The purpose of this study is to investigate the incidence of NUD in Japan and to describe the clinical presentation of NUD. The population of this study consisted of the patients initially visited to our gastroenterology clinic during the period of one year from Feb. 1990 to Jan 1991. Out of the total population, 106 patients with dyspepsia were suspected of NUD according to the definition of AGA, and have received the endoscopy and ultersonography to find the existence of organic disease. While 50 cases presented organic diseases (19 peptic ulcers, 16 gastritis, 7 carcinoma, 4 gall stone, 4 esophageal disease), 56 cases were with no organic diseases and were regarded as NUD. NUD was more common in younger generation and was especially so in women under 40 years old. There was no significant difference in symptoms between NUD and organic diseases. On the other hand, peptic ulcer disease was frequently associated with sever epigastralgia, and smoking habit as a external factor, while abdominal fullness was predominant feature observed in NUD.
Rats with water-immersion stress-induced ulcer were prepered to determine the levels of ET in blood and gastric tissues, and their relationship with the gastric mucosal blood flow, PGs and pathogenesis in the gastric mucosa were evaluated. Pathology in the gastric mucosa appeared an hour after stress loading, while blood flow rate decreased significantly 30 mimites later. PGE2 increased 30 minites later, then decreased. PGI2 decreased significantly. Blood ET level was 1.22±0.50pg/ml for the controls, but this increased remarkably after one hour and significantly peaked after two hours of water immersion. The level of ET in the gastric tissues was 25.87±1.63pg/g tissue for the controls, and this increased markedly after two hours of immersion, reaching a significant peak. In the present study, increased in endogenic ET due to stress were confirmed, and the results suggested the possibility of ET being involved in the pathogenesis of ulcer.
Hypergastrinemia is a very important clinical condition for the reason that a growing body of evidence obtained from animal and human experiments has revealed gastric carcinoids induced by hypergastrinemia. We investigated 35 patients with Basedow's disease (BD) to elucidate the mechanism of hypergastrinemia associated with BD as well as the relationship between type A gastritis and BD. Fasting serum gastrin levels in BD (296.1±251.4pg/ml; mean±S.D.) were significantly (p<0.001) higher than those in age-matched 27 healthy subjects (106.1±69.2), and in the BD group, significant positive correlation was detected between fasting serum gastrin levels and thyroid hormones (i.e. T3 and free T4). In the hyperchlorhydria group in BD with hypergastrinemia, the levels of fasting serum gastrin were normalized after euthyroidism was attained due to antithyroidal drugs. On the other hand, in the achlorhydria group in BD significant hypergastrinemia was persisted in spite of normalization of thyroid function. Twenty % of the BD patients had histologically proved type A gastritis with achlorhydria, and all patients with type A gastritis were older than 60 years old. Endoscopic examination revealed that one patient with type A gastritis had an early gastric cancer. However, no gastric carcinoids were demonstrated in this study. In conclusion, the results described as above suggested, 1) hypergastrineumia observed in patients with BD may be induced by gastrin hypersecretion due to hyperthyroidism as well as type A gastritis, 2) BD patients with type A gastritis were recommended to undertake regular endoscopic examination for detecting gastric cancers as well as gastric carcinoids.
To investigate the effect of the acid-base imbalance on the gastric mucosal defense mechanism, the intracellular pH of gastric surface epithelial cells were measured with double-barreled H+ selective microelectrodes in the isolated antral mucosa of bullfrog stomach. By knowing the intracellular pH and the PCO2 of the serosal perfusate, the intracellular HCO3- concentration was estimated, and the rate of HCO3- secretion was directly measured with the pH-stat method in mounted preparations on a Ussing's chamber. Both the calculated intracellular HCO3- concentration and the rate of HCO3- secretion were dependent on the exogenous HCO3- supplied from the serosal perfusate. The alkaline tide raised the intracellular HCO3- concentration, thus increasing the mucosal buffering power against acid. Under mild respiratory acidosis, the production of endogenous HCO3- from the serosal CO2 was enhanced, and both the intracellular HCO3- concentration and the rate of HCO3- secretion were increased. As a result, the intracellular pH was maintained at a physiologically optimal level, and the ability of gastric mucosal protection was strengthened by enrichment of cellular bicarbonate supply. It is confirmed in this study that the maintenance of acid-base status in the cell is indispensable in the protection of gastric mucosa against acid invasion.
Four markers for hepatic fibrosis-N-terminal peptide of Type III procollagen (PIIIP), Laminin P1 (laminin), Type IV collagen (Type IV-C), and 7S domain (7S)-were measured in the sera of 90 patients with various chronic liver diseases diagnosed by liver biopsy-fatty liver (FL), chronic inactive hepatitis (CIH), chronic active heptitis (CAH), and liver cirrhosis (LC)-and in the sera of 20 healthy controls. The values of markers were compared with the grade of histologic findings of the liver. Four markers were significantly raised in the CAH group and the LC group, and they were considered to be indicators of hepatic fibrosis. PIIIP reflected necrosis and inflammation as well as fibrosis of the liver. Laminin, Type IV-C, and 7S reflected severe fibrosis. 7S was considered to be useful marker for liver cirrhosis.
