Heterotopic gastric mucosa with focal intestinal metaplasia and squamous epithelium in the rectum

Heterotopic gastric mucosa has been described in all levels of the gastrointestinal tract. However, gastric heterotopia of the rectum is a rare finding. It is usually reported along with polyp located in the rectum between 5 and 8 cm from the anal verge. The most common symptom is painless rectal bleeding, and non-specific gastrointestinal symptoms may also be presented. We report an incidentally found case of a 46-year-old man without any gastrointestinal symptoms. The pathology showed gastric mucosa and squamous epithelium and focal intestinal metaplasia. This finding could be a clue as to the origins of the heterotopic gastric mucosa. Although there are no guidelines for treatment or the follow-up period, regular endoscopic surveillance is necessary for gastric cancer screening.     

Primary adenocarcinoma of the cervical esophagus arising from heterotopic gastric mucosa

Received: February 18, 2000 / Accepted: November 17, 2000     

Differential diagnosis of large-sized pedunculated polypoid lesions of the gallbladder by endoscopic ultrasonography: a prospective study

Purpose. We have previously reported the effectiveness of endoscopic ultrasonography (EUS) for the differential diagnosis of pedunculated polypoid lesions of the gallbladder, based on retrospective studies using resected specimens. We proposed the following diagnostic criteria for EUS findings: when the contour of a lesion is nodular or smooth, the lesion is diagnosed as a neoplasm, and when a lesion has a granular contour, it is diagnosed as a nonneoplasm. The present study was designed to verify the clinical utility of our EUS ctiteria prospectively. Methods. Forty-six consecutive patients with pedunculated polypoid lesions of the gallbladder 10 mm or greater in size diagnosed as nonneoplasms at the initial EUS, all of whom underwent follow-up examinations, were enrolled in this study. The occurrence of changes in these lesions during the observation period was examined. Results. No evident changes in lesions were observed in 43 of the 46 patients. Spontaneous self-detachment of lesions was recognized during the observation period in the other 3 patients. Conclusions. EUS is useful for determining treatment indications for pedunculated polypoid lesions of the gallbladder, even when the lesions are large, and contributes to avoiding unnecessary surgery. Received: December 7, 2000 / Accepted: March 30, 2001     

Heterotopic gastric mucosa of the gallbladder

A case of heterotopic gastric mucosa in the fundus of the gallbladder is reported. A 23-year-old man, who had been healthy and asymptomatic, visited our hospital because of abnormal findings in a liver enzyme test given during a routine health screening. Ultrasonography demonstrated a highly echogenic polypoid mass in the fundus of the gallbladder. The gallbladder mass was confirmed by both computed tomography and intravenous cholangiogram. After a 10-month follow up, laparoscopic cholecystectomy was performed. Intraoperative touch smear cytology of this lesion revealed class II cells. The surgical specimen revealed a 15×10×5 mm polypoid lesion in the fundus, with no gallstones in the gallbladder. Histologically, the polypoid lesion consisted of both fundic type and pyloric type gastric glands located in the mucosa of the gallbladder. In the literature, 42 cases of heterotopic gastric mucosa of the gallbladder have been reported, only 3 of which, including this present case, were found incidentally, with no apparent symptoms.     

Prevalence and risk factors for heterotopic gastric mucosa of the upper esophagus among men undergoing routine screening colonoscopy

The prevalence of heterotopic gastric mucosa of the upper esophagus (inlet patch) has a wide range depending on the method and detail of examination. The inlet patch is believed to be a congenital malformation that rarely leads to symptoms. We aimed to quantify the prevalence of the inlet patch in a non‐referred population and determine if there are any risk factors or associated symptoms. Men between ages 50 and 79 presenting for routine colonoscopy at two clinical sites were recruited to undergo an upper endoscopy. Endoscopists were prompted to examine for the presence of the inlet patch. Of the 822 enrolled patients, 795 had data regarding the presence of an inlet patch. Of these, 55 (6.9%) had an inlet patch identified. Education was inversely associated (odds ratio [OR] advanced degree vs. high school or less = 0.310; 95% confidence interval [CI] = 0.111, 0.869), and tobacco use was positively associated with the presence of an inlet patch (current vs. never smokers OR = 2.87; 95% CI = 1.23, 6.69; former vs. never smokers OR = 1.93; 95% CI = 0.922, 4.02). No association between the inlet patch and symptoms of heartburn, globus, or dysphagia was found. In a cross‐sectional study of colon cancer screenees, inlet patches were common and were not associated with symptoms. Tobacco use appears to be associated with the presence of an inlet patch.     

