消化不良病人胃窦胃体内镜表现及病理对比研究

目的研究功能性消化不良病人胃窦与胃体的内镜表现及病理检查的区别。方法2003-03~05对北京友谊医院门诊接受胃镜检查的132例有上消化道症状的病人,根据红斑、糜烂、出血和萎缩4种表现进行内镜评价,按胃黏膜慢性炎症、活动性、萎缩、肠化生、幽门螺旋杆菌和异型增生进行病理评价。分析胃窦与胃体内镜表现及病理的区别。结果胃窦与胃体相比,内镜下红斑和糜烂病变较为多发,P值均<0.01;病理诊断萎缩和慢性炎症,胃窦与胃体之间差异也很显著,P值分别为<0.001和<0.025。结论功能性消化不良病人胃窦与胃体在内镜和病理上存在差异,内镜下红斑和糜烂,以及病理萎缩和慢性炎症,在胃窦比胃体更常见。     

慢性萎缩性胃炎的相关因素及内镜与病理诊断比较的临床意义

目的 探究慢性萎缩性胃炎(CAG)的临床相关因素并比较临床中胃镜诊断与病理诊断结果的差别。方法通过在我院进行胃镜及病理检查的994例病人的临床相关因素资料、胃镜及病理检查结果的分析和差异的比较，了解慢性萎缩性胃炎的相关因素以及胃镜诊断与病理诊断结果差异的原因。结果慢性萎缩性胃炎和慢性非萎缩性胃炎在平均年龄、吸烟史、酗酒、既往有胃或十二指肠病史上有显著差异；肠上皮化生和活动性炎症伴随CAG的比例分别为91．2％、76．7％，明显比不伴CAG的比例(分别为8．8％、23．3％)高，两者有高度相关性。CAG在不同部位的萎缩程度有差别：胃窦部CAG以轻中度萎缩为主，重度萎缩很少。而在胃体部cAG和胃窦兼胃体部cAG病人中，重度萎缩占有相当的比例。正常胃黏膜与CAG内镜下诊断以及不同部位间的CAG内镜下诊断为正常胃黏膜、胃窦部CAG、胃窦兼胃体部CAG和胃体部CAG与病理诊断比较的符合率分别为52．5％、37．5％、8％、25％。结论慢性萎缩性胃炎与多方面因素有关，以胃窦部多见，在病理诊断上与胃黏膜的活动性炎症及肠上皮化生有关。胃镜诊断与病理诊断的符合率不高，要提高CAG诊断的正确率，必须在提高胃镜检查技术的同时结合黏膜病理活检。     

慢性萎缩性胃炎内镜与病理学诊断的临床分析

[目的]分析慢性萎缩性胃炎(CAG)内镜诊断与病理诊断的符合率及其相关要素。[方法]收集626例内镜诊断为慢性萎缩性胃炎患者为研究对象,统计内镜检查与病理学诊断的符合率。[结果]内镜诊断626例慢性萎缩性胃炎患者,其内镜与病理诊断的符合率为47.6%,胃体和胃角萎缩的检出率比胃窦低,但肠化的检出率比胃窦高;取材数量1块的胃镜符合率为27.27%,2块胃镜符合率为45.61%,≥3块胃镜符合率为62.34%。[结论]内镜诊断CAG的符合率较低;建议取≥3块活检数,更多的活检数能提高诊断的准确性。     

