十二指肠球部多发隆起病变与幽门螺杆菌和胃上皮化生的关系

目的探讨内镜下十二指肠球部多发隆起病变与幽门螺杆菌（Hp）感染和胃上皮化生等组织学异常关系.方法连续调查86例经胃镜检查证实十二指肠球部多发隆起病变患者,并以40例球部基本正常患者作为对照.病变组Hp阳性患者接受三联根除治疗（奥美拉唑20mg、克拉霉素250mg、甲硝唑400mg,每天2次）,疗程7 d,停药后随访6个月后复查胃镜;病变组Hp阴性者接受奥美拉唑20 mg,每天1次治疗,疗程4～6个月,停药后2周复查胃镜.比较2次胃镜检查结果,包括胃镜下隆起病变程度及球部黏膜胃上皮化生等组织学异常,分析Hp感染与上述胃镜下表现及组织学异常关系.结果对照组患者组织学仅部分发现轻度慢性炎症,未发现球部Hp感染.病变组患者Hp检出率为58.1%,胃上皮化生检出率为57.0%.Hp阳性与Hp阴性患者胃镜下隆起病变程度差异无统计学意义（P＞0.05）,但胃上皮化生检出率更高,程度更严重（P＜0.05）.76例患者复查胃镜,根除Hp或奥美拉唑治疗对Hp阳性或阴性患者球部多发隆起病变无明显作用,但根除Hp后6个月,53.6%（15/28）患者胃上皮化生消失,61.0%（25/41）患者绒毛萎缩恢复正常,所有患者淋巴滤泡完全消失（26/26）,杯状细胞减少完全恢复（25/25）,同时炎症和活动性显著减轻（P值均＜0.01）.奥美拉唑疗效不显著.结论十二指肠球部多发隆起病变患者半数以上有Hp感染.Hp感染与隆起病变伴随组织学炎症密切相关,而与其内镜下表现及严重程度无关.根除Hp可使炎症显著减轻,胃上皮化生范围缩小或消退.     

Characteristics of gastritis in patients with Helicobacter pylori-positive reflux esophagitis

BACKGROUND AND AIM: The influence of Helicobacter pylori on gastric acid secretion differs with the status of gastritis. The histological characteristics of gastritis in H. pylori-positive patients with reflux esophagitis have not been fully investigated. We therefore studied the pattern of endoscopic gastric mucosal atrophy and degree of histological gastritis in such patients. METHODS: Subjects comprised 41 H. pylori-positive patients with reflux esophagitis, 41 age- and sex-matched patients with duodenal ulcer, and 41 patients with early gastric cancer. The endoscopic pattern of gastric mucosal atrophy was reviewed, and the degree of histological gastritis in biopsy specimens from the antrum and corpus was assessed in accordance with the updated Sydney system. RESULTS: The grade of endoscopic and histological gastric mucosal atrophy in patients with reflux esophagitis was significantly lower than that in patients with gastric cancer, and the histological scores for antral atrophy and metaplasia in patients with reflux esophagitis tended to be lower than those in patients with duodenal ulcer. In patients with reflux esophagitis and duodenal ulcer, the scores for antral inflammation and activity tended to be higher than those for the corpus. Conversely, the inflammation and activity score in patients with early gastric cancer showed a corpus-predominant gastritis pattern. CONCLUSION: In H. pylori-positive patients with reflux esophagitis, the degree of endoscopic gastric mucosal atrophy is low and histologically there is an antral-predominant gastritis pattern. Therefore, gastric acid secretion in H. pylori-positive patients with reflux esophagitis may be augmented by H. pylori infection.     

Helicobacter pylori-induced inflammation masks the underlying presence of low-grade dysplasia on gastric lesions

BACKGROUND Helicobacter pylori(H. pylori) infection has been associated with a long-term risk of precancerous gastric conditions(PGC) even after H. pylori eradication.AIM To investigate the efficacy of High-Resolution White-Light Endoscopy with Narrow-Band Imaging in detecting PGC, before/after H. pylori eradication.METHODS We studied 85 consecutive patients with H. pylori-related gastritis with/without PGC before and 6 mo after proven H. pylori eradication. Kimura-Takemoto modified and endoscopic grading of gastric intestinal metaplasia classifications, were applied to assess the endoscopic extension of atrophy and intestinal metaplasia. The histological result was considered to be the gold standard. The Sydney System, the Operative-Link on Gastritis-Assessment, and the OperativeLink on Gastric-Intestinal Metaplasia were used for defining histological gastritis, atrophy and intestinal metaplasia, whereas dysplasia was graded according to World Health Organization classification. Serum anti-parietal cell antibody and anti-intrinsic factor were measured when autoimmune atrophic gastritis was suspected.RESULTS After H. pylori eradication histological signs of mononuclear/polymorphonuclear cell infiltration and Mucosal Associated Lymphoid Tissue-hyperplasia, disappeared or decreased in 100% and 96.5% of patients respectively, whereas the Operative-Link on Gastritis-Assessment and Operative-Link on Gastric-Intestinal Metaplasia stages did not change. Low-Grade Dysplasia prevalence was similar on random biopsies before and after H. pylori eradication(17.6% vs 10.6%, P = 0.19), but increased in patients with visible lesions(0% vs 22.4%, P 0.0001). At a multivariate analysis, the probability for detecting dysplasia after resolution of H. pylori-related active inflammation was higher in patients with regression or reduction of Mucosal Associated Lymphoid Tissue hyperplasia, greater alcohol consumption, and anti-parietal cell antibody and/or anti-intrinsic factor positivity [odds ratio(OR) = 3.88, 95% confidence interval(CI): 1.31-11.49, P = 0.01; OR = 3.10, 95%CI: 1.05-9.12, P = 0.04 and OR = 5.47, 95%CI: 1.33-22.39, P 0.04, respectively].CONCLUSION High-Resolution White-Light Endoscopy with Narrow-Band Imaging allows an accurate diagnosis of Low-Grade Dysplasia on visible lesions after regression of H. pylori-induced chronic gastritis. Patients with an overlap between autoimmune/H. pylori-induced gastritis may require more extensive gastric mapping.     