Heterotopic gastric mucosa in the cervical esophagus (inlet patch): endoscopic prevalence, histological and clinical characteristics

BACKGROUND AND AIM: Heterotopic gastric mucosal patch, which has a 0.1-10% frequency, is encountered when the cervical esophagus is examined carefully during endoscopy. In this study, we aimed to determine the prevalence of the patch in the cervical esophagus, to identify its macroscopic and histological characteristics and to evaluate demographic and clinical features. METHODS: Six hundred and sixty patients (317 male, 343 female; mean age 50.28 years, range 14-90) with upper gastrointestinal symptoms had elective esophagogastroduodenoscopy and the cervical esophagus was examined for the patch during withdrawal of the endoscope. Biopsies were obtained from the antrum and the patch. Helicobacter pylori was assessed using an immunohistochemical method. RESULTS: The patch was found in 11 patients of 660, with a prevalence of 1.67%. Patch size ranged between 5 and 30 mm, appeared as a single patch in nine patients and as twin patches in two patients. Mean age and male : female ratio were not significantly different from the patient population without patches, but the female sex was predominant (three men, eight women; mean age 43.6 years, range 32-64). In five of 11 patients, the upper esophageal and laryngopharyngeal symptoms were remarkable. Eight patients in whom histological confirmation was carried out showed three fundic and five antral-type mucosa. Two of five patients with antral H. pylori also had the bacteria in the patch. H. pylori prevalence in the patch was 25%. CONCLUSION: Heterotopic gastric mucosal patches in the proximal esophagus should not be overlooked during endoscopy because they may lead to important complications in relation to their acid secretion, which may vary according to their parietal cell mass.     

Three other types of duodenal polyps: Mucosal cysts,focal foveolar hyperplasia,and hyperplastic polyp originating from islands of gastric mucosa

Summary Seven cases are reported that initially presented on endoscopic examination as duodenal polyps originating from islands of gastric mucosa within the duodenal bulb. Microscopic examination revealed mucosal cysts (MC), focal foveolar hyperplasia (FFH), and hyperplastic polyp (HPP). These lesions must be added to the list of neoplastic and tumorlike lesions of the duodenum that may endoscopically present as polyps.     

Study ofHelicobacter pylori colonization of patches of heterotopic gastric mucosa (HGM) at the upper esophagus

Helicobacter pylori (HP), known to cause active chronic gastritis, has primarily been found in gastric-type mucosa. Even in the duodenum, the organism was detected in islands of metaplastic gastric mucosa. HP has also been found in gastric metaplasia of Barrett's esophagus in 15–50%. The aim of our study was to determine: (1) the frequency with which HP is found on histopathological sections of heterotopic gastric mucosa (HGM) patch(es) at the upper esophagus, as compared to that of the stomach proper, and (2) the histopathological significance of infection in the HGM patches. From 63 patients with HGM patches at the upper esophagus, 48 patients were found to have concurrent adequate specimen from the stomach for modified Steiner's stain. In 22 patients (45.8%), pair sections from HGM and stomach were negative for HP. Of 26 patients (54.1%) HP-positive on sections from the antrum and/or body (both in 21 cases) nine patients (18.7%) demonstrated HP in the HGM patches. Whereas focal acute inflammatory changes on the H&E section of HGM was present in six patients, HP was detected in HGM only in one. Chronic inflammatory cell infiltration was detected in all nine HP-positive HGM patches and in 37 of 39 HP-negative patches. A mixed acute and chronic inflammatory cell infiltration was found in five of these 37 patients. Our data demonstrate that HP infection of HGM patches at the upper esophagus is part of the HP gastritis and an independent colonization of HGM patches without gastric infection does not occur. No correlation was found between the presence of acute and chronic inflammatory changes in H&E-stained section and positivity of HP in modified Steiner's section of HGM.This study was presented in part, as poster, at the Digestive Disease Week of the AGA, May 12–18, 1990, in San Antonio, Texas.     

