312例胃底腺息肉临床及病理分析

目的探讨胃底腺息肉(fundic gland polyp,FGP)患者的临床及病理特点。方法回顾性分析312例FGP患者临床资料,包括临床表现、组织病理特点和幽门螺旋杆菌感染情况。结果 312例FGP中男女比例为1∶1.89,其中149例有长期服用质子泵抑制剂药物史;患者临床表现无明显特异性,病变主要分布于胃体及胃底,形态多为山田Ⅱ型,病变直径多为0.2~0.5cm,单发息肉占52.88%;组织病理学示胃腺体大量增生,壁细胞及主细胞增生,胃小凹短浅或缺如,偶伴黏膜急慢性炎症,被覆上皮及腺上皮细胞未见肠化及异型增生表现;幽门螺旋杆菌感染率为19.55%(61/312)。结论 FGP多见于女性,其发生可能与长期口服质子泵抑制剂有关,与幽门螺旋杆菌感染无明显相关性;胃底及胃体病变以山田Ⅱ型为主,胃体腺大量增生为其主要组织病理特点。     

365例胃息肉的临床特点分析

目的 分析不同组织学类型胃息肉的临床特点.方法 根据组织学不同,将胃息肉分为胃底腺息肉、增生性息肉、炎性息肉、腺瘤性息肉等,比较各型胃息肉在发病部位、幽门螺杆菌(Hp)感染、质子泵抑制剂(PPI)与胃息肉发生的关系等方面的异同,从而指导治疗.结果 10 197例接受胃镜检查的患者中检出胃息肉365例,检出率为3.6%.胃息肉的组织学类型依次为胃底腺息肉(61.1%),增生性息肉(23.3%),炎性息肉(12.3%),腺瘤性息肉(2.2%).289例(79.2%)为单发性息肉,各型胃息肉均以单发为主.胃息肉主要分布在胃体和底部,其次是胃窦和贲门.胃底腺息肉绝大多数分布在胃体和底部;增生性和腺瘤性息肉以胃窦部为主;炎性息肉以贲门、胃体和底部为主.胃底腺息肉患者应用PPI的比例较高(51.6%),与增生性息肉(8.2%)和炎性息肉(8.9%)患者比较,差异均有统计学意义(x2值分别为48.31、27.63,P均<0.01).增生性和炎性息肉的Hp感染率分别为72.4%和74.4%,均高于胃底腺息肉(20.2%)(X2值分别为46.50、35.04,P均<0.01).根除Hp后1年随诊,增生性息肉和炎性息肉再发病例明显降低[2.4%(1/41)和0(0/19)].结论 胃息肉的组织学类型以胃底腺息肉为最常见,其次为增生性息肉.胃息肉主要分布在胃体和底部,其次是胃窦和贲门.不同类型胃息肉在胃内的分布有一定的特点.长期应用PPI有发生胃底腺息肉的风险.增生性息肉和炎性息内的发生可能与Hp感染有关,根除Hp后可能有助于预防这两型胃息肉的再发.     

365例胃息肉的临床特点分析

目的 分析不同组织学类型胃息肉的临床特点.方法 根据组织学不同,将胃息肉分为胃底腺息肉、增生性息肉、炎性息肉、腺瘤性息肉等,比较各型胃息肉在发病部位、幽门螺杆菌(Hp)感染、质子泵抑制剂(PPI)与胃息肉发生的关系等方面的异同,从而指导治疗.结果 10 197例接受胃镜检查的患者中检出胃息肉365例,检出率为3.6%.胃息肉的组织学类型依次为胃底腺息肉(61.1%),增生性息肉(23.3%),炎性息肉(12.3%),腺瘤性息肉(2.2%).289例(79.2%)为单发性息肉,各型胃息肉均以单发为主.胃息肉主要分布在胃体和底部,其次是胃窦和贲门.胃底腺息肉绝大多数分布在胃体和底部;增生性和腺瘤性息肉以胃窦部为主;炎性息肉以贲门、胃体和底部为主.胃底腺息肉患者应用PPI的比例较高(51.6%),与增生性息肉(8.2%)和炎性息肉(8.9%)患者比较,差异均有统计学意义(x2值分别为48.31、27.63,P均<0.01).增生性和炎性息肉的Hp感染率分别为72.4%和74.4%,均高于胃底腺息肉(20.2%)(X2值分别为46.50、35.04,P均<0.01).根除Hp后1年随诊,增生性息肉和炎性息肉再发病例明显降低[2.4%(1/41)和0(0/19)].结论 胃息肉的组织学类型以胃底腺息肉为最常见,其次为增生性息肉.胃息肉主要分布在胃体和底部,其次是胃窦和贲门.不同类型胃息肉在胃内的分布有一定的特点.长期应用PPI有发生胃底腺息肉的风险.增生性息肉和炎性息内的发生可能与Hp感染有关,根除Hp后可能有助于预防这两型胃息肉的再发.     

