Tsuyoshi Yabana

Colonization of Helicobacter pylori in the Gastric Mucosa of Mongolian Gerbils

Helicobacter pylori was orally inoculated into Mongolian gerbils. The organisms were able to colonize in the gastro‐mucosal layer of the gerbils, especially in those gerbils which had mucosal lesions caused by indomethacin treatment. The pathological changes developed by H. pylori infection were restricted to the stomachs, and only slightly inflammatory cells were observed.

Stress-induced vascular damage and ulcer

Factors controlling gastric mucosal blood flow are now better understood, and improved techniques have been established to study microcirculation in the gastrointestinal tract. In this paper, four areas are reviewed: gross and microscopic vessels that supply blood to the stomach; factors that control gastrointestinal blood flow; pathogenic role of disturbed mucosal blood flow circulation induced by stress; and findings in early vascular permeability and injury caused by cold restraint stress in the rat.Factors controlling gastric mucosal blood flow are now better understood, and improved techniques have been established to study microcirculation in the gastrointestinal tract. In this paper, four areas are reviewed: gross and microscopic vessels that supply blood to the stomach; factors that control gastrointestinal blood flow; pathogenic role of disturbed mucosal blood flow circulation induced by stress; and findings in early vascular permeability and injury caused by cold restraint stress in the rat.

Gastric antral vascular ectasia causing severe anemia.

Gastric antral vascular ectasia (GAVE) that caused continuous gastrointestinal bleeding is reported in a 76-year-old woman who had been treated with repeated blood transfusions because of severe anemia. Endoscopic examination was performed and diffuse speckled telangiectasia of the entire antrum was observed. Laboratory data showed SGOT>SGPT, decreased chE level and the increased levels of serum gastrin and ICG at 15 min. Anti-HCV antibody was positive. Image examination revealed splenomegaly. There was no family history of telangiectasia, and no telangiectasia was found in other organs. The diagnosis was established as GAVE with liver cirrhosis. Surgical resection of the distal stomach resulted in termination of the bleeding, and the cirrhotic changes of the surface of the liver were revealed at that time, providing further evidence of liver cirrhosis. Although the pathogenesis of GAVE is unknown, liver cirrhosis and hypergastrinemia are thought to be associated with the condition. Importantly, this condition is a cause of severe gastrointestinal bleeding in elderly patients.

Mucosal Immune Response to Helicobacter pylori and Cytotoxic Mechanism

BACKGROUND Helicobacter pylori is widely accepted as a major pathogen in gastritis. The histologic features of H. pylori gastritis are the numerous infiltrating mononuclear cells (MNCs) and neutrophils. It is not clear what role the infiltrating MNCs and neutrophils play in H. pylori gastritis. METHODS In this study, we have established enzyme-linked immunospot (ELISPOT) assay for the measurement of H. pylori antibody-producing cells in gastric mucosa. RESULTS Using ELISPOT assay, we found that H. pylori-specific IgA-producing cells as well as IgG-producing cells were distributed in gastric mucosa. These H. pylori-specific antibodies in gastric mucosa and neutrophils are responsible for the induction of cytotoxic effect to cultured Vero cells. CONCLUSIONS These observations suggest that a mucosal immune response specific to H. pylori is closely associated with the pathogenesis of gastritis.

A pancreatic abscess 7 years after a pancreatojejunostomy for calcifying chronic pancreatitis

We present herein a case of a 75-year-old Japanese man who had developed a pancreatic abscess 7 years after a longitudinal pancreatojejunostomy for chronic pancreatitis. The patient, a heavy drinker of alcohol, underwent surgical decompression of a ductal obstruction to relieve persistent abdominal pain due to severely calcifying chronic pancreatitis. After the surgery, he stopped drinking alcohol and was treated with insulin to control secondary diabetes mellitus. Thereafter, his symptoms disappeared. Seven years after the surgery, however, he was hospitalized due to obstructive jaundice, high-grade fever, and right hypochondria pain. Ultrasound and computed tomographic scans of the abdomen both disclosed a cystic mass, approximately 6 cm in size, in the pancreatic head. Magnetic resonance imaging strongly suggested a pancreatic abscess with necrotic fluid and debris. First, percutaneous transhepatic cholangiodrainage (PTCD) was done to treat the progressively obstructive jaundice. Subsequently, fine-needle aspiration of the pancreatic abscess was performed under ultrasound guidance. Enterococcus avium and Klebsiella oxytoca were revealed by culture of abscess aspirates. He was successfully cured by treatment with both appropriate antibiotic and continuous PTCD for the obstructive jaundice.

Lansoprazole Versus Lansoprazole plus Amoxicillin Treatment for Eradication of Helicobacter pylori in Patients with Gastric Ulcer

Helicobacter pylori is a major cause of gastritis and an important factor in duodenal ulcer relapse. Eradication of H. pylori has usually been achieved by triple therapy, a combination of bismuth salts and two antibiotics. The disadvantage of these regimens is the large number of tablets and the high incidence of side effects. A new H+,K+-ATPase inhibitor, lansoprazole (LPZ), has a strong acid inhibitory effect and an anti-H. pylori effect in vitro. These dual effects have an advantage for the eradication of H. pylori by LPZ alone or by a combination of LPZ and antibiotics. In this study, we investigated an anti-H. pylori effect of LPZ alone and LPZ plus low-dose amoxicillin and the relation between the status of H. pylori colonization and the endoscopic healing stage. LPZ monotherapy suppressed H. pylori but did not eradicate it. LPZ plus low-dose amoxicillin dual therapy eradicated H. pylori in 45.5% of patients with gastric ulcer disease. However, this rate is not satisfactory for eradication therapy. The optimal dosage and duration of treatment need to be specified. A high rate of healing to the endoscopic S2 stage was achieved by eradication of H. pylori and the recurrence of gastric ulcer was suppressed in patients in whom H. pylori was eradicated. The eradication of H. pylori may change the natural course of gastric ulcer disease as it does in duodenal ulcer disease.