结节型十二指肠炎的内镜表现及其临床病理学特征

目的 探讨结节型十二指肠炎内镜下表现与其组织学特征的关系及其发病机制。方法 观察内镜下136例结节型十二指肠炎的表现，对其活检标本均行H-E染色，观察病理改变，Giemsa染色及快速尿素酶试验诊断幽门螺杆菌感染，十二指肠黏膜兼作AB／PAS染色，观察十二指肠胃上皮化生。结果 136例结节型十二指肠炎内镜下表现为直径0．2～1．0cm大小不等的结节，伴有不同程度的充血、水肿，其中伴糜烂21例，出血点及（或）瘀斑30例。检出率占同期15820例内镜检查的0．9％，十二指肠炎的3．8％。病理诊断为十二指肠炎107例，其中慢性十二指肠炎53例，表现为间质内可见慢性炎性细胞浸润，肠绒毛缩短或萎缩、变平．肠腺不同程度减少；活动性十二指肠炎54例，除慢性炎性细胞外，黏膜层及固有层内还有不同程度的中性粒细胞浸润，伴Brunner腺增生51例，胃型上皮化生59例。136例中检出胃黏膜异位增生7例以及血吸虫虫卵所致的炎性病变4例，107例结节型十二指肠炎中，幽门螺杆阳性（Hp^＋）者为45．8％（49／107）。其中，53例慢性十二指肠炎患者中HP^＋者为32．1％（17／53），54例活动性十二指肠炎中Hp^＋检出率为59．3％（32／54），后者的Hp^＋检出率显著高于前者（P〈0．01）。结论 结节型十二指肠炎是一类特殊的非特异性十二指肠炎，内镜下表现与组织学改变存在不一致性。其发生可能与Hp感染及胃上皮化生、Brunner腺增生有关。     

Histological changes of gastric atrophy and intestinal metaplasia after Helicobacter pylori eradication]

BACKGROUND/AIMS: Long-term Helicobater pylori infection results in atrophic gastritis and intestinal metaplasia, and increases the risk of gastric cancer. However, it is still controversial that eradication of H. pylori improves atrophy or metaplasia. Therefore, we investigated histological changes after the H. pylori eradication in patients with atrophy or metaplasia. METHODS: One hundred seven patients who received successful eradication of H. pylori infection in Hanyang University, Guri Hospital from March 2001 to April 2006, were enrolled. Antral biopsy was taken before the eradication to confirm the H. pylori infection and grade of atrophy or metaplasia by updated Sydney System. After a certain period of time, antral biopsy was repeatedly taken to confirm the eradication and investigate histological changes of atrophy or metaplasia. RESULTS: Mean age of the patients was 55.3+/-11.3, and average follow-up period was 28.7+/-13.9 months. Endoscopic diagnosis included gastric ulcer, duodenal ulcer, non-ulcer antral gastritis. Atrophy was observed in 41 of 91 and their average score was 0.73+/-0.92. After the eradication of H. pylori, atrophy was improved (0.38+/-0.70, p=0.025). However, metaplasia which was observed in 49 of 107, did not significantly improve during the follow-up period. Newly developed atrophy (7 of 38) or metaplasia (18 of 49) was observed in patients who without atrophy or metaplasia initially. Their average scores were slightly lower than those of cases with pre-existing atrophy or metaplasia without statistical significance. CONCLUSIONS: After the eradication of H. pylori infection, atrophic gastritis may be improved, but change of intestinal metaplasia is milder and may take longer duration for improvement.     