365例胃息肉的临床特点分析

目的 分析不同组织学类型胃息肉的临床特点.方法 根据组织学不同,将胃息肉分为胃底腺息肉、增生性息肉、炎性息肉、腺瘤性息肉等,比较各型胃息肉在发病部位、幽门螺杆菌(Hp)感染、质子泵抑制剂(PPI)与胃息肉发生的关系等方面的异同,从而指导治疗.结果 10 197例接受胃镜检查的患者中检出胃息肉365例,检出率为3.6%.胃息肉的组织学类型依次为胃底腺息肉(61.1%),增生性息肉(23.3%),炎性息肉(12.3%),腺瘤性息肉(2.2%).289例(79.2%)为单发性息肉,各型胃息肉均以单发为主.胃息肉主要分布在胃体和底部,其次是胃窦和贲门.胃底腺息肉绝大多数分布在胃体和底部;增生性和腺瘤性息肉以胃窦部为主;炎性息肉以贲门、胃体和底部为主.胃底腺息肉患者应用PPI的比例较高(51.6%),与增生性息肉(8.2%)和炎性息肉(8.9%)患者比较,差异均有统计学意义(x2值分别为48.31、27.63,P均<0.01).增生性和炎性息肉的Hp感染率分别为72.4%和74.4%,均高于胃底腺息肉(20.2%)(X2值分别为46.50、35.04,P均<0.01).根除Hp后1年随诊,增生性息肉和炎性息肉再发病例明显降低[2.4%(1/41)和0(0/19)].结论 胃息肉的组织学类型以胃底腺息肉为最常见,其次为增生性息肉.胃息肉主要分布在胃体和底部,其次是胃窦和贲门.不同类型胃息肉在胃内的分布有一定的特点.长期应用PPI有发生胃底腺息肉的风险.增生性息肉和炎性息内的发生可能与Hp感染有关,根除Hp后可能有助于预防这两型胃息肉的再发.     

胃增生性息肉和胃底腺息肉患者血清胃功能指标及幽门螺杆菌感染情况的分析

目的分析比较胃增生性息肉和胃底腺息肉患者血清胃功能指标及幽门螺杆菌(Helicobacter pylori,Hp)感染情况.方法选取2017年12月至2018年12月于徐州医科大学附属医院行胃镜检查发现胃息肉且病理证实为胃增生性息肉和胃底腺息肉患者135例,其中增生性息肉组68例,胃底腺息肉组67例.采用免疫印迹法对两组患者血清Hp抗体[尿素酶A(urease A,UreA)、尿素酶B(urease B,Ure B)、细胞毒素相关蛋白(cytotoxin associated gene A, CagA)、空泡细胞毒素(vacuolating cytotoxin,VacA)]进行定性检测.选取慢性浅表性胃炎80例为对照组.酶联免疫吸附(enzymelinkedimmunosorbent assey,ELISA)法检测3组血清胃功能指标[胃蛋白酶原(pepsinogen,PG)Ⅰ、PG-Ⅱ、胃泌素-17(gastrin,G-17)],并计算PGⅠ、PGⅡ比值(PGⅠ and PGⅡ ratio,PGR).结果胃增生性息肉组血清PGⅡ(13.13(8.15,20.30)μg /L)、G17(8.44(3.72,27.17)pmol/L)水平高于对照组(9.16(5.56,15.14)μg /L与1.83(0.87,5.95)pmol/L)(P均<0.05),PGR水平低于对照组(P<0.05);胃底腺息肉组血清PGⅠ(120.12(86.72,174.70)μg /L)、PGⅡ(11.92(7.27,22.26)μg/L)、G17(5.68(1.79,14.65)pmol/L)水平高于对照组(101.32(79.17,131.33)μg /L、9.16(5.56,15.14)μg /L、1.83(0.87,5.95)pmol/L)(P 均<0.05);胃增生性息肉组血清 G17 (8.44 (3.72, 27.17)pmol/L)水平高于胃底腺息肉组(5.68(1.79,14.65)pmol/L)(P<0.05);胃增生性息肉组Hp感染率61.76%(42/68)高于胃底腺息肉组40.30%(27/67)(P<0.05),且以Ⅰ型Hp为主(P<0.05);胃增生性息肉组Hp阳性者血清PGⅡ、G17水平均高于Hp阴性者(P均<0.05);胃底腺息肉组Hp阳性与阴性者血清PGⅠ、PGⅡ、G17、PGR水平比较差异无统计学意义;胃增生性息肉组Hp Ⅰ型者血清PGⅠ、PGR水平高于Hp Ⅱ型者(P<0.05),胃底腺息肉组Hp Ⅰ型血清PGⅠ、PGⅡ、G17、PGR水平与Ⅱ型比较差异无统计学意义.结论胃增生性息肉、胃底腺息肉患者血清PG、G17水平高于慢性浅表性胃炎患者,胃增生性息肉患者较胃底腺息肉患者Hp感染率高且胃功能指标存在异常.     

