cystic dilatation of the common bile duct and 14 did not. Five of the 50 (10%) and 10 of the 14 (71.4%) had gallbladder carcinoma (p<0.01), and this carcinoma seems to be related to anomalous ductal union rather than to cystic dilatation of the common bile duct. It was also demonstrated in this study by analysis of serial cholangiograms that the sphinecter of Oddi mechanism seen as mural motility and measured in 25 cases of anomalous ductal union was operative only below the junction of the two ductal systems, whereas in 25 control subjects without anomalous ducts, the sphincter mechanism was demonstrated along the entire length of the common channel and beyound. These observations are compatible with a theory suggesting an etiologic role of regurgitation of pancreatic juice into the biliary tract as already documented in anomalous ductal union.
Effects of ursodeoxycholic acid (UDC) administration and bile refeeding on biliary excretion of cefotiam (CTM) were studied in eight patients with percutaneous transhepatic biliary drainage (PTBD) for obstructive jaundice. Peak concentration of CTM in the bile and biliary output of CTM were significantly increased by UDC administration, and slightly increased by bile refeeding. There was a significant correlationship between CTM and bile acid in biliary output (p<0.01). It is suggested that UDC administration is useful in preventing biliary infection in PTBD patients, and that UDC is one of the important factors affecting biliary excretion of CTM.
Although pancreatic juice trypsinogen is generally understood to be activated totally and completely into trypsin in the duodenum, intraduodenal conditions are also suited for degradation as well as for activation. In vitro experiments of trypsinogen activation at 37°C using rabbit pancreatic juice, duodenal juice and bile revealed the simultaneous occurrence of activation and degradation processes, resulting in partial activation of the original trypsinogen with the degree of 30 to 60%, dependent on bile content in the mixture. Bile accelerated the activation and inhibited the degradation chiefly by means of calcium ion. In in vitro incubation of solutions of crystallized enzymes at 37°C, pH 8, Ca2+ below 3mM, being approximated the intraduodenal conditions, trypsinogen was activated almost entirely by enterokinase and not by trypsin, which reversely provoked degradation both of trypsinogen and of trypsin. It is suggested that pancreatic juice trypsinogen is simultaneosly activated into trypsin and degradated into inert protein immediately after being secreted into the duodenal lumen, resulting in the partial activation, and that bile increased the degree of activation to about 60% at the maximum.
Evaluation of severity in acute pancreatitis is still controversial. We studied about thirteen cases of acute pancreatitis and calculated CT score using findings of early whole body CT scanning within forty eight hours after initial symptoms. Simultaneously we calculated clinical score too. CT score was constituted by ten points (changes limitted in pancreas itself, extension of inflammation and extrapancreatic fluid collection etc.). And clinical score was constituted by eight clinical symptoms and fourteen laboratory findings in fatal pancreatitis reported in Japan. From these studies, we conclude that early CT scanning is more useful for objective determination of severity and therapy (surgical or medical) in acute pancreatitis than clinical findings. So we made new classification of severity in acute pancreatitis by CT score as follows: severe (6_??_: surgical therapy), moderate (4 or 5: medical therapy possible) and mild (3_??_: medical therapy).