AIM： To evaluate fecal calprotectin （FC） as a surrogate marker of treatment outcome of relapse of inflammatory bowel disease （IBD） and, to compare FC with fecal myeloperoxidase （MPO） and fecal eosinophil protei...AIM： To evaluate fecal calprotectin （FC） as a surrogate marker of treatment outcome of relapse of inflammatory bowel disease （IBD） and, to compare FC with fecal myeloperoxidase （MPO） and fecal eosinophil protein X （EPX）. METHODS： Thirty eight patients with IBD, comprising of 27 with ulcerative colitis （UC） and 11 with Crohn＇s disease （CD） were investigated before treatment （inclusion）, and after 4 and 8 wk of treatment. Treatment outcomes were evaluated by clinical features of disease activity and endoscopy in UC patients, and disease activity in CD patients. In addition, fecal samples were analyzed for FC by enzyme-linked immunosorbent assay （ELISA）, and for MPO and EPX with radioimmunoassay （RIA）. RESULTS： At inclusion 37 of 38 （97%） patients had elevated FC levels （〉 94.7 μg/g）. At the end of the study, 31 of 38 （82%） patients fulfilled predefined criteria of a complete response IUC 21/27 （78%）; CD 10/11 （91%）]. Overall, a normalised FC level at the end of the study predicted a complete response in 100% patients, whereas elevated FC level predicted incomplete response in 30%. Normalised MPO or EPX levels predicted a complete response in 100% and 90% of the patients, respectively. However, elevated MPO or EPX levels predicted incomplete response in 23% and 22%, respectively. CONCLUSION： A normalised FC level has the potential to be used as a surrogate marker for successful treatment outcome in IBD patients. However, patients with persistent elevation of FC levels need further evaluation. FC and MPO provide superior discrimination than EPX in IBD treatment outcome.展开更多
AIM： To investigate the relationship between myeloperoxidase polymorphisms as a host-related factor and atrophy caused by H pylori. METHODS： Our study enrolled 77 patients. Biopsy materials obtained during gastroint...AIM： To investigate the relationship between myeloperoxidase polymorphisms as a host-related factor and atrophy caused by H pylori. METHODS： Our study enrolled 77 patients. Biopsy materials obtained during gastrointestinal endoscopies were evaluated for the presence of H pylori. Polymerase chain reaction-restriction fragment length polymorphism assay was used to characterize myeloperoxidase genothpes. RESULTS： Forty four patients （57.1%） were lip （＋） and 33 （42.9%） were Hp （-）. Sixty six （85.7%） had GG genotype, 10 （12.9%） had GA genotype and 1 （1.29%） had AA genotype. The change in atrophy in relation to neutrophil infiltration was significant in Hp （＋） patients （P = 0.0001）. The change in atrophy in relation to neutrophil infiltration in patients with GG genotype was significant （P = 0.002）. However, the change in atrophy in relation to neutrophil infiltration was not significiant in patients with Hp （＋） GG genotype （r = 0.066, P = 0.63）. CONCLUSION： Myeloperoxidase genotype is critical for development of atrophy in relation to the severity of inflammation. However, it is interesting to note that, H pylori does not show any additive effect on development of atrophy.展开更多
AIM: To elucidate the relations between the myeloperoxidase ^(-468)G→a polymorphism and the development of duodenal ulcer (DU), and to investigate the impacts of this host genetic polymorphism on the histopathologica...AIM: To elucidate the relations between the myeloperoxidase ^(-468)G→a polymorphism and the development of duodenal ulcer (DU), and to investigate the impacts of this host genetic polymorphism on the histopathological features of Helicobacter pylori (H py/ori)-related gastritis. METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase ^(-468)G→A polymorphism was genotyped. Additionally, gastric mucosal changes were examined according to the updated Sydney System. RESULTS: The two study groups differed in the distributions of myeloperoxidase genotypes (P=0.008). All six individuals carrying myeloperoxidase A/A genotypes were in the DU group. The carriage of myeloperoxidase allele A and H pylori infection were associated with an increased risk of DU with odds ratios (OR) of 2.3 and 5.8, respectively. The combined risk of the carriage of myeloperoxidase allele A and H pylori infection for DU was 8.7 (95% CI, 3.5-21.8). In the H pylori-infected individuals, allele A carriers displayed higher bacterial density scores (P=0.04) in the antrum than did non-carriers. CONCLUSION: This work verifies for the first time the association of myeloperoxidase ^(-468)G→A polymorphism with antral H pylori density and DU disease. The mechanisms underlying this genetic polymorphism in developing DU disease merit further investigations.展开更多