质子泵抑制剂联合促胃动力药治疗胃底食管反流性咳嗽26例临床观察

目的 观察质子泵抑制剂联合促胃动力药治疗胃底食管反流性咳嗽的临床疗效.方法 回顾性分析2010年10月至2011年10月方城县人民医院收治的26例胃底食管反流性咳嗽患者的临床资料,26例患者均应用质子泵抑制剂雷贝拉唑钠肠溶胶囊联合促胃动力制剂进行治疗,观察其支气管咳嗽评分和胃食管反流症状评分.结果 与治疗前比较,支气管咳嗽评分和胃食管反流症状评分较前降低,差异均有统计学意义(P＜0.01).结论 质子泵抑制剂联合促胃动力药治疗胃底食管反流性咳嗽疗效显著,值得临床推广.     

胃增生性息肉和胃底腺息肉临床特征对比分析

目的对比分析胃增生性息肉和胃底腺息肉的临床特征。方法选取内镜下取病理组织检查诊断为胃增生性息肉38例(A组)和胃底腺息肉59例(B组)患者临床资料行回顾性分析,比较两组患者性别,息肉直径、部位及幽门螺杆菌(HP)感染情况。结果 A组男性(22例)多于B组(20例),女性(16例)少于B组(39例);A组息肉好发于胃窦(18例),B组息肉好发于胃底(50例);A组HP感染(29例)多于B组(1例);A组息肉直径为(9.8±2.2)mm,B组为(7.1±1.3)mm,A组长于B组(P0.05)。结论胃增生性息肉好发于男性、胃窦部,胃底腺息肉好发于女性、胃底部,胃增生性息肉直径较胃底腺息肉大,胃增生性息肉发生与HP感染有相关性,临床可根据上述临床特征和差异进行初步预防、诊断。     

胃镜下胃息肉的临床病理分析

目的　了解胃镜下胃息肉的临床及病理特点。方法　对 2年间胃镜下胃息肉进行重新分型并对息肉本身的急、慢性炎症、癌前改变、癌变以及不同类型息肉与幽门螺杆菌 (helicobacterpylori,H .pylori)的关系进行分析。结果　胃镜下胃息肉的检出率为 3.0 % ( 2 5 0 / 8319) ,男性 1.6 % ( 71/ 4 4 4 8) ,女性 4 .6 % ( 179/ 3871) ;单发和多发息肉分别占 6 6 .8%和 33.2 % ,平均 ( 2 .2± 2 .9)枚 ;2 36例进入病理分析 ,胃底腺、增生性、腺瘤及炎性纤维性息肉分别占 2 8.0 % ,2 5 .0 % ,0 .8%和 0 .4 % ,有 4 5 .3%镜下息肉病理检查无息肉组织发现(组织学阴性息肉 ) ;胃底腺 ( 3.8± 4 .8)较增生性 ( 1.7± 1.4 )和组织学阴性息肉 ( 1.4± 1.0 )多发 ;胃底腺、增生性和组织学阴性息肉本身中度以上慢性炎症分别占 0 ,6 1.0 %和 5 4 .2 % ,有中性粒细胞浸润分别为 0 %、4 0 .7%和 31.8% ,萎缩分别占 0 ,8.5 %和 12 .1% ,肠化生分别为 1.5 % ,37.3%和 17.8% ,不典型增生分别占1.5 % ,8.5 %和 3.7% ,胃窦粘膜H .pylori检出率分别为 7.6 % ,2 0 .3%和 33.6 % ,未发现癌变改变 ;胃底腺息肉全部分布在底、体部 ,增生性息肉分布于全胃 ,组织学阴性息肉分布于全胃但以胃窦多见。结论　胃息肉的检出率较低 ,女性多见 ,单     