pH profile of esophagus in patients with inlet patch of heterotopic gastric mucosa after tetragastrin stimulation

In a series of 1771 endoscopic examinations from 1988 to 1990, we observed 62 cases (3.3%) of inlet patch of heterotopic gastric mucosa (IPHGM) in the upper esophagus. Ten of the IPHGM patients complained of throat discomfort or globus sensation, and these symptoms were relieved by histamine H₂-antagonists, suggesting that these symptoms could be caused by acid secretion from IPHGM. Acidity under tetragastrin stimulation was measured in the esophagus and compared with the pool of gastric juice and saliva under direct vision by a newly devised endoscopic method. Congo red staining was also carried out after pH measurement. Significant pH reduction at IPHGM was observed in three cases, and black coloration with Congo red staining in the IPHGM was observed in four cases. These findings suggest that IPHGM is a mucosal change with latent acid secretion.     

硫氧还蛋白-1在急性坏死性胰腺炎并急性胃黏膜损伤中的作用

目的探讨硫氧还蛋白-1（TRX-1）在实验性急性坏死性胰腺炎（ANP）并急性胃黏膜损伤发病机制中的作用以及抗氧化剂褪黑素对其的影响。方法72只大鼠随机分为对照组（C组,n=24）、ANP组（A组,n=24）和褪黑素干预组（M组,n=24）。A组分3次腹腔内注射6％L-精氨酸（L—Arg）1．5g／kg建立ANP模型;C组同法注射等量生理盐水;M组于首次注射L—Arg前0．5h腹腔内注射1％褪黑素50μg／kg。各实验组大鼠于末次腹腔内注射后6h、12h和24h分批处死。光镜下观察胰腺和胃组织并进行病理学评分,采用免疫组化检测TRX-1在胃黏膜的表达,并检测胃黏膜中MDA、MPO的含量。结果A组各时点胃黏膜TRX-1的染色积分及MDA、MPO的含量明显高于C组（P均〈0．05）;M组各时点胃黏膜中TRX一1的染色积分及MDA、MPO的含量明显低于A组（P均〈0．05）,胰腺和胃组织病理改变较A组明显减轻（P均〈0．05）。结论内源性的TRX-1可能是胃黏膜组织抵御氧化应激损伤的重要因子之一,TRX-1的表达量可能与组织氧化应激损伤的严重程度有关。外源性的褪黑素在ANP时可能通过其抗氧化作用,减轻胃黏膜氧化应激损伤的程度,对胃黏膜有一定的保护作用。     

Benign pseudotumorous lesion (fibroangiomyomatous hyperplasia with elastosis) in the gallbladder

Received: November 12, 1999 / Accepted: September 8, 2000     

Adenocarcinoma arising from heterotopic gastric mucosa in the cervical esophagus and upper thoracic esophagus: two case reports and literature review

Primary adenocarcinoma arising from heterotopic gastric mucosa (HGM) is rare and the clinicopathological characteristics are not well known. We present two cases of esophageal adenocarcinoma arising from HGM with a review of a case series. Case 1 was a 78-year-old woman who underwent a periodic medical examination without complaining of any symptoms. Preoperative evaluation suggested esophageal adenocarcinoma arising from the HGM. The patient was treated with endoscopic submucosal dissection. Definitive pathological diagnosis confirmed adenocarcinoma arising from the HGM. Case 2 was a 70-year-old man who underwent a medical examination after complaining of dysphagia. Preoperative diagnosis suggested esophageal adenocarcinoma; however, its origin was unclear. The patient was treated with surgical resection. Definitive pathological diagnosis revealed adenocarcinoma arising from the HGM. In this article, the authors report the clinicopathological features of esophageal adenocarcinoma arising from HGM that were collected from a literature review and our cases.     