Expression of neural cell adhesion molecule (NCAM) in the healing process of gastric ulcer

Cell adhesion molecules are ligands that can participate in cell to cell recognition during the formation of tissue structures. NCAM is a glycoprotein, which belongs to the immunoglobulin superfamily and functions in a Ca2+-independent, homophilic adhesion manner II. NCAM is mainly expressed on neurogenic cells, myogenic cells and NK cells. However, there is no report that NCAM is expressed on the gastric epithelium. We describe here the expression of NCAM in the healing process of human gastric ulcer. Biopsy specimens were taken from the margin of ulceration and the normal epithelium with informed consent, fixed in buffered formalin and embedded in paraffin blocks. Tissue sections reacted with monoclonal anti-NCAM antibody (Sigma,USA), anti-epithelial membrane antigen(EMA) antibody(DAKO, Denmark) and anti-proliferating cell nuclear antigen(PCNA) antibody (DAKO, Denmark), and were stained with the ABC method. Human gastric epithelial cells adjacent to the ulcer at the active and healing stages were strongly stained with anti-NCAM antibody(Fig.l) and the same cells were stained with anti-PCNA antibody and anti-EMA antibody (n=7) . NCAM was mainly expressed in the cytoplasma of epithelial cells, and weakly expressed on the membrane. The normal epithelial cells were not, or weakly, stained with anti-NCAM or anti-PCNA (n=7) . These results suggest that NCAM is preferentially expressed on the marginal epithelial cells of ulceration, which could be in a proliferating stage. On the other hand, NCAM was not expressed on the marginal epithelial cells at the scarring stage(n=3) . In conclusion, NCAM may play an important role in gastric mucosal repair. Reference l)Edelman GM: Ann Rev Cell Biol 1986;2:81-116 Fig.l NCAM is expressed on the epithelial

Hepatocellular Carcinoma with Metastasis to the Duodenum: —A Case Report—

Abstract: A case of hepatocellular carcinoma with metastasis to the duodenum is reported on together with a review of the literature. A 61‐year‐old male was admitted with hematemesis and melena. An endoscopic examination revealed a large hemorrhagic ulcer at the duodenal bulbi. A biopsied specimen taken from the bottom of the ulcer revealed an infiltrating hepatocellular carcinoma. The postmortem examination revealed a hepatocellular carcinoma with metastasis in the duodenum. This is the third report of hepatocellular carcinoma with metastasis in the duodenum.

A Solid-Phase Enzyme-Linked Immunospot (ELISPOT) Assay for Detection of Helicobacter pylori Antibody-Producing Cells in Gastric Mucosa

Helicobacter pylori(H.pylori) is considered to be associated w~th gastritis. The histological features of H.pylori-associated gastritis are the numerous infiltrating mononuclear cells and neutrophils. However, it is not clear how the infiltrating mononuclear cells play a role in the pathogenesis of H.pylor~associated gastritis. In this study, we attempted to establish an assay system for the detection of H.pylori antibody-producing cells in gastric mucosa. Type strain H.pylori(NCTCl1637) was cultured and sonicated according to a previously described method. One hundred Bg of the sonicated antigen were fixed in a 96-well plate. The mononuclear cells(MNC) were separated from gastric biopsy specimens by Ficoll-Hypaque solution. Ten thousand MNC from gastric mucosa were added to each well and incubated. One hundred ~i of biotinylated anti-human IgG(2~g/ml) or IgA(2~g/ml) antibody were added and incubated. After washing, I00 ~i of diluted avidin-biotinylated alkaline phosphatase(ALP) complex were added and then warm agaroseALP substrate(2.3mM of BCIP)solut~on was added and colored. The blue spots were counted under microscope. IgA antibody-producing cells to H.pylori were 3841• and IgG antibodyproducing cells were 1933~2506/I0~MNC in H.pylori positive gastritis patients(Fig.l). On the other hand,H.pylori antibody-producing cells in gastric mucosa were negligible in H.pylori negative gastritis Mononuclear cells(MNC) of Gastric Mucosa

Serum gastrin and gastrin-like immunoreactivity of gastrointestinal mucosa in fetal, neonatal and adult rats

SummarySerum gastrin concentration became detectable in rats at one week after birth (56 pg/ml), and a rapid rise to 198 pg/ml was seen at two weeks after birth. Gradual decreases were seen again at three weeks and four weeks, and thereafter it attained the adult level of 132 ± 17.6 pg/ml.In regards to the gastrin-like immunoreactivity (GLI) in the gastrointestinal mucosa during the fetal period, the values were extremely low even in the antral mucosa. However, the GLI showed an increase during the neonatal suckling period, and was accompanied by a remarkable increase at the commencement of feeding.This GLI coincided with so-called little gastrin, and while an increase accompanied by the development of growth was seen, no qualitative changes were evident. GLI values were high in the duodenal mucosa followed by the antrum, and positive evidence was also seen in the corpus of the stomach and jejunum. High values of GLI in the mucosae were gradually seen at two weeks after birth coinciding with the rise in serum gastrin levels, and the significance of the increases was discussed from the angle of the trophic effect of gastrin.