Hyperplastic polyps of the esophagus and esophagogastric junction: histologic and clinicopathologic findings.

Hyperplastic polyps of the esophagus and esophagogastric junction region (EGJ) are uncommon lesions characterized by hyperplastic epithelium (foveolar-type, squamous, or both) with variable amounts of inflamed stroma. They have been reported almost exclusively in the radiologic and clinical literature as occurring predominantly in association with gastroesophageal reflux disease (GERD). Comprehensive histologic and clinicopathologic evaluation of these polyps, their association with background mucosal pathology, and their association with Barrett's esophagus has not been previously performed. We studied 30 hyperplastic polyps from 27 patients and characterized the histologic, endoscopic, and clinical features of both the polyps and the background esophagus. Hyperplastic polyps were most common in the region of the EGJ (67%), followed by the distal esophagus (30%) and mid-esophagus (3%). Most (80%) were composed of predominantly cardiac-type mucosa, predominantly squamous mucosa (17%), or an admixture (3%). Intestinal metaplasia of the polyp was present in only 7% and low-grade dysplasia in only 3%. In the majority of cases (67%) hyperplastic polyps were associated with concurrent or recent ulcers or erosive esophagitis. In most cases (48%) esophageal injury was associated with GERD, but other potential etiologies included medications, infection, anastomotic or polypectomy sites, vomiting, and photodynamic therapy. Four patients (15%) had Barrett's esophagus, three of whom had or developed dysplastic Barrett's mucosa. These results underscore the pathogenesis of esophageal/EGJ region hyperplastic polyps as a mucosal regenerative response to surrounding mucosal injury. Careful clinical history and biopsy of the nonpolypoid mucosa are essential for determining the clinicopathologic context in which the polyps have developed.     

Gastric adenomas: intestinal-type and gastric-type adenomas differ in the risk of adenocarcinoma and presence of background mucosal pathology

Gastric adenomas are neoplastic growths characterized by localized, polypoid proliferations of dysplastic epithelium. They frequently arise in stomachs with a background of mucosal atrophy and intestinal metaplasia, and a higher risk of adenocarcinoma elsewhere in the stomach has been reported in patients with gastric adenomas. Additionally, some gastric adenomas themselves demonstrate neoplastic progression to infiltrating adenocarcinoma. However, previous studies have not comprehensively evaluated the background gastric mucosa and risk of adenocarcinoma, particularly in relation to the histologic classification of adenomas as either intestinal-type or gastric-type. We studied 61 gastric adenomas from 51 patients between 1985 and 2001. The adenomas were classified as intestinal-type (containing at least focal goblet cells and/or Paneth cells), gastric-type (lined entirely by gastric mucin cells on PAS/alcian blue stain), or indeterminate. We evaluated the histologic features of both the adenomas (location, multiplicity, degree of dysplasia, presence of adenocarcinoma within the polyp) and the surrounding gastric mucosa (presence of gastritis, intestinal metaplasia, and adenocarcinoma). Gastric adenomas were distributed equally throughout the stomach, were most frequently solitary (82%), and contained adenocarcinoma in nine cases (14.8%). There were 34 intestinal-type adenomas (56%) in 31 patients, 25 gastric-type adenomas (41%) in 18 patients (including 10 patients with familial adenomatous polyposis), and 2 of indeterminate type (3%). Intestinal-type adenomas were significantly more likely than gastric-type adenomas to show high-grade dysplasia (p <0.0001), adenocarcinoma within the polyp (p = 0.016), intestinal metaplasia in the surrounding stomach (p <0.000001), and gastritis (p = 0.002). Patients with intestinal-type adenomas were also more likely to have separate adenocarcinomas (five cases vs 0 cases), although this did not reach statistical significance. Gastric adenomas are rarely truly "sporadic" lesions. In any individual patient complete removal of the adenoma should be performed, and thorough biopsy of the surrounding gastric mucosa is essential to understand the clinicopathologic context of the adenoma.     