胃息肉与幽门螺旋杆菌感染关系分析

目的分析胃息肉与幽门螺旋杆菌感染关系。方法选取2012年1月~2014年6月我院收治的120例胃息肉患者。均行胃息肉病理检查与幽门螺杆菌(Hp)检查。结果 120例胃息肉患者的胃息肉分布情况为:53例位于胃窦、4例为胃角、28例为胃体,24例为胃底,11例为贲门。胃窦、胃角、胃体、胃底、贲门分布Hp感染率分别为30(56.6%)、2(50.0%)、10(35.7%)、7(29.2%)、4(36.6%);120例为息肉患者的胃息肉病理类型:77例为炎性,34例为增生性,6例为胃底腺,3例为腺瘤性息肉。炎性、增生性、胃底腺、腺瘤性息肉Hp感染率分别为38(49.3%)、14(41.2%)、0(0.0%)、1(33.3%)。炎性胃息肉、增生性息肉Hp感染率于胃窦、胃角与胃体、胃底、贲门差异具有统计学意义(P0.05)。结论幽门螺旋杆菌与胃息肉形成有关,因此在胃息肉治疗过程中对Hp检查与治疗具有重要临床意义。     

质子泵抑制剂对老年人磁控胶囊胃镜图像质量的影响

目的探讨应用质子泵抑制剂对老年人磁控胶囊胃镜（MCE）图像质量的影响。 方法回顾性分析2018年1月至2019年4月北京大学第一医院接受MCE检查的老年患者（≥60岁）临床资料,根据是否应用质子泵抑制剂分为2组,比较2组的胃视野清洁度、黏膜可视度、疾病检出率及不良反应事件情况。采用Mann-Whitney U检验比较MCE胃视野清洁度和黏膜可视度积分的组间差异,采用χ²检验或Fisher精确检验比较2组患者疾病检出率的差异。 结果共纳入93例患者[男性70例,中位年龄75.0（60~93）岁],未应用质子泵抑制剂组（N组）54例;应用质子泵抑制剂组（P组）39例。N组胃总体视野清洁度评分高于P组[22.0（6.0,23.0）分vs 19.5（11.0,23.0）分],差异具有统计学意义（Z=-3.186,P<0.001）。N组胃总体黏膜可视度评分高于P组[18.0（6.0,18.0）分vs 17.0（11.0,18.0）分],差异具有统计学意义（Z=-2.158,P=0.031）。N组患者的整体胃视野好于P组,尤其是胃底、胃体部视野更清晰。N组和P组胃部病变总检出率比较（57.4% vs 51.3%）,差异无统计学意义（χ²=0.343,P=0.558）。2组均未发生不良反应及胶囊滞留。 结论对于老年人群,应用质子泵抑制剂虽会影响MCE视野,但不影响病变检出率,MCE对老年人群是安全的检查选择。     

Gastric epithelial cell modality and proton pump inhibitor

Proton pump inhibitors (PPIs) are now commonly used for the treatment of acid related diseases such as peptic ulcer and reflux esophagitis. Because of their ability to produce direct inhibition of the proton pump, PPIs provide more sustained increase of the gastric pH than H(2)-receptor (H(2)R) antagonists. Diverse reports have been published on gastric epithelial cell modality associated with PPI treatment both in animal models and clinical settings. The present review summarizes the recent accumulated evidence on gastric epithelial cell modality associated with PPI treatment, including the formation of gastric carcinoid tumors and fundic gland polyps, and the development of gastric mucosal atrophy. Long-term PPI treatment has been reported to cause enlargement of the parietal cells and enterochromaffin-like cells, and to decrease the number of chief cells without affecting A-like cell. Although the development of gastric carcinoid tumors after chronic PPI treatment has been reported in animal studies, no such occurrences have been demonstrated in humans. The effect of PPIs on the formation of fundic gland polyps and the development of atrophic gastritis should be investigated in future studies.     