智能分光染色放大内镜在胃平坦型病变诊断中的应用价值

目的:对胃平坦型病变进行富士能智能分光染色内镜(Fujinon intelligent chromoendoscopy,FICE)放大内镜观察,对比FICE放大内镜与病理检查的一致性,探讨FICE放大内镜在胃平坦型病变诊断中的应用价值.方法:2012-09/2014-08对江汉大学附属医院发现的248个胃黏膜平坦性病变进行富士能FICE放大内镜检查.在FICE及放大模式观察病灶腺管开口与毛细血管形态,对其形态进行分型,并结合整体内镜下表现预测病理诊断.将FICE放大内镜下的内镜判定结果与病理组织学结果进行对比,评价其一致性与关联性.FICE内镜与病理诊断的一致性评价采用Kappa检验.结果:萎缩在FICE内镜下主要表现为C、D、E型胃小凹形态;肠上皮化生在F I C E内镜下主要表现为D、E型胃小凹形态;高级别上皮内瘤变及早期癌在FICE内镜下主要表现为E、F型胃小凹形态.FICE放大内镜技术判定萎缩、肠上皮化生、异型增生及早期癌的结果与病理诊断的结果具有较好的一致性.结论:FICE放大内镜技术有助于对病变性质如炎症、萎缩、肠上皮化生、上皮内瘤变及早期癌等的判断,有较好的临床应用价值.     

胃黏膜萎缩胃小区形态变化的可视性研究

慢性萎缩性胃炎是以胃黏膜固有腺体的萎缩为基础的一系列慢性炎症过程。可表现为黏膜固有腺体萎缩,全层变薄,或表现为上皮、腺体、黏膜肌及淋巴滤泡的代偿性增生使黏膜变厚。胃小区的微细结构——胃小凹的形态变化,可引起胃小区形态结构的改变。据此,我们通过内镜直视下观察胃小区形态结构的变化以诊断胃黏膜萎缩及肠化,结果如下。     

幽门螺杆菌相关性萎缩性胃炎酸分泌与杆菌定植的关系

目的研究胃酸分泌和粘膜萎缩对胃体和胃窦幽门螺杆菌（ Hp）定植的影响。方法将 95例 Hp阳性的慢性萎缩性胃炎患者分组。组一：胃窦中度萎缩伴胃体轻、中或重度萎缩性胃炎;组二：胃体轻度萎缩伴胃窦轻、中或重度萎缩性胃炎。分别测定基础酸分泌、最大酸分泌和胃泌素, Warthin-Starry染色诊断 Hp,同一组织诊断萎缩并分度。内因子抗体阳性者除外。结果组一中胃窦萎缩固定不变的各组之间,酸分泌显著降低组胃窦部 Hp定植率显著降低（ P< 0.05）;组一中胃体萎缩中度与重度组比较,最大酸分泌差异无统计学意义 (P >0.05),胃体重度萎缩组 Hp定植率较中度萎缩组明显低下 (P< 0.05)。组二中胃体萎缩固定不变的各组之间,酸分泌显著降低组胃体 Hp定植率显著降低 (P< 0.05);组二中胃窦萎缩中度与重度组比较,基础酸、最大酸分泌差异无统计学意义 (P >0.05),胃窦重度萎缩组 Hp定植率较中度萎缩组明显低下（ P< 0.05）。结论慢性萎缩性胃炎的低酸和萎缩明显影响胃窦、体部 Hp的定植,两种影响因素既独立又互补。     

胃黏膜萎缩、肠上皮化生及异型增生的放大内镜表现及其诊断价值

目的 确定胃黏膜萎缩、肠上皮化生及异型增生的形态学特征，探讨放大内镜结合染色对上述病变诊断的可行性和准确性。方法 应用Fujinon EG485 ZH型放大内镜对100例患者进行检查及0．5％美蓝染色，在确定A、B、C、D、E 5型基本胃小凹形态的基础上，制订放大内镜的诊断分型及放大内镜对萎缩、肠上皮化生和异型增生的判定标准，与相应部位活检所获得的417个病变组织的病理组织学检查结果进行比较分析。结果 胃黏膜萎缩主要表现为胃小凹粗大而分布稀疏，肠上皮化生表现为C、D、E型小凹形态伴美蓝着色阳性，异犁增生表现为轻度凹陷、隆起或平坦性病变伴细微结构消失、细微小凹或细微结构粗糙紊乱放大内镜对萎缩诊断的敏感性、特异性分别为95．85％和95．09％；对肠上皮化生分别为88．30％和90．83％；对异型增生分别为91．52％和94．41％，均明显高于普通内镜。结论 根据放大内镜下萎缩、肠上皮化生和异型增生的形态学特征可以使内镜对上述病变诊断的准确性明显提高。     