Gastric pit dysplasia in adjacent gastric mucosa in 414 gastric cancers: prevalence and characteristics

Despite wide acceptance of the chronic gastritis-intestinal metaplasia-dysplasia-carcinoma sequence, especially for intestinal-type gastric adenocarcinoma, the precise nature of the subtle precursor lesions of gastric cancer remains to be delineated. For example, pit dysplasia with surface foveolar maturation is not well defined, nor is its prevalence and biological characteristics well characterized. We have evaluated the surrounding gastric mucosa of 414 gastric cancers for the presence of gastric pit dysplasia. We investigated its relationship with various clinicopathological and immunophenotypic features of gastric adenocarcinoma, as well as the severity and extent of any surrounding gastritis and intestinal metaplasia. p53 expression and Ki-67 proliferation index were also evaluated. We have found that 21.0% (n=87) of gastric cancer cases showed pit dysplasia in adjacent gastric mucosa. Gastric cancers with pit dysplasia were significantly associated with older age, male sex, body/fundic location, and intestinal histologic type (P<0.05). Interestingly, gastric mucin-containing intestinal metaplasia (incomplete intestinal metaplasia) was highly associated with adenocarcinoma with pit dysplasia (P=0.000). In addition, MUC6 expression in gastric adenocarcinoma was associated with pit dysplasia (P=0.036). p53 overexpression and increased Ki-67 proliferation index were more evident in gastric pit dysplasia compared with adjacent gastric mucosa. We suggest that gastric pit dysplasia is an important candidate precursor of gastric adenocarcinoma and may represent another morphologic step in the pathogenesis of gastric adenocarcinoma, especially of intestinal type. More detailed prospective studies are needed to determine the precise significance of these findings.     

Poorly Differentiated Adenocarcinoma with Signet-Ring Cell Carcinoma in a Hyperplastic Polyp of the Stomach: Report of a Case

Hyperplastic polyps (HPs) of the stomach have been reported to be mostly benign. However, in rare cases, carcinomas have been found in HPs. We treated a 59-year-old Japanese male who underwent a total gastrectomy, and a gross examination of the resected stomach revealed a 4.8 × 3.8-cm polyp on the greater curvature of the antrum and multiple small polyps in the whole gastric mucosa. Histologically, the large polyp consisted mainly of hyperplastic foveolar epithelium, while the presence of variously colored lobules demonstrated a poorly differentiated adenocarcinoma mixed with signet-ring cell carcinoma. Hyperplastic polyps should therefore be carefully examined microscopically as a polypectomy specimen and in resected stomach specimens.     

胃镜下胃息肉组织与背景胃黏膜活检标本病理变化的研究

目的探讨胃镜下活检不同类型胃息肉组织与背景胃黏膜癌前病变及瘤变的关系。方法对2003～2008年胃镜检查、病理证实的1825例胃息肉进行分型并对息肉组织和背景黏膜的肠上皮化生（肠化）、异型增生和瘤变关系进行分析。结果胃息肉检出率为4.3%（1825/42003）;胃底腺、增生性、腺瘤性、炎症性及并发息肉（2种息肉同时发生于同一病例）分别占62.5%（1141/1825）、32.2%（587/1825）、0.8%（14/1825）、1.7%（31/1825）和2.8%（52/1825）。增生性息肉息肉组织肠化发生率（5.3%,31/587）和异型增生发生率（6.8%,40/587）均高于胃底腺息肉（0.2%,2/1141;0.4%,4/1141）（均P〈0.001）。增生性息肉息肉组织癌变率为0.3%（2/587）,其余类型息肉组织未发现癌变病例。息肉组织与背景胃黏膜病理变化对比分析,各型息肉病例的背景胃黏膜肠化发生率均显著高于相应息肉组织（均P〈0.05）,并且胃底腺息肉、增生性息肉和炎症性息肉病例的背景胃黏膜肠化程度重于息肉组织（均P〈0.05）。胃底腺息肉病例的背景胃黏膜异型增生发生率显著高于息肉组织（P=0.000）,且背景胃黏膜异型增生程度重于息肉组织（P=0.000）。息肉病例背景胃黏膜瘤变率（0.5%,7/1355）高于息肉组织（0.1%,2/1773）,胃底腺息肉、增生性息肉和腺瘤性息肉病例的背景胃黏膜瘤变病例数分别为3例、1例和3例。结论胃息肉检出率较低;增生性息肉的息肉组织可以发生癌变;息肉背景胃黏膜存在癌前病变及瘤变,内镜检查时应重视对息肉背景胃黏膜的检查。     

Intragastric bile acids and histological changes in gastric mucosa

Multiple gastric biopsies and gastric juice aspirates were taken in 108 patients undergoing routine or review gastroscopy for a variety of upper gastrointestinal disorders. The gastric juice was measured for free and total bile acids and the biopsies examined for premalignant mucosal changes. Total bile acid levels were significantly higher in patients with atrophic gastritis, intestinal metaplasia and dysplasia but not chronic gastritis. There was no correlation between the severity of the dysplasia and total bile acid levels. Free bile acid levels were significantly higher in patients with atrophic gastritis but not in patients with chronic gastritis, intestinal metaplasia or dysplasia. These results suggest that intragastric bile acids may be implicated in premalignant histological changes of gastric mucosa and thus play a part in gastric carcinogenesis.     

Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis

We present the case of a 52 years old man, with significant familial history, diagnosed with familial adenomatous polyposis-attenuated form, with no clinical and endoscopic surveillance until 2001 when he was admitted for an upper gastrointestinal haemorrhage episode. Upper gastrointestinal scopy revealed duodenal adenomatous polyps and gastric hyperplastic polyps. The patient underwent duodenopancreatectomy with total gastrectomy. The histopathological exam revealed duodenal G2 adenocarcinoma pT3N0, and gastric hyperplastic polyps with no signs of dysplasia. The surgical procedure was followed by chemotherapy. In 2002 the patient was admitted for rectal bleeding and colonoscopy showed 2 sigmoid polyps, appropriate for endoscopic removal and a poly-lobate polyp in the transverse colon. The patient underwent transverse colectomy (the histopathological exam--in situ carcinoma). March 2003--the patient underwent endoscopic removal for a rectal polyp (histopathological exam: moderate dysplasia). In 2005 was noted a pulmonary nodule, located in the postero-apical segment of upper left lobe, for which left superior lobe resection was performed (the histopathological exam: metastatic adenocarcinoma). In May 2006 was performed an exploratory laparotomy. Intraoperatively were noted: peritoneal carcinomatosis and multiple liver metastasis. The surgical procedure recommended in patients with attenuated form of familial adenomatous polyposis and suspect periampullary lesions is duodenopancreatectomy. The particularity of the case is the association of total gastrectomy for gastric hyperplastic polyps.     

Effect of duodenal diversion on low-grade dysplasia in patients with Barrett’s esophagus: Analysis of 37 patients

It is well known that in patients with Barrett’s esophagus (BE), even after antireflux surgery, intestinal metaplasia can progress to dysplasia or even adenocarcinoma. However, the opposite—that is regression of dysplastic changes to intestinal metaplasia after antireflux surgery—has been documented in only a few reports. The objective of this study was to determine the effect of a duodenal diversion operation on lowgrade dysplasia in patients with BE. Thirty-seven patients with either short-segment (n = 12) or longsegment (n = 25) BE underwent antireflux surgery plus either a duodenal switch procedure (13 patients) or a partial distal gastrectomy with Roux-en-Y gastrojejunal anastomosis (24 patients). All of them were subjected to complete clinical, endoscopic, histologic, manometric, and 24-hour pH testing, and 24-hour monitoring of the bile exposure in distal esophagus. There were no deaths in this series, and morbidity occurred in only one patient (2.7%). Manometric assessment after surgery showed a significant increase in sphincter pressure, abdominal length, and total length (P < 0.001). Acid reflux showed a significant decrease after surgery, and duodenal reflux was completely abolished in all except one patient. Follow-up in all patients was longer than 24 months (mean 60 months). Three to four endoscopic procedures were performed after surgery in each patient, and several biopsy specimens were taken distal to the squamo-columnar junction during each endoscopic procedure. Eleven patients (91%) with short-segment BE demonstrated histologic regression to either cardiac mucosa or nondysplastic intestinal metaplasia. Among the 25 patients with long-segment BE, there was a 62.5% rate of histologic regression to nondysplastic epithelium when the length of BE measured between 31 and 99 mm and 33 % histologic regression when the length of BE was 101 mm or more. There were no cases of progression to high-grade dysplasia or adenocarcinoma. The endoscopic length of the columnar-lined esophagus did not change late after surgery. In 65% of patients with BE, antireflux surgery, gastric acid reduction, and duodenal diversion produced histologic regression of low-grade dysplasia to nondysplastic mucosa. This effect was even more pronounced when the length of BE was shorter. It seems to be permanent, and no progression to high-grade dysplasia or adenocarcinoma has occurred.     