Une cause rare d’hémorragie digestive: la polypose gastrique induite par inhibiteur de la pompe à protons au long cours

Proton pump inhibitors are responsible with gastric polyps’ development. Generally asymptomatic, their proliferative and inflammatory properties may trigger a digestive hemorrhage.We report the rare case of a 73-year-old man treated by a long-term proton pump inhibitor for a gastro-esophageal reflux disease. Gastrointestinal bleeding and iron deficiency anemia require a gastroscopy which reveals diffuse glandulocystic and hyperplastic gastric polyps. After a polypectomy therapy failure, an argon plasma coagulation treatment of the most inflammatory polyps is processed. The proton pump inhibitor is stopped and the control gastroscopy done one month later does not find any inflammatory polyps.This case report is a chronic digestive hemorrhage due to gastric polyposis secondary long-term treatment by proton pump inhibitor.This case demonstrates the efficiency, the simplicity of a treatment by argon plasma coagulation compared to treatment by polypectomy. The case also shows the polyposis regression after stopping proton pump inhibitors and introducing a treatment by histamine H2-receptor antagonists.     

Serum chromogranin A as a screening test for gastric enterochromaffin-like cell hyperplasia during acid-suppressive therapy

BACKGROUND: Serum chromogranin A (CgA), a marker of neuroendocrine neoplasia, increases during profound gastric acid inhibition, possibly reflecting the trophic effect of gastrin on the enterochromaffin-like (ECL) cells. AIMS: This study investigated the clinical value of serum CgA as a screening test for gastric fundic enterochromaffin-like (ECL) cell hyperplasia during acid-suppressive therapy. METHOD: A consecutive series of 230 dyspeptic patients referred for upper gastrointestinal endoscopy was investigated in a cross-sectional design. They were 154 patients on continuous medium-term (6 weeks to one year) or long-term (longer than one year) acid inhibition with either proton pump inhibitors (PPIs, n = 117) or histamine2-receptor antagonists (H2RAs, n = 37) for gastro-oesophageal reflux disease, and 76 nontreated subjects, with normal endoscopic findings (control group). Fasting blood samples were analysed for gastrin and CgA. Gastric biopsy specimens (oxyntic mucosa) were examined for histological evaluation of gastritis (Sydney classification) and of ECL cell hyperplasia (Solcia classification). RESULTS: Serum CgA levels correlated positively with serum gastrin, following a quadratic function (r = 0.78, P < 0.0001). Elevated serum CgA values during long-term acid inhibition correlated with the presence and severity of fundic ECL cell hyperplasia. Multivariate analysis identified hypergastrinaemia (P < 0.0001), duration of acid inhibition (P < 0.0001), H. pylori infection (P = 0.008), ECL cell hyperplasia (P = 0.012), and body gland atrophy (P = 0.043) as independent predictors of elevated serum CgA. In subjects on long-term acid inhibition (n = 123), serum CgA was equally sensitive but more specific than serum gastrin for the detection of ECL cell hyperplasia (sensitivity, 91.3% for both; specificity, 73% vs. 43%, P < 0.0001). CONCLUSIONS: During long-term gastric acid inhibition, serum CgA levels reflect the presence and severity of fundic ECL cell hyperplasia. Serum CgA is therefore a useful screening test for gastric ECL cell proliferative changes within this context.     