胃体溃疡性病变的内镜鉴别诊断探讨

溃疡性病变的性质不同,其治疗方法及预后亦不同。本文分析了我院近年来经内镜检查发现的直径<1cm 的胃体溃疡性病变124例,以探讨胃体良恶性溃疡性病变的内镜鉴别诊断。     

进镜胃体反转法在胃底间质瘤治疗中的应用(含视频)

为评价进镜胃体反转法在胃底间质瘤治疗中的应用价值, 前瞻性纳入2020年6月—2021年6月在中国医科大学附属第四医院消化内镜科经胃镜及超声内镜诊断的胃底固有肌层间质瘤患者进行本次研究。所有患者在气管插管全麻下进行内镜全层切除术治疗, 记录进镜胃体反转法成功情况、内镜手术情况、操控性能评价、病理类型及并发症等相关信息。共入组患者12例, 术后病理均证实为间质瘤, 极低危险度10例, 低危险度2例。进镜胃体反转法成功9例, 失败3例, 最终内镜手术成功9例。所有患者未发生术中出血。内镜切除过程中, 内镜同向进退功能、内镜视野及镜身稳定性评分均为2.00分。进镜胃体反转法在内镜治疗胃底间质瘤方面具有一定的临床应用价值。     

窄带成像放大内镜下胃小凹形态观察的临床价值

目的探讨窄带成像放大内镜(NBI)技术下胃小凹的形态分型及其临床价值。方法应用窄带成像放大内镜技术对113例患者进行检查,观察胃小凹形态,并于各不同形态处行活组织检查。结果 A、B型胃小凹主要见于慢性浅表性胃炎,C、D、E型胃小凹主要见于慢性萎缩性胃炎,D、E型胃小凹与肠上皮化生及异型增生密切相关。结论通过窄带成像放大内镜对5种胃小凹的形态观察可以推测病理组织学诊断,使镜下准确诊断胃黏膜萎缩、肠上皮化生及异型增生成为可能,以指导正确的治疗方法及内镜下随诊。     

Improvement of gastric atrophy after Helicobacter pylori eradication therapy

BACKGROUND: It remains controversial whether gastric atrophy is reversible after Helicobacter pylori eradication therapy. AIM: To clarify whether gastric atrophy improves after H. pylori eradication therapy using a histologic approach. METHODS: Subjects were 87 H. pylori infection-cured patients (treatment group) and 29 continuously H. pylori-infected patients (control group). The subjects in the treatment and control groups were followed for 10-49 months (mean, 22 months) and 11-50 months (mean, 22 months), respectively. Biopsy specimens were obtained from the greater curvature of the antrum and corpus at the beginning and end of the observation period; histologic analyses of these specimens were performed for detection of activity, inflammation, atrophy, and intestinal metaplasia. Results were scored without any clinical information according to the Sydney system. RESULTS: In the treatment group, the histologic score for atrophy was improved in the corpus but not in the antrum. Intestinal metaplasia was not improved in either the antrum or the corpus. There were no significant differences during the follow-up in gastric atrophy and intestinal metaplasia in the control group. CONCLUSION: Gastric atrophy was improved in the corpus approximately 2 years after H. pylori eradication therapy.     