Prevalence of Helicobacter pylori infection in 160 patients with Barrett's oesophagus or Barrett's adenocarcinoma

BACKGROUND: The role of Helicobacter pylori infection in the development of Barrett's oesophagus and its complications is uncertain. The aim of the present study was to determine the importance of H. pylori infection in this disease by comparing the frequency of oesophageal and gastric H. pylori infection in a group of patients with Barrett's oesophagus or adenocarcinoma, with the frequency of infection in a control group without Barrett's disease. METHODS: The study group included 160 patients (123 male, 37 female; mean age: 61.2 years) who were classified (according to the highest grade pathological lesion in the oesophagus) as having Barrett's intestinal metaplasia (IM; 88 patients), Barrett's oesophagus with low-grade dysplasia (LGD; 28 patients), high-grade dysplasia (HGD; five patients), Barrett's indefinite for dysplasia (n = 4), and Barrett's adenocarcinoma (33 patients). A total of 91 of these patients had gastric antral specimens available for study. The control group consisted of 214 consecutive, prospectively enrolled symptomatic patients (122 male, 92 female; mean age: 57.2 years) who underwent upper gastrointestinal endoscopy and in whom Barrett's oesophagus or Barrett's adenocarcinoma was not found. A modified Warthin-Starry method was used to detect H. pylori infection. RESULTS: Oesophageal H. pylori infection was found in eight of 160 (5%) patients with Barrett's oesophagus or Barrett's adenocarcinoma. Holicobacter pylori organisms in the oesophagus were found only on non-intestinalized cardiac or oxyntocardiac mucosa. All patients with oesophageal H. pylori infection and an antral biopsy available for study had antral H. pylori infection. Gastric antral H. pylori infection was significantly less prevalent in patients in the Barrett's study group (15/91, 16.5%) than in the non-Barrett's control group (67/214, 31.3%; Fisher's exact test, P = 0.01). Patients from the control group with an endoscopic diagnosis of duodenal ulcer, gastric ulcer, gastritis, or duodenitis had a significantly higher prevalence of infection compared with the Barrett's group, but there was no difference in the infection prevalence in patients in the Barrett's group and patients with reflux oesophagitis, hiatal hernia, no endoscopic abnormality, or any other diagnosis. CONCLUSIONS: Oesophageal H. pylori infection is uncommon in patients with Barrett's IM, dysplasia, or adenocarcinoma, and may be restricted to non-intestinalized columnar epithelium. Gastric H. pylori infection may have a protective effect for the development of Barrett's oesophagus.     

Second follow-up study of mucosal changes in the gastric remnant after resection for peptic ulcer disease

Second follow-up 36-37, 26-27 and 15-18 years after gastric resection for peptic ulcer disease was performed for 72 patients who in the first screening five years earlier had severe atrophic gastritis and/or intestinal metaplasia in the gastric remnant mucosa. Of the 72 patients 60 were still alive. The death certificates revealed no gastric stump carcinomas among the 12 deceased patients. Neither were any cases of gastric stump carcinoma found among the 38 endoscopically screened patients. Severe atrophic gastritis, which was present in 37 patients in 1982-83, had regressed in 14 cases (p less than 0.01) and proceeded in one case. The extent of intestinal metaplasia had increased in 11 cases and decreased in five cases (p = 0.149, NS). Dysplasia, which was not seen five years ago, was now detected in four cases (10.5%). There was an association between dysplasia and incomplete intestinal metaplasia in three cases. Although these mucosal changes may be premalignant it is not possible to be categorical about the prognosis. Thus, endoscopic screening of all patients whose stomach has been resected for peptic ulcer disease cannot be recommended. Endoscopy, however, is always indicated when gastric symptoms appear in a patient with history of gastric resection.     

Hyperplastic polyposis: association with colorectal cancer

Hyperplastic polyposis is a loosely defined syndrome initially thought not to confer a clinically important predisposition to colorectal cancer. The aim of the current study was to examine the clinical, histologic, and molecular features of a prospective series of cases meeting a strict definition of the condition. Twelve patients were identified, seven of whom had developed colorectal cancer. Most polyps were hyperplastic, but 11 patients also had polyps containing dysplasia as either serrated adenomas. mixed polyps, or traditional adenomas. The mean percentage of dysplastic polyps in patients with cancer was 35%, and in patients without cancer, 11% (p < 0.05). Microsatellite instability (MSI) was present in 3 of 47 hyperplastic polyps and two of eight serrated adenomas. Kras was mutated in 8 of 47 hyperplastic polyps and two of eight serrated adenomas. No polyps showed loss of heterozygosity of chromosomes 5q, 1p, or 18q. Two of seven cancers showed a high level of MSI. It is concluded that hyperplastic polyposis is associated with a high risk of colorectal cancer. Hyperplastic polyps are the dominant type of polyp, but most cases have some dysplastic epithelium. A higher proportion of dysplastic polyps is associated with increased cancer risk. Clonal genetic changes are observed in some hyperplastic polyps and serrated adenomas.     

