ABSTRACT
To analyze the causes of failure in conventional treatment to refractory gastroesophageal reflux diseases (GERD) patients, 16 refractory GERD patients (group R) and 16 cases of GERD primarily diagnosed (group P) were studied. Endoscopy, pathologic examination and 14C urea breath test were conducted in every patient. 24 h ambulatory pH and bilirubin monitoring were performed with Digitrapper MK III and Synetics Bilitec 2000. It was found that esophagitis in group R was more severe than in group P. The rate of Helicobacter pylori infection in group R was significantly lower than in group P. Fraction time pH below 4.00 was not longer while the bile reflux represented by fraction time abs above 0.14 was greater for patients in the group R as compared with those in the group P. The mixed refluxes and pure bile refluxes between the two groups had significant difference. The reflux episodes in the group R mainly occurred during nights. These results indicated that severe esophagitis, especially Barrett's esophagus with complications makes it difficult to control GERD. Severe duodenogastroesophageal refluxes (DGER) are often accompanied by refractory GERD. Mixed refluxes aggravate the esophageal injuries. Pure bile refluxes and nocturnal refluxes may cause failure of administration of proton pump inhibitors (PPI) in the morning. Helicobacter pylori infection and acid refluxes may not be the direct cause of refractoriness. Individual refractory GERD patient without abnormal results on pH or bile reflux recently should be diagnosed again.
Subject(s)
Barrett Esophagus/complications , Esophagitis/complications , Esophagitis/microbiology , Gastroesophageal Reflux/complications , Gastroesophageal Reflux/diagnosis , Gastroesophageal Reflux/therapy , Helicobacter Infections/complications , Helicobacter pylori , Treatment FailureABSTRACT
The vacuolated effect of Helicobacter (H. pylori) and its relationship to vacuolated cytotoxin antigen (VacA) were investigated by the method of cytotoxic test and SDS-pobyacrylamide gel electrophoresis (SDS-PAGE). Of the 62 clinical isolates, the broth culture filter (BCF) of 43 strains caused the Vero cell intracytoplasmically vacuolated. H. pylori strains were divided into H. pylori (Toxin+) group with vacuolated effect and H. pylori (Toxin-) group without vacuolated effect. The analysis of the BCF of H. pylori (Toxin+) and that of H. pylori (Toxin-) was studied by SDS-PAGE and Scan reader. A kind of protein with 87 ku molecular weight was recognized in the BCF of 30.23% (13/43) H. pylori (Toxin+) strains but in none of that of H. pylori (Toxin-) strains, the difference was statistically significant (P < 0.05). There was a significant and concordant relationship between OD of the protein band with 87 ku molecular weight and titer of vacuolated activity of H. pylori (Toxin+) (r = 0.67 and P < 0.05 by linear regression analysis). H. pylori strains were divided into H. pylori (Toxin+) group with vacuolated effect and H. pylori (Toxin-) group without vacuolated effect. The vacuolated effect of H. pylori (Toxin+) was caused by the protein with 87 ku molecular weight (VacA).
Subject(s)
Bacterial Proteins/genetics , Genotype , Helicobacter Infections/microbiology , Helicobacter pylori/genetics , Peptic Ulcer/microbiology , Stomach Diseases/microbiology , VacuolesABSTRACT
The vacuolated effect of Helicobacter (H. pylori) and its relationship to vacuolated cytotoxin antigen (VacA) were investigated by the method of cytotoxic test and SDS-pobyacrylamide gel electrophoresis (SDS-PAGE). Of the 62 clinical isolates, the broth culture filter (BCF) of 43 strains caused the Vero cell intracytoplasmically vacuolated. H. pylori strains were divided into H. pylori (Toxin+) group with vacuolated effect and H. pylori (Toxin-) group without vacuolated effect. The analysis of the BCF of H. pylori (Toxin+) and that of H. pylori (Toxin-) was studied by SDS-PAGE and Scan reader. A kind of protein with 87 ku molecular weight was recognized in the BCF of 30.23% (13/43) H. pylori (Toxin+) strains but in none of that of H. pylori (Toxin-) strains, the difference was statistically significant (P < 0.05). There was a significant and concordant relationship between OD of the protein band with 87 ku molecular weight and titer of vacuolated activity of H. pylori (Toxin+) (r = 0.67 and P < 0.05 by linear regression analysis). H. pylori strains were divided into H. pylori (Toxin+) group with vacuolated effect and H. pylori (Toxin-) group without vacuolated effect. The vacuolated effect of H. pylori (Toxin+) was caused by the protein with 87 ku molecular weight (VacA).
Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Bacterial Proteins , Genetics , Genotype , Helicobacter Infections , Microbiology , Helicobacter pylori , Genetics , Peptic Ulcer , Microbiology , Stomach Diseases , Microbiology , VacuolesABSTRACT
To analyze the causes of failure in conventional treatment to refractory gastroesophageal reflux diseases (GERD) patients, 16 refractory GERD patients (group R) and 16 cases of GERD primarily diagnosed (group P) were studied. Endoscopy, pathologic examination and 14C urea breath test were conducted in every patient. 24 h ambulatory pH and bilirubin monitoring were performed with Digitrapper MK III and Synetics Bilitec 2000. It was found that esophagitis in group R was more severe than in group P. The rate of Helicobacter pylori infection in group R was significantly lower than in group P. Fraction time pH below 4.00 was not longer while the bile reflux represented by fraction time abs above 0.14 was greater for patients in the group R as compared with those in the group P. The mixed refluxes and pure bile refluxes between the two groups had significant difference. The reflux episodes in the group R mainly occurred during nights. These results indicated that severe esophagitis, especially Barrett's esophagus with complications makes it difficult to control GERD. Severe duodenogastroesophageal refluxes (DGER) are often accompanied by refractory GERD. Mixed refluxes aggravate the esophageal injuries. Pure bile refluxes and nocturnal refluxes may cause failure of administration of proton pump inhibitors (PPI) in the morning. Helicobacter pylori infection and acid refluxes may not be the direct cause of refractoriness. Individual refractory GERD patient without abnormal results on pH or bile reflux recently should be diagnosed again.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Barrett Esophagus , Esophagitis , Microbiology , Gastroesophageal Reflux , Diagnosis , Therapeutics , Helicobacter Infections , Helicobacter pylori , Treatment FailureABSTRACT
ObjectiveTo investigate the gastric adaptation to aspirin in rats. MethodsMucosal in-jury was induced by repeated doses of acidified aspirin (ASA) in rats. Mucosal lessions and necrosis depth were measured. Mucosal contents of epidermal growth factor (EGF) were tested by radioimmunoassay. To test the possible implication of endogenous nitric oxide in gastric adaptation to aspirin. L-Arg, L-NAME and L-Arg +L-NAME were given intravenously 30 minutes before the exposure to ASA. ResultsThe lession areas of gas-tric mucosa in first exposure to ASA was (50.4 ± 6.2)mm2. After repeated dose of ASA, the mucosal lessions were significantly alleviate, P ＜0.01. The mucosal contents of EGF were significantly increased, P < 0.01.The rat mucosa had adaptation to ASA after pretreated L-Arg、L-NAME and L-Arg + L-NAME. The lession areas of the pretreated L-NAME rats were significantly bigger than that of the pretreated L-Arg rats. Conclu-sionGastric mucosa exhibits the ability to adapt to ulcerogenic action of aspirin. After four days repeated doses of ASA, the full adaptation to ASA was achieved. The mechanism of the adaptation was possibly through increased gastric mucosal EGF. NO played a part of role in the gastric adaptation to ASA.
ABSTRACT
Gastric emptying time of liquid meal was detected by using ultrasonography in 28 gas tric ulcer patients with continual or recurrent dyspepsia symptoms after the ulcer healing. Sixteen out of 28 patients (57.1%) with a delay of gastric emptying time (T1/2) were randomly divided into two groups: 8 cases were treated with cisapride 5 mg three times a day and 8 cases with cis apride 10 mg three times a day respectively. The results showed that cisapride could relieve the symptoms with the effective rate being 68.8% in the two groups. T1/2 in the patients after treat ment with cisapride was significantly shorter than before treatment (P＜0.001). It was concluded that there is a delay of T1/2 in some patients with gastric ulcer healing. Cisapride could promote gastric empty of liquid meal and relieve the symptoms efficiently. The effect of lower dose of cis apride is similar to that of higher dose.
ABSTRACT
Gastric emptying time of liquid meal was detected by using ultrasonography in 28 gas tric ulcer patients with continual or recurrent dyspepsia symptoms after the ulcer healing. Sixteen out of 28 patients (57.1%) with a delay of gastric emptying time (T1/2) were randomly divided into two groups: 8 cases were treated with cisapride 5 mg three times a day and 8 cases with cis apride 10 mg three times a day respectively. The results showed that cisapride could relieve the symptoms with the effective rate being 68.8% in the two groups. T1/2 in the patients after treat ment with cisapride was significantly shorter than before treatment (P＜0.001). It was concluded that there is a delay of T1/2 in some patients with gastric ulcer healing. Cisapride could promote gastric empty of liquid meal and relieve the symptoms efficiently. The effect of lower dose of cis apride is similar to that of higher dose.
ABSTRACT
p53 gene mutation (exon4 , 5 , 6 . 7 . 8 and intron6) in gastric cancer and precancerous le- sions and p53 gene (exon4 and intron6) .APC gene deletion in gastric carcinomas were studied by PCR/ SSCP and PCR/RFLP. Results showed: mutation rate of p53 in intestinal metaplasia ,dysplasia and gas- tric carcinoma was 37. 5% (3/8) ,42. 1 % (8/19) , 53. 3% (16/30) ,respectively. There was significant dif- ference between groups of metaplasia、dysplasia、cancer and that of normal control. We found there were no exon8 mutation in metaplasia and dysplasia , but 4 cases in cancer group. lt is suggestted that exon8 mutation occurs at the late stage of gastric cancer , but exon 5 , 6 , 7 mutation occur in the course of pre- cancerous lesions to cancer. Loss of heterozygosity (LOH) of exon4 . intron6 . APC was 47. 4 % ( 9/19) . 8. 7%C2/23).16. 7%(3/18) ,respectively. There are some relationship between LOH of exon4 and poor- ly differentiation , lymph node metastas , depth of invasion. LOH of exon4 may be one of prognostic marker of gastric cancer. We concluded that p53 gene mutation is an early event and perhaps has syner- gism with ras oncogene in gastric carcinogenesis