Distribution of atrophy in Helicobacter pylori-infected subjects taking proton pump inhibitors

BACKGROUND: Gastric atrophy is associated with Helicobacter pylori infection. Conflicting results have been obtained as to whether acid suppressant therapy hastens the development or changes the distribution of atrophy in the stomach. The aim of this study was to investigate whether concomitant proton pump inhibitor (PPI) therapy in H. pylori-infected individuals resulted in an increase or an alteration in atrophy distribution and whether this was reflected by the plasma gastrin. METHODS: Multiple gastric biopsy specimens were taken from the antrum and corpus from 46 H. pylori-infected subjects, 18 of whom were taking PPIs, and assessed histologically by the updated Sydney System. The control group was age- and sex-matched to the index group. Fasting gastrin levels were measured. RESULTS: In the control group there was no significant tendency for either antral or corpus atrophy to predominate (P = 0.44). In the treatment group there was a significant tendency for corpus as opposed to antral atrophy to develop (P < 0.001). There was no significant difference in the overall atrophy score between the treated and untreated groups (P = 0.76). Fasting gastrin levels were significantly higher in the treated group (P < 0.001). CONCLUSIONS: Treatment with PPIs in H. pylori-infected subjects does not lead to an overall increase in gastric atrophy. It does, however, result in an increased prevalence of corpus as opposed to antral atrophy. This is associated with a significantly higher gastrin level.     

GASTRIC CANCER DETECTED AFTER HELICOBACTER PYLORI ERADICATION

Background: Helicobacter pylori is associated with progression to gastric cancer. However, it is still unclear whether eradication therapy can prevent the development of gastric cancer. Methods: Subjects were 242 patients in whom success in eradication of Helicobacter pylori had been continuous for more than 3 years. Clinical, endoscopic and histological findings were compared retrospectively between those who developed gastric cancer (cancer group) and those who did not (non‐cancer group). Clinical features of each cancer case were also evaluated. Results: Gastric cancer was found in six of the 242 subjects (2.5%) during a mean follow‐up period of 4.6 years (range: 3.0–7.0). The mean age of the cancer group tended to be higher than that of the non‐cancer group. Endoscopy revealed a more severe grade of gastric corpus atrophy in the cancer group, and histological findings showed that the degree of intestinal metaplasia in the upper corpus was higher in the cancer group. Four of the six cancers were located in the gastric antrum. All were early cancers and five were of 0‐IIc type endoscopically. All were intestinal type histologically. Conclusions: Gastric cancer was discovered at a rate of 2.5% during the mean follow‐up period of 4.6 years after H. pylori eradication. Careful endoscopic follow up is necessary even after successful eradication, especially in cases characterized by an endoscopically high grade of gastric atrophy and pathologically severe intestinal metaplasia at the upper corpus.     

Is screening for and surveillance of atrophic gastritis advisable?

Gastric cancer remains a leading cause of cancer-related deaths in many parts of the world. At present, prevention seems to be the most effective means to reduce its the incidence and mortality rate. Gastric atrophy is considered the first relevant step in the histogenesis of gastric adenocarcinoma. However, whether screening for and surveillance of atrophic gastritis is advisable is debated. The prevalence and pattern of chronic atrophic gastritis varies greatly from country to country, being higher and mainly diffuse pangastritis or localized in those countries with a high gastric cancer incidence. The only method available to detect gastric atrophy is histopathological examination of endoscopic specimens, but there is no consensus about diagnosis. Serum gastric secretion may be a marker of gastric atrophy, although it has high specificity but low sensitivity. Gastric atrophy is mainly related to chronic Helicobacter pylori (H. pylori) infection. Thus, the only effective strategy for gastric cancer prevention is eradication of H. pylori infection to arrest atrophy progression in selected populations. In conclusion, there is insufficient evidence to suggest screening for and surveillance of atrophic gastritis in the general population; however, this strategy should be applied in countries with a high incidence of gastric cancer.     