Oxyntic mucosa pseudopolyps: a presentation of atrophic autoimmune gastritis

Gastric polyps are often present in the setting of atrophic gastritis. Although the majority of these polyps are nonneoplastic, such as hyperplastic polyps, neoplastic polyps may be present. We discuss nine cases that illustrate an additional nonneoplastic cause of polyps in atrophic gastritis. Specifically, preserved islands of relatively normal oxyntic mucosa in a background of gastric atrophy may appear polypoid endoscopically. The patients (seven women, two men, mean age 64 years) presented with nonspecific abdominal or reflux symptoms (n = 8) and diarrhea (n = 1). Five of five patients tested were confirmed to have hypergastrinemia, and three of three patients tested had antiparietal cell antibodies. Biopsies from the gastric body or fundus of our nine patients showed fragments of atrophic mucosa and separate fragments of preserved oxyntic mucosa. Based upon the histologic characteristics of the atrophic fundic and relatively normal antral biopsies, the gastric atrophy appeared to be of autoimmune-type. The relatively preserved oxyntic glands showed parietal cell hypertrophy and focal mild chronic inflammation. The number of polyps observed endoscopically ranged from less than five to multiple/diffuse. Three patients had persistent nodularities in their stomachs for 1, 3, and 7 years of their follow-up. Our study shows that some patients with atrophic gastritis, autoimmune-type, may present with gastric polyps/nodules that represent relatively preserved oxyntic mucosa. This presentation may be more common than is presently recognized because biopsies of the polyps alone will not show histologic features of atrophic gastritis or reveal the etiology of the polyp itself. Although a limited number of previous studies have suggested this type of polypoid presentation may represent "early" atrophic gastritis, its persistence in three of our patients argues against this hypothesis.     

Chronic atrophic gastritis and the risk of cancer

Chronic gastritis, which is frequent in subjects over 50 years old, is caused by the concurrence of predisposing and congenital conditions and exogenous harmful factors, in particular foods. In etiopathogenetic terms it is worth considering autoimmune diseases and duodenogastric back-flow separately. Lesions develop progressively from superficial gastritis to atrophic gastritis and finally to gastric atrophy; they are frequently found together with intestinal metaplasia, formed by areas of the epithelium with the morphological and histochemical characteristics of intestinal mucosa, which are the expression of a modified regeneration of the gastric wall. It is acknowledged that chronic atrophic gastritis is a precancerous phenomenon which is the majority of cases leads to the onset of intestinal cancer, passing through the stages of chronic gastritis, metaplasia and dysplasia. Identification of this lesion may therefore help to prevent cancer: diagnosis is essentially performed using endoscopy (together with histocytological tests and bioptic staining) and laboratory tests (enzyme and CEA assays in the gastric juices). Rather than prescribing generic medical therapy or surgical treatment, which is only possible in selected cases of alkaline gastritis, attention is focused on curing unhealthy habits and on an endoscopic follow-up (every 2 years in cases of gastritis, and more frequently in cases of metaplasia or dysplasia).     

Dysplasia and Adenocarcinoma After Classic Antireflux Surgery in Patients With Barrett’s Esophagus: The Need for Long-Term Subjective and Objective Follow-Up