Serum levels of monomeric, dimeric and tetrameric pseudocholinesterases were measured by means of enzyme-linked immunosorbent assay in patients with various liver diseases and normal controls in order to evaluate their clinical significance. In patients with liver cirrhosis, serum levels of monomeric, dimeric and tetrameric were significantly lower than those in normal controls, patients with fatty liver and chronic hepatitis. The ratio of monomeric and dimeric to tetrameric in patients with liver cirrhosis was also significantly lower than that in normal controls, patients with fatty liver and chronic hepatitis. Serum levels of tetrameric, dimeric and monomeric were not significantly higher in the patients with fatty liver than in normal controls, but the ratio of monomeric and dimeric to tetrameric was significantly higher in patients with fatty liver than that in normal controls, patients with chronic hepatitis and liver cirrhosis. These findings suggest that the selective determinations of serum levels of monomeric, dimeric and tetrameric pseudocholinesterases are useful to estimate the metabolism of fat and protein in various liver diseases.
Both effect of LAK cells and neuraminidase treated LAK (N-LAK) cells on liver regeneration were investigated after 70% partial hepatectomy in mice. Intravenous transfusion of LAK cells suppressed the liver regeneration depending on cell numbers injected. N-LAK cells accumulated into regenerating liver 1.7 times in cell number compared with LAK cells. Injection of 5×107 LAK cells and N-LAK cells into hepatectomized mice suppressed the liver regeneration by 16.5% and 53.8% respectively. These results indicated that suppression of the liver regeneration by LAK cells was dependent upon the number of injected LAK cells and the degree of accumuration of LAK cells into the liver, namely, LAK cells down-regurate the regeneration of liver cells in the micromilieu.
PTCD was performed in 206 of our patients during the past 6 years and 7 months. Of the 206, hemobilia occurred in 14 patients (6.8%). The hemorrhage was completely stopped by irrigation of the bile duct in 3 patients, compression with a larger catheter in 7 patients, and transcatheter arterior embolization (TAE) in 4 patients. TAE was performed on the patients whose hemobilia could not controlled by the compression with a larger catheter. In TAE, either a steel coil or a spongel was used as an embolus. Rebleeding occurred in one patients for whom the right hepatic artery was chosen as a embolization site. Therefore, it was decided that the embolization was going to be done in all the hepatic arteries when the blood stream in the portal vein and preserved functions of the liver of the subjected patients including the one with rebleeding were fully normal. A complete control of the hemorrhage was obtained in all patients. The PTCD root caused hemobilia was removed after TAE in considering the possibility or rebleeding from the root, and a new PTCD root was made.
The role of oxygen derived free radicals or tissue lipid peroxides in the pathogenesis of chronic pancreatitis has not been established. To evaluate long-term effects of tissue lipid peroxides in the pathogenesis of chronic pancreatitis, we treated Wistar male rats with 2, 2'-azobis-(2-amidinopropane) dihydrochloride (AAPH) and/or linoleic acid (LA) for 3 or 6 months. Rats were divided into eight groups. A: Saline-treated rats for 3 months as control, B: AAPH 40 mg/kgw intraperitoneally, twice a week for 3 months, C: LA 0.5ml/kgw intraperitoneally, every other week for 3 months, D: AAPH and LA for 3 months, E: Saline-treated for 6 months, F: AAPH for 6 months, G: LA for 6 months, H: AAPH and LA for 6 months. The results were as follows: Lipid peroxide contents of the pancreas were elevated in groups: C, D, G and H. Histological examination revealed epithelial hyperplasia of large pancreatic ducts, vacu0olization of ductal epithelium, intraepithelial neutrophilic infiltration, periductal mononuclear cell infiltration (ductulitis and periductulitis), and sporadically in the lobules, destruction of acinar cells, neutrophilic infiltration and ductular proliferation in the same groups. These findings indicate that tissue damage was more severe in the pancreatic ducts than in the acinar cells, however no damage was seen in the endocrine pancreas. Vitamin E content of the pancreas was decreased in groups: B, C, D, F, G and H. Tissue glutathione peroxidase (GSH-Px) activity was increased in groups: D and H. Tissue catalase activity was increased in groups: D, G and H, but no change of superoxide dismutase (SOD) activity was seen in any of the groups. These results indicate that vitamin E may play the role of the main scavenger in the situation of a smaller dose of lipid peroxides, but when larger doses are administered, GSH-Px may play the main role as the scavenger in this experimental system.