Sucralfate protection against ethanol-induced injury of rat gastric mucosa in vitro and in vivo

A number of mechanisms for sucralfate protection of gastric mucosa during ulcer healing and protection from experimental injury have been proposed. One currently held postulate that sucralfate acts by inhibiting acid/pepsin attack and creating, at acid pH, a barrier to diffusion of hydrogen ions was tested. The experiments took advantage of a cultured rat antral mucosal model in which ethanol injury is assessed by release of radiolabel from ⁵¹chromiumloaded mucosa. In this model, with mucosa cultured in the absence of pepsin activity at a neutral pH, sucralfate conferred marked protection; specific ⁵¹chromium release fell from 12.4% (s.e.m. = 0.7) in controls to 8.9% (s.e.m. = 0.9) at 0.5 mg/ml (P < 0.05) and 3.4% (s.e.m. = 0.5) at 2.0 mg/ml (P < 0.001) of sucralfate and was abolished at 10 mg/ml and 40 mg/ml (P < 0.001). Pretreatment with sucralfate in vivo also protected the mucosa against subsequent ethanol challenge in the cultured mucosal model, control 12.3% (s.e.m. = 1.9) versus sucralfate pretreatment 6.9% (s.e.m. = 0.7) (P < 0.02). Using computer-assisted macroscopic assessment of mucosal damage after ethanol dosage by gavage, it was further demonstrated that sucralfate protection in vivo is dose-dependent and prolonged, lasting for at least 5 h at a dose of 200 mg/kg. It is concluded that sucralfate-induced protection of the gastric mucosa is long-lasting and can occur via mechanisms other than minimization of acid/peptic attack.     

Morphologic changes in gastric mucosa of aging rats

We examined histologic and ultrastructural changes in the gastric mucosa of aging rats. Standardized gastric specimens from Sprague-Dawley rats 3 months of age (young) and 24 months of age (old) were evaluated by qualitative and quantitative histology and transmission electron microscopy. Old rats had the following histologic changes: (1) partial atrophy of the gastric glands and their replacement with hyalinlike connective tissue; (2) cystic dilatation of the gastric glands at the bases with occasional squamous cell metaplasia; and (3) extensive perivascular depositions of PAS-positive material, negative for amyloid. The total mucosal thickness was 484±100 m in young rats vs 1122 ±240m in old rats (P<0.01). Electron microscopy demonstrated degenerative changes in parietal and chief cells, hyperplasia of surface and foveolar mucous cells, and prominent accumulation of disorganized collagen fibrils in perivascular connective tissue. This study indicates that the gastric mucosa of aging rats that have not been exposed to damaging agents does show definite histologic and ultrastructural changes.Preliminary data have been published as an abstract inGastroenterology 90:1658, 1986.These studies were supported by grant AG02767-04 from the National Institute on Aging and in part by the Goldsmith Foundation.     

Effects of collagen solution on the prevention of acute gastric mucosa injuryin rats

AIM To investigate the effects of collagen solution on the prevention of acute gastric mucosal injury inrestricted rats inflicted by cooling in low temperature (4℃),METHODS Thirty healthy Wistar rats were randomly divided into normal (N, n = 10),injury (I, n = 10)and prevention (P, n = 10) groups. The rats were fasted for 48 h but free access to water without restrictionand cooling in normal group, fasted for 48 h but free access to water with restriction of rats onto the fixationframe for cooling in 4℃ for 4 h, so to cause stress injury of gastric mucosal membrane in I group and fed with3 mL of collagen solution 30min before injury in P group in addition to the procedures in I grobp. Gastricmucosal potential difference, blood flow volume, content of nitrite (NO2-) and hydrogen ion concentration(H+ ) in gastric juice were determined under aneasthesia at 48 h after fast in N group and at 4 h after injuryin I and P groups to evaluate the degree of injury (injury index).RESULTS Gastric mucosal potential difference was 22.10±5.27 in N group and 11.46±5.25 in I groupwith obvious difference (P<0.01), but 16.98±4.84 in P group which was remarkably improved whencompared to that in I group. Gastric mucosal blood flow volume was 23.65±10.65 in I group and 57.20±11.75 in N group with evident difference (P<0.01), but 37.49±5.87 in P group with sound effects incontrast to that in I group (P<0.01). Gastric injury index was 18.40±8.35 in I group and 7.9±2.13 in Pgroup with significant difference (P<0.01). Hydrogenion concentration in gastric juice was 118.0±41.2mmol/L in N group, 186.9±74.7 mmol/L in I group and 96.4±57.2 mmol/L in P group with prominentdifference (P< 0.01 ) between those in I and P group. Gastric mucosal nitrite concentration was 1.15±0.46in N group, 0.69±0.15 in I group and 1.04±0.44 in P group with obvious differences between N and Igroups (P<0.01) and between I and P group (P<0.01).CONCLUSION Ischemic and hypoxic injury of gastric mucosal due to low blood perfusion during restrictionand cooling injury at 4℃ was supposed to be an important factor in inducing gastric mucosal stress injury. Butcollagen solution could maintain the integrity of gastric mucosal barrier, buffer gastric acid, promotethrombocytic agglutination and ameliorate direct injury to gastric mucosa caused by various factors.     