OBJECTIVE: To assess the clinical, endoscopic, and functional results in a group of patients with Barrett's esophagus undergoing classic antireflux surgery in whom dysplasia and adenocarcinoma were found at a late objective follow-up. SUMMARY BACKGROUND DATA: There have been isolated reports of patients with Barrett's esophagus undergoing antireflux surgery who show dysplasia or even adenocarcinoma on follow-up. METHODS: Of 161 patients undergoing surgery, dysplasia developed in 17 (10.5%) at late follow-up and adenocarcinoma developed in 4 (2.5%). These 21 patients represent the group assessed and were compared with 126 surgical patients with long-segment Barrett's in whom dysplasia did not develop. They were evaluated by clinical questionnaire, multiple endoscopic procedures and biopsy specimens, 24-hour pH studies, and 24-hour bilirubin monitoring. RESULTS: Of the 17 patients with dysplasia, 3 were asymptomatic at the time that dysplastic changes appeared; all patients with adenocarcinoma had symptoms. Two patients (12%) in the dysplasia group had short-segment Barrett's; all patients with adenocarcinoma had long-segment Barrett's. Manometric studies revealed an incompetent lower esophageal sphincter in 70% of the dysplasia group, similar to nondysplasia patients with recurrence, and in 100% of the adenocarcinoma group. The 24-hour pH study showed pathologic acid reflux in 94% of the patients with dysplasia, similar to patients with recurrence without dysplasia, whereas bilirubin monitoring showed duodenal abnormal reflux in 86% of the patients. Among patients with dysplasia, three different histologic patterns were identified. All patients with adenocarcinoma had initially intestinal metaplasia, with appearance of this tumor 6 to 8 years after surgery. CONCLUSIONS: Patients with Barrett's esophagus who undergo antireflux surgery need close and long-term endoscopic and histologic surveillance because dysplasia or even adenocarcinoma can appear at late follow-up. Metaplastic changes from fundic to cardiac mucosa and then to intestinal metaplasia and later to dysplasia or adenocarcinoma can clearly be documented. There were no significant differences in terms of clinical, endoscopic, manometric, 24-hour pH, and bilirubin monitoring studies between patients with recurrence of symptoms without dysplastic changes, and patients with dysplasia. Therefore, the high-risk group for the development of dysplasia is mainly the group with failed antireflux surgery.     

Endoscopic and Histologic Findings in the Gastric Pouch and the Roux Limb after Gastric Bypass

Background: Despite the large number of gastric bypasses performed for morbid obesity, very little is known about the endoscopic and histologic aspects of the gastric pouch and the Roux-limb late after surgery. We performed prospective routine endoscopic and histologic studies of the pouch and Roux-limb 2 years after gastric bypass. Methods: The present study includes 227 patients submitted to resectional gastric bypass and followed for a mean of 27 months after surgery. Mean BMI before bypass was 44 kg/m². In all patients, upper endoscopy of the pouch and of the jejunal limb was performed, taking 3 biopsy samples of the gastric pouch in 171 patients and 2 samples of the jejunum in 40 patients. Results: Macroscopic appearance of the gastric pouch was normal in 99% of the patients and of the jejunal limb in 100%. Histologic analysis revealed normal fundic mucosa in 56%. Chronic active gastritis was the most frequent abnormal histologic finding. 7 patients (4.1%) showed intestinal metaplasia. H. pylori infection was present in the gastric pouch in 31% of the patients. Conclusions: The proximal gastric pouch after gastric bypass is endoscopically normal in 99% of patients 2 years after surgery, while the Roux-limb is normal in 100%. Histologic analysis of gastric mucosa revealed normal fundic mucosa in 56%. There are some chronic histologic changes, even intestinal metaplasia, whose behavior at late follow-up is not yet known. H. pylori is present in nearly 1/3 of the patients.     

良性和恶性病因术后残胃黏膜组织学变化特征及幽门螺杆菌感染状况

目的分析良性和恶性病因术后残胃黏膜组织学变化特征与幽门螺杆菌感染状况的关系。 方法回顾性分析2014年2月至2019年2月于四川省石棉县人民医院因良性和恶性病因行胃部手术治疗患者共80例,其中36例为良性消化性溃疡患者（良性组）,44例为早期胃患癌者（胃癌组）,两组患者术后均行黏膜组织学与胃镜检测。分析入组患者病例资料（首次行胃大部切除手术时年龄、性别、术后病程、行胃镜检测年龄、幽门螺杆菌感染、手术病因、病理和胃镜检测结果和手术方式等）,观察患者胃黏膜病变[慢性萎缩性胃炎（CAG）、肠化生（IM）和异型增生（DYS）发生率]、幽门螺杆菌感染率与胃黏膜炎症与活动性异常等,比较两组患者中幽门螺杆菌感染者与未感染者胃黏膜的病理特征。 结果良性组患者手术年龄为（40.46 ± 6.71）岁,低于胃癌组[（54.08 ± 8.17）岁],胃镜检测年龄及术后病程分别为（67.78 ± 11.36）岁、（27.26 ± 8.87）年,高于胃癌组[（61.99 ± 11.03）岁和（8.04 ± 6.57）年],差异均有统计学意义（t = 10.419、P < 0.001,t = 3.102、P = 0.003,t = 13.964、P < 0.001）;良性组患者幽门螺杆菌感染和胃黏膜活动性异常比例分别为47.22%（17/36）和66.67%（24/36）,均显著高于胃癌组[31.82%（14/44）和40.91%（18/44）],差异有统计学意义（χ² = 4.147、P = 0.039,χ² = 8.239、P = 0.003）。良性组、胃癌组患者中幽门螺杆菌感染者胃黏膜活动性异常、CAG及癌前病变比例均高于无幽门螺杆菌感染者,而NAG比率低于无幽门螺杆菌感染者,差异均有统计学意义（P均< 0.05）。 结论胃大部切除手术后残胃黏膜病变与进展和幽门螺杆菌感染存在一定关系,为预防残胃黏膜癌变可在幽门螺杆菌检测基础上加强胃镜随访。     

