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Objective To investigate colonoscopic presentation and explore biopsy style of lower gastrointestinal graft-versus-host disease (GI-GVHD) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).Methods The endoscopic findings including mucosa erythema,edema,erosion,ulcer,tortoiseshell-pattern and sloughing were observed in 36 patients with GI-GVHD and the rate of apoptotic cell yields in colon and end-ileum was calculated.Results Mucosa lesions were found in almost all of the patients both in colorectal and end-ileum (97.2％ vs 94.1％,P =0.609).Mucosa erythema was more often seen in end-ileum (47.2％ vs 79.4％,P =0.007) and tortoiseshell-pattern was mainly in colorectal mucosa (63.9％ vs 5.9％,P =0.000).Mucosa edema,erosion and oozing bleeding were the same prevalence in large intestine and end-ileum (97.2％ vs 94.1％,80.6％ vs 79.4％,47.2％ vs 47.1％,P ＞ 0.05,respectively).Sloughing was found in 76.5％ (26/34) GI-GVHD patients,and it was almost the same prevalence in large intestine and end-ileum (52.8％ vs 47.1％,P ＞0.05).Almost all of the colorectal mucosa sloughing located in the tortoiseshell-pattern mucosa.Rates of apoptotic cell in rectal,colonic and end-ileal mucosa were 88.9％,91.3％ and 75.9％,respectively,and the rates were 88.2％ and 93.9％ in ileum plus rectum and ileum plus colon respectively,showing that biopsy only in ileum was not sufficient for the pathologic diagnosis of GI-GVHD (93.9％ vs 75.9％,P =0.070).Conclusion Endoscopic presentations of GI-GVHD after allo-HSCT are not the same between colorectal and end-ileal mucosa.Sloughing with GIGVHD feature is not rarely seen in lower GI.Tortoiseshell-pattern mucosa should also be pathognomonic feature of colorectal GVHD in endoscopy.Pathologic tissue should not only be biopsied in end-ileum,but also in colorectal mucosa in the same time.
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Objective To investigate the relationship between helicobacter pylori (H. pylori) infection and reflux esophagitis (RE). Methods H.Pylori infection rates of RE in patients with simple chronic gastritis(CG),which was confirmed by gastrospcope combined with pathological diagnosis were researched.The relationship between HP infection and RE classifications using gastroscope and pathology was explored.Results ⑴H.pylori infection was found in 29(27.1%) in 107 cases of RE and 43(40.2%) in 107 cases of simple CG patients respectively,HP infection positive in RE patients less than that of simple CG patients.RE of class Ⅰ,Ⅱand Ⅲ using gastroscopy classification were 62.1%, 10.3% and 27.6% in H. Pylori-positive cases respectively, while they were 56.4%, 6.4% and 37.2% respectively in H. Pylori-negative ones. However, mild, moderate and severe RE identified by pathohistology were 72.4%, 13.8% and 13.8% in H.Pylori-positive cases respectively, and they were 57.7%, 17.9% and 24.4% respectively in H.Pylori-negative ones.Conclusions All above results suggested that H.Pylori possibly has prevention role in some extent to pathogenesis of RE. RE more commonly was seen in H.Pylori-negative cases.RE could inhibit the H.Pylori survive,So that,the RE was occurred frequently in H.Pylori-negative patients.The inflammatory extent of RE is not serious in H.Pylori-positive patients.
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0.1) were not significantly different.Conclusion The seropositivity of H.pylori,anti-CagA and anti-H.pylori-IgG are associated with the risk of gastric cancer.
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Objective To investigate serologic manifestation of Helicobacter Pylori (H. pylori) infection in patients with inflammatory bowel disease (IBD) and the role of H. pylori infection in pathogenesis of IBD.Methods We measured anti-H.pylori-IgG and anti-H.pylori-CagA of 45 IBD patients and their with sex and age matched 45 chronic gastritis(CG) control patients during 4 years, and analyzed the relationship between seroprevalence of H.pylori and inflammatory range of ulcerative colitis(UC).Results There were 40 UC patients and 5 Crohn's disease(CD) patients; the positive anti-H.pylori-IgG patients in IBD was 40 0% and in chronic gastritis was 66 7% respectively(? 2=6 43,P0 05).Conclusions The anti-H.pylori-IgG positive rate is in high level in IBD patients, but that is lower than chronic gastritis patients.H. pylori infection could play a inhibition role in the inflammation range of UC. The anti-H.pylori-CagA positive rate of IBD patients and pan-colorectal UC are lower than their controls respectively, but there is no obviously different in statistics.
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0. 1). All the GI-GVHD and CMV colitis patients presented with a variety of colonic mucosal lesions. Besides the tortoiseshell-pattern mucosa and deep ulcer were characteristic lesions in GI-GVHD and CMV colitis respectively, the remaining mucosa lesions including edema, reddish patchy, erythma, erosion and superficial ulcer could not differentiate GI-GVHD from CMV colitis. Three GI-GVHD cases presented with pseud-omembrane, and 1 CMV colitis patient with herpes-like mucosa. Oozing bleeding of terminal-ileum mucosa and ileocecal valve inflammation could easily be found in GC patients. 63. 8% tissue samples were taken biopsies from rectosigmoid in GI-GVHD, and 70. 0% and 43. 8% in CMV colitis and GC patients respectively. Conclusion The positivity of peripheral blood CMV-DNA can not distinguish GI-GVHD from CMV colitis in allo-HSCT patients. GI-GVHD and CMV colitis manifest with a variety of lesions in colonoscopy, the tor- toiseshell-pattern mucosa in GI-GVHD and deep ulcer in CMV colitis are characteristic lesions. The patients of GI-GVHD complicated with CMV colitis readily present oozing bleeding of terminal-ileum mucosa and ileo-cecal valve inflammation. Colonoscopy and tissue biopsy of left-colon can diagnose the most of GI-GVHD and CMV colitis, but it's better to undertake pan-colon as well as terminal ileum examination for more accurate diagnosis.