The effect of iodoacetamide-induced fundic ulcers on gastric carcinogenesis produced by N-methyl-N'-nitro-N-nitrosoguanidine in rats

This study was undertaken to determine the effect of ulcer induced by iodoacetamide on the development of gastric carcinoma by N-methyl-N'-nitro-N-nitrosoguanidine in male Wistar rats. Fifty-six of the 62 ulcers induced by IAM were located in the fundic gland area along the limiting ridge. The incidence of fundic carcinoma was 16% in the groups treated with IAM and MNNG, while no fundic carcinoma was found in the group treated with MNNG alone. This difference was statistically significant. All the carcinomas in the fundic gland area were confined within the ulcer itself or its scar tissue, produced by IAM. These findings indicate that if an ulcer is present, carcinoma develops even in the fundic mucosa which is, if intact, resistant to the carcinogenic stimulation of MNNG. It was concluded that gastric ulcer predisposes the development of gastric carcinoma.     

Changes in the rat stomach after long-term administration of proton pump inhibitors (AG-1749 and E-3810)]

E-3810 and AG-1749, new proton pump inhibitors, were administrated in single doses or over a long period of time in order to evaluate their effect on the rat stomach. E-3810 inhibited gastric acid secretion for a shorter period of time than AG-1749 in both the single dose and long-term administration. While hypergastrinemia persisted with long-term administration of AG-1749, serum gastrin levels returned to normal upon cessation of treatment with E-3810. Both E-3810 and AG-1749 caused vacuolar formation of parietal cells and an increase in gastric acid secretion after cessation of long-term treatment, suggesting that these changes are common after treatment with proton pump inhibitors.     

Gastric hamartomatous polyp without polyposis coli: Radiologic diagnosis

Gastric hamartomatous polyps were found in 25 patients over a period of 4 1/2 years, for an incidence of 11% in all endoscopically biopsied polyps. The number of polyps was fewer than 5 in most patients. All polyps were sessile, sharply demarcated, hemispheric protrusions, measuring up to 10 mm in diameter but most were less than 5 mm. The most characteristic finding differing from hyperplastic polyps, adenoma, and polypoid carcinoma was that hamartomatous polyps were located in the fundic gland mucosa, which was demonstrated as a rugal area on moderately distended double-contrast radiographs.     

Overuse of proton pump inhibitors

BACKGROUND: There have been concerns raised about the potential adverse effects of proton pump inhibitors, especially with long-term use. In particular, their potent action can suppress the features and delay the diagnosis of gastric cancer, while prolonged exposure may hasten the development of gastric carcinoids. AIM: To examine the use of proton pump inhibitors in patients at the major teaching hospital in Tasmania, Australia, principally to determine the appropriateness of the therapy according to published guidelines. METHODS: A retrospective review of the medical records of all patients prescribed any of the proton pump inhibitors at the hospital over a 7-month period, was performed. An extensive range of demographic and clinical variables was recorded for each patient. The patients were also asked a series of questions during their hospitalization to extract some of the relevant information - in particular, if and when they had undergone endoscopy. RESULTS: The 200 patients (52% males) had a mean age of 69 +/- 16.4 years. The most common indications for using proton pump inhibitors were acute gastrointestinal bleeding (20.9%), severe refractory ulcerating oesophagitis (17.3%), mild/moderate oesophageal reflux (17.3%) and refractory peptic ulcer (11.7%). A large number of patients were using a proton pump inhibitor for 'other' indications (39.6%). The prescribing of proton pump inhibitors satisfied the approved indications, as outlined in the Australian Schedule of Pharmaceutical Benefits, in only 37.1% of cases. Endoscopy had been performed in 54.1% of patients prior to commencing therapy with a proton pump inhibitor and within the next 7 days in another 12.8% of patients. Only 59% of patients had previously been treated with an H2-receptor antagonist before commencing therapy with a proton pump inhibitor. Even worse, only 58.5% of patients had used an H2-receptor antagonist before a proton pump inhibitor for mild/moderate oesophagitis. The median duration of proton pump inhibitor therapy for patients admitted to the hospital and already receiving one of the drugs was 450 days. Over half of the patients were being concurrently treated with other drugs which are known to cause or exacerbate gastro-oesophageal disease, and 18% were smokers. CONCLUSION: Whereas the proton pump inhibitors are undoubtedly effective agents, studies of their prescribing in practice consistently suggest over-use prior to endoscopy, use in patients who do not fit the approved criteria, and prescribing for indications in which 'less powerful' agents should have been sufficiently effective for the patient's symptoms. This poses economic and safety concerns, particularly in light of the suggestion that these drugs could delay the diagnosis of gastric cancer.