RÉSUMÉ
BACKGROUND: During Helicobacter pylori (HP) gastritis, the organisms cause an impairment of DNA repair that results in accumulation of mutations in the genome of epithelial cells and an increased risk of gastric carcinoma. The aim of this study was to determine whether microsatellite instability (MSI) could be induced by chronic HP infection in the Mongolian gerbil model. METHODS: Seven-weeks old, specific pathogen-free male Mongolian gerbils were infected with the HP strain CA20. They were sacrificed at the each time points (1, 2, 3, 6, 9, 12 months). Areas of gastritis were carefully microdissected. DNA from tissues was analyzed for the presence of MSI by genomic DNA amplification with five gerbil microsatellite markers per sample. Gerbil markers labelled with Fam or Hex were obtained to perform MSI analysis using the 310 Genetic Analyzer. RESULTS: MSI was more frequent in the area of gastritis than in that of normal (p<0.05). Six showed MSI-low and one showed MSI-high within the area of gastritis (p<0.05). CONCLUSIONS: This study shows that chronic HP infection in the Mongolian gerbil induces MSI. This finding indicates that HP infection causes a decrease in DNA MMR proteins in epithelial cells of the stomach that may reach critically low levels, allowing for the accumulation of mutations such as those seen in microsatellite regions.
Sujet(s)
Humains , Mâle , ADN , Réparation de l'ADN , Cellules épithéliales , Gastrite , Génome , Gerbillinae , Helicobacter pylori , Helicobacter , Instabilité des microsatellites , Répétitions microsatellites , Modèles animaux , EstomacRÉSUMÉ
BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed medicine but induce damage throughout the entire gastrointestinal tract including small intestine with protein and blood loss. Impaired epithelial barrier function, overgrowth of luminal bacteria and others have been implicated in the pathogenesis of NSAID induced enteropathy. Colostrum is a first milk produced after birth and is particularly rich in growth factors, immunoglobulins and antimicrobial peptides. The present study aimed to exam whether defatted bovine colostrum reduce small intestinal injury caused by diclofenac in the animals. METHODS: 64 rats were utilized in four groups; control group, diclofenac group, diclofenac with 5% colostrum group and diclofenac with 10% colostrum group. The animals with colostrum were fed with 5% or 10% colostral solution for 5 days before diclofenac administration. Small intestinal injury was induced by administering a single dose of diclofenac (50 mg/kg subcutaneously). Epithelial permeability, enteric aerobic bacterial counts, serum albumin and protein levels, and pathologic findings of distal ileum were measured. RESULTS: Diclofenac caused marked increase in intestinal permeability, enteric bacterial numbers and intestinal villous damage, and declines in serum levels of total protein and albumin. Co-administration of bovine colostrum reduced intestinal permeability and enteric bacterial numbers, declines in serum albumin and protein levels, and mucosal damage of small intestine induced by diclofenac. CONCLUSION: Bovine colostrums may have beneficial effects on preventing NSAID induced small intestinal injury and bacterial translocation.
Sujet(s)
Animaux , Rats , Bactéries , Charge bactérienne , Translocation bactérienne , Colostrum , Diclofenac , Tube digestif , Iléum , Immunoglobulines , Protéines et peptides de signalisation intercellulaire , Intestin grêle , Lait , Modèles animaux , Parturition , Peptides , Perméabilité , Phénobarbital , SérumalbumineRÉSUMÉ
BACKGROUND/AIMS: Increased intestinal permeability has been possible contributing factors to the pathogenesis of alcoholic liver disease. Moreover, it can contribute to the development of bacterial infection and intestinal endotoxemia in patients with liver cirrhosis. This study aimed to examine the difference of intestinal barrier dysfunction between alcoholic and viral liver disease patients through the comparison of the intestinal permeabilities of patients with clinical characteristics. METHODS: Intestinal permeabilities were measured in 18 healthy controls, 41 patients with alcoholic liver disease (17 cases of alcoholic liver disease without cirrhosis and 24 cases of alcoholic liver cirrhosis) and 46 patients with viral liver disease (14 cases of chronic viral hepatitis and 32 cases of viral liver cirrhosis) by measuring 24 hour urine excretion of 51Cr-EDTA. RESULTS: The intestinal permeability was significantly increased in the patients with alcoholic liver disease without cirrhosis (5.62 +/- 2.80%), alcoholic liver cirrhosis (5.29 +/- 2.48%) and viral liver cirrhosis (3.15 +/- 1.39%) compared with that in control subjects (1.99 +/- 0.53%). On the contrary, it was not increased in the patients with chronic viral hepatitis (2.05 +/- 0.57%) versus controls. The significant correlation was not found between intestinal permeability and clinical and laboratory findings. CONCLUSIONS: The intestinal permeability was elevated in patients with alcoholic liver disease compared to those with viral liver cirrhosis. The pathophysiology of liver injury secondary to intestinal epithelial damage may be different between alcoholic and viral liver diseases.