Endoscopic management of multiple large antral hyperplastic polyps causing gastric outlet obstruction

Gastric hyperplastic polyps are often asymptomatic and are found incidentally at upper endoscopy performed for unrelated reasons. Although they are considered a benign lesion, all symptomatic polyps should be removed for a more reliable histological diagnosis, resolution of symptoms and to prevent potential malignant transformation. In fact, there are no significant difference between pure gastric hyperplastic polyps and gastric hyperplastic polyps with neoplastic transformation in the number, location, or gross appearance of polyps. If symptomatic, patients usually complain of dyspepsia, heartburn, abdominal pain or upper gastrointestinal bleeding leading to anaemia. Complete or incomplete gastric outlet obstruction with intermittent symptoms, may rarely be caused by gastric hyperplastic polyps. We described the management of a rare case of intermittent gastric outlet obstruction caused by a large hyperplastic antral polyp prolapsing through the pylorus. Using hydroxypropylmethylcellulose, a new lifting agent, firstly from pyloric side, we obtained a reliable long-lasting submucosal cushion under the lesion which allowed a stable repositioning of the polyp in the gastric lumen without making additional infiltration during the endoscopic mucosal resection. Innovative lifting agents could significantly reduce the procedure time, but additional studies should be performed on this area to confirm preliminary results. Endoscopic mucosal resection not only provides tissue to determine the exact histopathologic type of the polyp, but also achieves symptomatic treatment.     

Pyloric gland adenoma: an entity distinct from gastric foveolar type adenoma

Pyloric gland adenoma (PGA) is a rare neoplasm demonstrating gastric epithelial differentiation. In this series, we studied 41 PGAs from 36 patients. We compared them to 28 gastric foveolar type gastric adenomas (GTAs) from 25 patients. PGAs occurred in an older population with a mean age of 73 compared with 48 in GTAs (P<0.001). There was a significant female predominance, particularly for gastric PGAs. Morphologically, PGAs were characterized by closely packed pyloric gland-type tubules with a monolayer of cuboidal to low columnar epithelial cells containing round nuclei and pale to eosinophilic cytoplasm with a ground glass appearance. The cells lacked an apical mucin cap, a feature distinct from GTAs. An immunohistochemical panel of mucin core peptides (MUCs) and CDX2 was performed on a subset of the lesions. All PGAs expressed MUC6 with coexpression of MUC5AC, whereas GTAs expressed predominantly MUC5AC without MUC6. Both lesions lacked CDX2 and MUC2 except in areas of intestinal metaplasia (IM) found in some PGAs. Histologic features consistent with conventional dysplasia were found in 26 (63.4%) PGAs. Using a 2-tier grading system, 5 (12.2%) cases demonstrated low-grade dysplasia whereas 21 (51.2%) cases showed high-grade dysplasia including 5 (12.2%) cases with an associated intramucosal or more deeply invasive adenocarcinoma. This was significantly different from GTAs; all cases showed only low-grade dysplasia (P<0.001). In addition, 60% of gastric PGAs were associated with IM in the surrounding mucosa and 40% of lesions arose in a background of autoimmune gastritis, whereas these 2 conditions were only associated with 1 case (3%) of GTA. In summary, PGA is a distinct entity. Despite its bland histologic appearance, it is much more likely to be accompanied by background IM and autoimmune gastritis and can evolve into invasive adenocarcinoma displaying pyloric gland differentiation.