基金Grants from the Medical Faculty, Uppsala University, Uppsala, Sweden
文摘AIM： To evaluate fecal calprotectin （FC） as a surrogate marker of treatment outcome of relapse of inflammatory bowel disease （IBD） and, to compare FC with fecal myeloperoxidase （MPO） and fecal eosinophil protein X （EPX）. METHODS： Thirty eight patients with IBD, comprising of 27 with ulcerative colitis （UC） and 11 with Crohn＇s disease （CD） were investigated before treatment （inclusion）, and after 4 and 8 wk of treatment. Treatment outcomes were evaluated by clinical features of disease activity and endoscopy in UC patients, and disease activity in CD patients. In addition, fecal samples were analyzed for FC by enzyme-linked immunosorbent assay （ELISA）, and for MPO and EPX with radioimmunoassay （RIA）. RESULTS： At inclusion 37 of 38 （97%） patients had elevated FC levels （〉 94.7 μg/g）. At the end of the study, 31 of 38 （82%） patients fulfilled predefined criteria of a complete response IUC 21/27 （78%）; CD 10/11 （91%）]. Overall, a normalised FC level at the end of the study predicted a complete response in 100% patients, whereas elevated FC level predicted incomplete response in 30%. Normalised MPO or EPX levels predicted a complete response in 100% and 90% of the patients, respectively. However, elevated MPO or EPX levels predicted incomplete response in 23% and 22%, respectively. CONCLUSION： A normalised FC level has the potential to be used as a surrogate marker for successful treatment outcome in IBD patients. However, patients with persistent elevation of FC levels need further evaluation. FC and MPO provide superior discrimination than EPX in IBD treatment outcome.
文摘AIM： To investigate the relationship between myeloperoxidase polymorphisms as a host-related factor and atrophy caused by H pylori. METHODS： Our study enrolled 77 patients. Biopsy materials obtained during gastrointestinal endoscopies were evaluated for the presence of H pylori. Polymerase chain reaction-restriction fragment length polymorphism assay was used to characterize myeloperoxidase genothpes. RESULTS： Forty four patients （57.1%） were lip （＋） and 33 （42.9%） were Hp （-）. Sixty six （85.7%） had GG genotype, 10 （12.9%） had GA genotype and 1 （1.29%） had AA genotype. The change in atrophy in relation to neutrophil infiltration was significant in Hp （＋） patients （P = 0.0001）. The change in atrophy in relation to neutrophil infiltration in patients with GG genotype was significant （P = 0.002）. However, the change in atrophy in relation to neutrophil infiltration was not significiant in patients with Hp （＋） GG genotype （r = 0.066, P = 0.63）. CONCLUSION： Myeloperoxidase genotype is critical for development of atrophy in relation to the severity of inflammation. However, it is interesting to note that, H pylori does not show any additive effect on development of atrophy.
基金Supported by the grants from the Research Foundation of Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan, China VGHKS9274 and the National Science Council, Taiwan, China NSC-92-2314B-075B-006
文摘AIM: To elucidate the relations between the myeloperoxidase ^(-468)G→a polymorphism and the development of duodenal ulcer (DU), and to investigate the impacts of this host genetic polymorphism on the histopathological features of Helicobacter pylori (H py/ori)-related gastritis. METHODS: In a case-control study of 115 consecutive DU patients and 182 controls, the myeloperoxidase ^(-468)G→A polymorphism was genotyped. Additionally, gastric mucosal changes were examined according to the updated Sydney System. RESULTS: The two study groups differed in the distributions of myeloperoxidase genotypes (P=0.008). All six individuals carrying myeloperoxidase A/A genotypes were in the DU group. The carriage of myeloperoxidase allele A and H pylori infection were associated with an increased risk of DU with odds ratios (OR) of 2.3 and 5.8, respectively. The combined risk of the carriage of myeloperoxidase allele A and H pylori infection for DU was 8.7 (95% CI, 3.5-21.8). In the H pylori-infected individuals, allele A carriers displayed higher bacterial density scores (P=0.04) in the antrum than did non-carriers. CONCLUSION: This work verifies for the first time the association of myeloperoxidase ^(-468)G→A polymorphism with antral H pylori density and DU disease. The mechanisms underlying this genetic polymorphism in developing DU disease merit further investigations.
