成年人慢性胃炎50例临床分析

目的:研究成年人慢性胃炎的症状、病因、诊治等问题。方法:对2010年1月—2010年9月我院消化内科50例成年人慢性胃炎患者的病因、临床症状、Hp检验以及治疗情况等进行回顾性分析。结果:成年人中,男性患慢性胃炎的总例数多于女性。随年龄的增加,发病率会增高;病因:不规律饮食或偏食者28例(56%),Hp感染14例(28%),血常规Hb或RBC较为低下4例(8%),患慢性扁桃腺炎或者鼻炎2例(4%),长期服用解热镇痛药2例(4%)。患者不良饮食习惯和Hp感染是最主要的致病因素;临床表现:因食欲不振和反复呕吐而就医者26例(52%),因腹部饱胀和反酸而就医者10例(20%),因呕血而就医者8例(16%),因乏力消瘦和头晕失眠而就医者6例(12%)。结论:饮食不当与Hp感染是当前临床上成年人慢性胃炎最主要的病因,应以改善饮食习惯与进行抗Hp治疗,坚持对症治疗,才能加以改善患者的症状。     

胃粘膜幽门螺旋菌感染发病学探讨——江苏省3013例胃粘膜病理组织学观察

从江苏省3013例胃粘膜病理组织学观察中发现幽门螺旋菌(HP)检出率为58.71%。它对胃粘膜有直接致病作用,可能是慢性活动性胃炎的病原,但不能提示它与胃癌有直接的病因学联系。50岁以下的男性、集体生活者可能为易感人群。宿主、环境因素在HP发病学中的作用值得重视。     

Leptin in the Control of Gastric Secretion and Gut Hormones in Humans Infected with Helicobacter pylori

Background: Leptin, a protein product of obese gene expressed primarily by adipocytes, provides feedback information on the size of energy stores to central OB receptors controlling the food intake, energy expenditure and body weight homeostasis. It has recently been detected in the rat stomach, especially after cholecystokinin (CCK) administration and in human stomach infected with Helicobacter pylori , but its role in gastric secretory functions in humans has not been revealed. This study was designed to determine the involvement of leptin in the control of basal, CCK- and meal-induced gastric H + secretion and plasma gastrin and CCK levels in humans before and after an eradication of H. pylori. Methods: Two groups (A and B) of subjects were used; group A ( n = 7), for comparison of the effects of CCK and leptin on basal gastric H + and plasma hormone (leptin, gastrin and CCK) levels, and group B ( n = 6), for studies on the involvement of leptin in gastric secretory and plasma hormonal responses to vagal stimulation and gastric peptone meal before and after H. pylori eradication. Results: In H. pylori -positive subjects, CCK (12-200 pmol kg -1 h -1 ) given i.v. caused a dose-dependent increase of gastric H + accompanied by a dose-dependent rise in plasma CCK and leptin levels. In contrast, leptin administered i.v. in graded doses (5-80 pmol kg -1 h -1 ) resulted in a gradual inhibition of basal gastric H + secretion and in adose-dependent increment in plasma leptin accompanied by an increase in plasma gastrin without alteration of plasma CCK level. Following eradication of H. pylori by 1- weektriple therapy in group B patients, the infusion of CCK produceda significantly smaller increase in gastric H + secretion and significantly smaller rise in plasma leptin as compared to those before the eradication. Cephalic phase stimulation of gastric secretion induced by modified sham-feeding in group B H. pylori positive subjects increased gastric H + secretion to about 40% of pentagastrin maximum without affecting plasma leptin, gastrin, or CCK level, while gastric peptone meal resulted in the increase in gastric H + response reaching about 70% of pentagastrin maximum accompanied by a marked rise in plasma leptin, gastrin and CCK. The treatment with a standard dose of leptin (20 pmol kg -1 h -1 ) failed to affect sham-feeding-induced gastric H + secretion but reduced significantly the peptone meal-stimulated H + secretion, while raising plasma gastrin in response to this meal. Plasma CCK under basal conditions and after sham-feeding was not affected, but plasma CCK response to gastric meal was significantly reduced by leptin infusion. Eradication of H. pylori did not affect basal or sham-feeding-induced H + secretion but resulted in a significant fall in gastric mealinduced H + and plasma leptin, gastrin and CCK levels. Conclusions: 1) The gastric meal and CCK enhance the release of leptin in H. pylori -positive patients and this leptin is capable of inhibiting basal and meal stimulated gastric H + secretion, while raising plasma gastrin and reducing the plasma CCK levels, and 2) the eradication of H. pylori reduces the postprandial gastric H + and plasma gastrin responses as well as the release of leptin in response to CCK and meal.     

Helicobacter pylori,Non-steroidal Anti-inflammatory Drugs and Smoking in Risk Pattern of Gastroduodenal Ulcers

Background: Helicobacter pylori , NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. Methods: 5967 dyspeptic patients underwent 13 C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. Results: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. Conclusions: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).     

Helicobacter pylori‐negative extra‐nodal marginal zone B‐cell lymphoma of Mucosa‐Associated Lymphoid Tissue (MALT) type following Roux‐en‐Y Gastric Bypass (RYGB)

Gastric MALT lymphoma is a common type of non‐Hodgkin''s lymphoma that has the potential for cure in patients found to have concomitant Helicobacter pylori (H. pylori) infection. This case report explores the evaluation, diagnosis, and treatment of H. pylori‐negative MALT lymphoma in a patient with a history of a RYGB.     

102例小儿纤维胃镜检查结果分析

本文对临床疑诊上消化道疾病的１０２例病儿进行了纤维胃镜检查，其中５８例做了ＨＰ尿素酶试验。结果显示：胃镜的病变检出率为９３．１％，其中以浅表性胃炎、十二指肠炎最多，其次为消化性溃疡。ＨＰ检出率为６２．０％，胃窦部有微小结节样改变者阳性率高达９１．７％，有家族史者阳性率高于无家族史者，ＨＰ感染随年龄增长而增加。