Sujet(s)
Sujet âgé , Femelle , Humains , Mâle , Adulte d'âge moyen , Maladie chronique , Résumé en anglais , Hépatites virales humaines/physiopathologie , Intestins/physiopathologie , Cirrhose alcoolique/physiopathologie , Maladies alcooliques du foie/physiopathologie , PerméabilitéRÉSUMÉ
BACKGROUND: Gut barrier dysfunction occurs in experimental models and humans of obstructive biliary disease. This phenomenon promotes infectious complications including bacterial translocation and intestinal endotoxemia. The aims of this study were to examine correlations between gut barrier dysfunction and clinical characteristics in obstructive biliary disease. METHODS: The intestinal permeability were measured in 18 normal healthy controls, 20 patients with cholestasis caused by benign disease and 23 of them with cholestasis caused by malignant disease (common bile duct cancer; 16, pancreatic head cancer; 5) by measuring 24 hour urine excretion of 51Cr-EDTA (51Cr-ethylenediaminetetraacetic acid). RESULTS: The increase in intestinal permeability in malignant cholestatic disease was more higher than benign cholestatic disease (p<0.05). The increase in intestinal permeability showed significant correlation with shortening of prothrombin and activated partial thromboplastin time (p<0.05). No significant correlation was found between the increase in intestinal permeability and pancreatitis, inflammation or liver function including the changes of serum bilirubin level in patients with obstructive biliary disease. CONCLUSION: The increase in intestinal permeability in obstructive biliary disease was more in malignant cholestatic disease than benign cholestatic disease. Activation of coagulation may be predictive factor for gut barrier dysfunction in patients with obstructive jaundice.
Sujet(s)
Humains , Translocation bactérienne , Tumeurs des canaux biliaires , Conduits biliaires , Bilirubine , Coagulation sanguine , Cholestase , Endotoxémie , Tumeurs de la tête et du cou , Inflammation , Intestins , Ictère rétentionnel , Foie , Modèles théoriques , Pancréatite , Temps partiel de thromboplastine , Perméabilité , ProthrombineRÉSUMÉ
BACKGROUND: Liver cirrhosis may be considered one of the most common cause of acquired immunodeficiency. Alcohol abuse may be predisposing factor to infections in patients with liver cirrhosis, so we compared the rate of spontaneous bacterial peritonitis (SBP) and other bacterial infections in alcoholic and viral liver cirrhosis. METHODS: We studied 188 patients who had been diagnosed with liver cirrhosis from January 1995 to June 2000 and evaluated the frequency of bacterial infections (SBP, pneumonia, urinary track infection, bacteremia, infectious colitis) retrospectively according to cause and degree of cirrhosis. RESULTS: Among 188 patients (alcoholic 76, viral 112), 64 patients (34%) presented with bacterial infection at hospitalization, 33 (43%;33/76) of 64 subjects were alcoholic and 31 (28%;31/112) of 64 subjects were viral liver cirrhosis. The rate of bacterial infections was higher in alcoholic liver cirrhosis than viral cirrhosis (p0.05). CONCLUSION: This results suggest that the rate of bacterial infections are more common in alcoholic than viral liver cirrhosis in relatively early stage and it may be influence the prognosis of liver cirrhosis.
Sujet(s)
Humains , Alcooliques , Alcoolisme , Bactériémie , Infections bactériennes , Causalité , Fibrose , Hospitalisation , Cirrhose du foie , Cirrhose alcoolique , Péritonite , Pneumopathie infectieuse , Pronostic , Études rétrospectivesRÉSUMÉ
BACKGROUND/AIMS: In clinical practice, among the technique to detected Helicobacter pylori (H. pylori) infection, IgG serological test is noninvasive, safe, quick, widely available, and inexpensive. We studied that whether the titers of anti-H. pylori IgG antibody were correlated with endoscopic finding, and the degree of microscopic gastric damage and H. pylori density in dyspeptic patients. METHODS: Gastric biopsy specimens were obtained in 109 patients with H. pylori infection undergoing upper gastric endoscopy. The titers of serum IgG antibodies to H. pylori were measured by enzyme immunoassay. Macroscopic gastric damages and histologic grades were scored by the Sydney system. RESULTS: Endoscopic findings showed no significant association with H. pylori antibody titers (p=0.111). There was significant correlation between H. pylori antibody titers and lymphocyte infiltration (p=0.002), neutrophil infiltration (p=0.002), H. pylori density (p=0.0001), respectively. There was no significant correlation between H. pylori antibody titers and atropy (p=0.142), intestinal metaplasia (p=0.368), respectively. CONCLUSIONS: H. pylori antibody titer has significant association with the H. pylori density, neutrophil and lymphocyte infiltration. The serological test using EIA method is a useful in detecting H. pylori infection and it may be used as a predictor for the H. pylori density and degree of inflammation.
Sujet(s)
Humains , Anticorps , Biopsie , Endoscopie , Helicobacter pylori , Helicobacter , Techniques immunoenzymatiques , Immunoglobuline G , Inflammation , Lymphocytes , Métaplasie , Infiltration par les neutrophiles , Granulocytes neutrophiles , Tests sérologiquesRÉSUMÉ
OBJECTIVE: This study was aimed to characterize the clinical features and course of acute hepatitis A in Korean adults. METHODS: One-hundred and thirteen cases of acute hepatitis A, diagnosed between Jan. 1995 to July 1998 at 6 medical centers in Korea, were reviewed retrospectively. The clinical course of 94 cases with follow-up duration longer than 3 months were analyzed. RESULTS: The median age was 26 (16-65) years and 97.3% of the patients were under 40 years. The presumed sources of infection were identifed in 62 cases (54.9%). Among those, the leading source was ingestion of raw food. All patients showed normalization of bilirubin level within 8 weeks. The ALT levels normalized within 8 weeks in all patients except three patients (3.2%). Three patients with prolonged elevation of ALT showed second rise of ALT, suggesting a possibility of relapsing hepatitis. Prolonged fever (>38 degree C) more than 10 days was observed in 3 patients (3.2%). One case showed prolonged elevation of alkaline phosphatase (> x3 upper normal limit). No case of fulminant hepatic failure or death was observed. CONCLUSION: The majority of cases with acute hepatitis A in Korean adults showed self-limited course with full recovery.