Distribution of Atrophy in Helicobacter pylori-Infected Subjects Taking Proton Pump Inhibitors

Background: Gastric atrophy is associated with Helicobacter pylori infection. Conflicting results have been obtained as to whether acid suppressant therapy hastens the development or changes the distribution of atrophy in the stomach. The aim of this study was to investigate whether concomitant proton pump inhibitor (PPI) therapy in H. pylori-infected individuals resulted in an increase or an alteration in atrophy distribution and whether this was reflected by the plasma gastrin. Methods: Multiple gastric biopsy specimens were taken from the antrum and corpus from 46 H. pylori-infected subjects, 18 of whom were taking PPIs, and assessed histologically by the updated Sydney System. The control group was age- and sex-matched to the index group. Fasting gastrin levels were measured. Results: In the control group there was no significant tendency for either antral or corpus atrophy to predominate (P = 0.44). In the treatment group there was a significant tendency for corpus as opposed to antral atrophy to develop (P &lt; 0.001). There was no significant difference in the overall atrophy score between the treated and untreated groups (P = 0.76). Fasting gastrin levels were significantly higher in the treated group (P &lt; 0.001). Conclusions: Treatment with PPIs in H. pylori-infected subjects does not lead to an overall increase in gastric atrophy. It does, however, result in an increased prevalence of corpus as opposed to antral atrophy. This is associated with a significantly higher gastrin level.     

Frequent and rapid progression of atrophy and intestinal metaplasia in gastric mucosa of patients with MALT lymphoma

OBJECTIVES: Association of gastric mucosa-associated lymphoid tissue (MALT) low-grade lymphoma and adenocarcinoma has repeatedly been reported. The aim of this study was to evaluate the frequency and the spreading of atrophy and intestinal metaplasia in gastric mucosa of patients with gastric MALT lymphoma followed after conservative treatment. METHODS: Forty-five patients (mean age 45 +/- 2.1 yr) with gastric MALT lymphoma, treated by Helicobacter pylori eradication, chemotherapy with per os single alkylating agents, or both treatments have been followed by gastroscopy with biopsies in antrum and corpus at least once a year. Univariate and multivariate analysis evaluated the association between the appearance of atrophy and intestinal metaplasia in antrum or corpus and different factors related to patients, H. pylori status, lymphoma features, and treatment. In addition, histological aspects of gastric biopsies at the diagnosis period and at the end of follow-up were compared with those of two control groups of age-matched patients with H. pylori gastritis. RESULTS: At the diagnosis time, only intestinal metaplasia in corpus was more frequent in patients with gastric MALT lymphoma than in patients with nonulcer dyspepsia. Within median follow-up of 54.4 months (range 9-196), the percentage of patients with gastric atrophy and intestinal metaplasia increased significantly and became significantly higher than in age-matched nonulcer dyspepsia patients. Multivariate analysis showed significant association between corpus intestinal metaplasia and corpus atrophy, intestinal metaplasia in antrum, and duration of the follow-up. CONCLUSIONS: Conservative management of gastric MALT lymphoma including H. pylori eradication is associated with progression of gastric atrophy and intestinal metaplasia with frequent involvement of the corpus which is known to be a precancerous condition. These findings show that long-term endoscopic monitoring should be recommended in such patients.     

Helicobacter pylori infection as a risk factor for gastric ulceration

BACKGROUND/AIMS: Recent reports have shown that Helicobacter pylori infection is closely related to pathogenesis of gastric ulcers. But there have been no reports on the prospective follow-up study of the patients with H. pylori infection to determine whether H. pylori infection puts patients at high risk of developing gastric ulcers. METHODOLOGY: Fifty-two patients with H. pylori infection and 34 patients without H. pylori infection, who were found endoscopically not to have localized lesions in the esophagus, stomach, or duodenum, underwent endoscopy follow-ups during the average observation period of 52 months. During each endoscopy, biopsy specimens were obtained from the antrum and the middle corpus. The grade of atrophy and intestinal metaplasia in the biopsy specimens were assessed histologically in accordance with the guidelines of the Updated Sydney System. RESULTS: Gastric ulcers developed in 8 (15%) of 52 patients with H. pylori infection, but not in patients without H. pylori infection: the difference was statistically significant (P<0.05). The development and the location of gastric ulcers was correlated to the development or progression of mucosal atrophy. In 8 (38%) of 21 patients in whom mucosal atrophy developed or progressed, gastric ulcers developed, but no ulcers developed in 31 patients without development or progression of gastric mucosal atrophy. Gastric ulcers developed in the gastric mucosa in which atrophy developed or progressed. CONCLUSIONS: H. pylori infection increases the risk for development of gastric ulcers and gastric ulcers developed through the progression of H. pylori-associated gastric mucosal atrophy.     