Pathological development of the gastric mucosa in Helicobacter pylori‐related diseases

OBJECTIVE : To study the relationship between Helicobacter pylori eradication and the pathological development of the gastric mucosa in H. pylori‐related diseases. METHODS : One hundred and ninety‐one H. pylori‐infected patients were randomly given anti‐H. pylori or non‐anti‐H. pylori medications. Endoscopic examination was carried out 1 year after treatment. Pathological classifications followed the Sydney System. RESULTS : Of the 191 patients, those with chronic inflammation of the gastric mucosa improved (P < 0.05), as did those with atrophy and intestinal metaplasia (P < 0.05). Helicobacter pylori was eradicated in 107 patients, but not in 84 patients. Compared with those patients in whom H. pylori was not eradicated, those with H. pylori eradicated had ameliorated chronic inflammation of the gastric mucosa (P < 0.05) and active inflammation reduced in some cases (P < 0.05). Notwithstanding a stratification of different gastric diseases and different treatments, patients with H. pylori eradicated showed a more marked improvement in mucosal chronic inflammation than did patients in whom H. pylori was not eradicated (P < 0.05). CONCLUSIONS : These results suggest that H. pylori infection is closely related to active inflammation of the gastric mucosa. Helicobacter pylori eradication is beneficial in improving chronic inflammation of the gastric mucosa.     

脾虚患者胃粘膜超氧化物歧化酶与前列腺素的关系

目的 观察脾虚患者胃粘膜超氧化物歧化酶(SOD)活性与前列腺素(PG)的关系。 方法 72例慢性胃病住院患者,按中医辨证分成脾虚组和肝气犯胃组,分别测出胃粘膜SOD活性,以及前列腺素和血栓素A_2的代谢产物6-酮-PGF_(1a)和血栓素B_2(TXB_2)的含量,分析SOD与6-酮-PGF_(1a)和TXB_2的相关性。 结果 脾虚组患者胃粘膜SOD活性为2.7±1.1 U/mg湿重,明显低于肝气犯胃组的4.2±1.7 U/mg湿重(P<0.01);脾虚组胃粘膜6-酮-PGF_(1a)含量为115.7±60.7 pg/mg湿重,亦明显低于肝气犯胃组的289.6±154.2 pg/mg湿重(P<0.01)。SOD活性与6-酮-PGF_(1a)含量呈线性正相关(P<0.05)。 结论 脾虚证患者胃粘膜内自由基代谢紊乱,表现为SOD活性及抗氧化能力低下,并且与胃粘膜PG代谢的改变存在着一定的关系。     

电针足三里穴抗大鼠应激性胃黏膜损伤的作用途径

[目的]探讨电针（EA）足三里穴抗大鼠应激性胃黏膜损伤的作用途径。[方法]采用束缚-冷应激方法制备大鼠应激性胃溃疡模型，观察切断膈下迷走神经或切除腹腔交感神经节及注射受体阻断剂对EA抗应激性胃黏膜损伤的影响。[结果]EA-模型组胃黏膜损伤明显减轻，溃疡指数（UI）与模型组比较差异有统计学意义（P〈0．01）。切断双侧膈下迷走神经或切断腹腔交感神经节，大鼠UI减小，分别与腹部假手术组比较差异有统计学意义（P〈0．01）。静脉给予β受体阻断剂普萘洛尔，可部分削弱EA对胃黏膜损伤的保护作用，与0．85％氯化钠组比较P〈0．01；而给予M受体阻断剂阿托品、α受体阻断剂酚妥拉明对EA保护胃黏膜损伤作用无明显影响（P〉0．05）。[结论]迷走神经和交感神经参与了电针对应激性胃黏膜损伤的调控作用，其作用部分是由β受体介导实现的。