Helicobacter pylori in gastric corpus of patients 20 years after partial gastric resection

AIM: To determine the long-term prevalence of Helicobacter pylori (H pylori) gastritis in patients after partial gastric resection due to peptic ulcer, and to compare the severity of H pylori-positive gastritis in the corpus mucosa between partial gastrectomy patients and matched controls. METHODS: Endoscopic biopsies were obtained from 57 patients after partial gastric resection for histological examination using hematoxylin/eosin and Warthin-Starry staining. Gastritis was graded according to the updated Sydney system. Severity of corpus gastritis was compared between H pylori-positive partial gastrectomy patients and H pylori-positive duodenal ulcer patients matched for age and gender. RESULTS: In partial gastrectomy patients, surgery was performed 20 years (median) prior to evaluation. In 25 patients (43.8%) H pylori was detected histologically in the gastric remnant. Gastric atrophy was more common in H pylori-positive compared to H pylori-negative partial gastrectomy patients (P<0.05). The severity of corpus gastritis was significantly lower in H pylori-positive partial gastrectomy patients compared to duodenal ulcer patients (P<0.01). There were no significant differences in the activity of gastritis, atrophy and intestinal metaplasia between the two groups. CONCLUSION: The long-term prevalence of H pylori gastritis in the gastric corpus of patients who underwent partial gastric resection due to peptic ulcer disease is comparable to the general population. The expression of H pylori gastritis in the gastric remnant does not resemble the gastric cancer phenotype.     

消化性溃疡中胃粘膜病变的特点分析

分析４９１例消化性溃疡伴随胃溃膜病变的特点。结果：性别年龄因素对病变发生率无影响。粘膜炎症较之萎缩和溃疡关系更密切。十二指溃肥广泛粘膜炎症及体部慢性轻度炎症为特点；胃溃疡以广泛萎缩，窦部重度萎缩及重度慢性活动性炎症为特点。两者粘膜病变特点和现有关于两者发病机理的认识相吻合。     

Helicobacter pyloriin gastric corpus of patients 20 years after partial gastric resection

AIM:To determine the long-term prevalence of Helicobacterpylori(H pylori)gastritis in patients after partial gastricresection due to peptic ulcer,and to compare the severityof Hpylori-positive gastritis in the corpus mucosa betweenpartial gastrectomy patients and matched controls.METHODS:Endoscopic biopsies were obtained from 57patients after partial gastric resection for histologicalexamination using hematoxylin/eosin and Warthin-Starrystaining.Gastritis was graded according to the updatedSydney system.Severity of corpus gastritis was comparedbetween Hpylori-positive partial gastrectomy patients andHpylori-positive duodenal ulcer patients matched for ageand gender.RESULTS:In partial gastrectomy patients,surgery wasperformed 20 years(median)prior to evaluation.In 25patients(43.8%)Hpyloriwas detected histologically inthe gastric remnant.Gastric atrophy was more common inH pylori-positive compared to H pylori-negative partialgastrectomy patients(P<0.05).The severity of corpusgastritis was significantly lower in Hpylori-positive partialgastrectomy patients compared to duodenal ulcer patients(P<0.01).There were no significant differences in theactivity of gastritis,atrophy and intestinal metaplasiabetween the two groups.CONCLUSION:The long-term prevalence of Hpylorigastritisin the gastric corpus of patients who underwent partialgastric resection due to peptic ulcer disease is comparableto the general population.The expression of Hpylorigastritisin the gastric remnant does not resemble the gastric cancerphenotype.