Helicobacter pylori infection and development of gastric cancer in Korea: long-term follow-up

BACKGROUND AND AIM: Infection of Helicobacter pylori is viewed as a major driver of progression to the precancerous state or to gastric cancer. This study was performed to investigate the effect of H. pylori infection on gastric cancer development and to determine to what extent H. pylori eradication is likely to reduce the prevalence of gastric cancer. METHODS: Gastric cancer development was investigated in 1790 Korean subjects who underwent gastroscopy and H. pylori testing between 1992 and 1998. The effects of H. pylori-positive and eradicated states on gastric cancer development were analyzed. RESULTS: Gastric cancer developed in 5 of the study cohort during a mean follow-up period of 9.4 years. All of these patients were positive for H. pylori infection, and 4 of the 5 had antral intestinal metaplasia (IM) at the time of study enrollment. One of these 5 patients was in an eradicated state when the gastric cancer was diagnosed, and had histologic IM before eradication therapy was performed. Gastric cancer was found to develop 10.9 times more frequently in the presence of IM than in its absence. CONCLUSIONS: The present study shows a close relationship between H. pylori infection and IM, and between IM and the development of gastric cancer. In addition, our finding suggests that chronic H. pylori infection looks like an important risk factor for the development of gastric cancer in Korea, where the prevalence of H. pylori remains high. This study indicates that to prevent gastric cancer H. pylori eradication is best performed before the development of IM.     

Effects of Helicobacter pylori Infection on gastric mucin expression

AIMS: This study was performed to determine the gastric distributions of MUC5AC and MUC6 depending on Helicobacter pylori (H. pylori) infection, and to evaluate whether the expressions of MUC5 and MUC6 change in H. pylori-associated gastroduodenal diseases. In addition, MUC5AC and MUC6 expressional changes were investigated before and after H. pylori eradication. METHODS: In the 224 individuals (136 H. pylori-positive and 88 H. pylori-negative) who came from control (N=48), duodenal ulcer (N=35), benign gastric ulcer (N=61), dysplasia plus stomach cancer (N=80) groups, MUC5AC and MUC6 expressions were determined by immunohistochemical staining in the antrum and body, respectively. This staining for MUC5AC and MUC6 were reperformed in 113 of the 136 H. pylori-positive patients after successful H. pylori eradication by proton pump inhibitor-based triple therapy. RESULTS: (1) No difference was found between the H. pylori-positive and negative groups in terms of MUC5AC expression. In contrast, MUC6 expression was significantly lower in the H. pylori-positive group than in the H. pylori-negative group in the gastric body. Moreover, reduced MUC6 expression increased to the H. pylori-negative level after eradication. (2) Expressions of MUC5AC and MUC6 were significantly lower in the dysplasia plus cancer group than those of control in case of H. pylori positive. Similarly, MUC5AC and MUC6 expressions were significantly lower in the presence of atrophic gastritis with intestinal metaplasia in case of H. pylori positive. (3) Aberrant expressions of MUC6 in foveolar cells were observed in both antrum (11.3%) and body (5.3%) only in the H. pylori-positive group, but this reverted to normal after H. pylori eradication. CONCLUSION: These results suggest that H. pylori infection causes alterations of mucin expression, closely related with the development of gastric atrophy with intestinal metaplasia, probably contributing to carcinogenesis.     

Multifocal atrophic gastritis and gastric carcinoma

Gastric carcinoma remains a major cause of morbidity and mortality worldwide despite its significant decline in recent years. H. pylori infection begins with nonatrophic gastritis, and most individuals continue to have nonatrophic H. pylori gastritis throughout their lifetime. A minority of those with severe antral inflammation will develop a duodenal ulcer, and a few, for unknown reasons, may develop gastric MALT lymphoma. Others, who acquired the H. pylori infection in early childhood, develop progressive multifocal atrophic gastritis with loss of gastric glands. A small proportion of these individuals develop extensive, incomplete (type III) intestinal metaplasia, and an even smaller proportion will progress to dysplasia and intestinal-type gastric carcinoma. H. pylori-associated gastritis is also a risk factor for diffuse-type gastric carcinoma, which is not preceded by atrophy, intestinal metaplasia, or dysplasia. Appropriate screening and preventive measures should be considered in high-risk groups. It is also crucial to identify cofactors such as genetic susceptibility and environmental factors that might interact with H. pylori infection to increase gastric cancer risk. To make an impact on gastric cancer incidence and mortality, serious consideration should be given to early H. pylori eradication in high-risk groups and endoscopic surveillance according to the updated Sydney system in some patients with high-risk preneoplastic lesions, whereas dysplastic lesions should be removed without delay. Studies currently in progress may tell us whether H. pylori eradication can prevent later development of gastric carcinoma and thus eliminate a major cause of mortality worldwide.     

Short-segment Barrett��s esophagus and cardia intestinal metaplasia: A comparative analysis

AIM:To investigate the endoscopy and histology of short-segment Barrett’s esophagus (SSBE) and cardia intestinal metaplasia (CIM),and their correlation with Helicobacter pylori (H. pylori) gastritis and gastroesophageal reflux disease (GERD). METHODS:Biopsy specimens were taken from 32 SSBE patients and 41 CIM patients with normal appearance of the esophagogastric junction. Eight biopsy specimens from the lower esophagus,cardia,and gastric antrum were stained with hematoxylin/eosin,Alcian blue/periodic acid-Schiff,Alcian blue/high iron diamine and Gimenez dye. Results were graded independently by one pathologist. RESULTS:The SSBE patients were younger than the CIM patients (P < 0.01). The incidence of dysplasia and incomplete intestinal metaplasia subtype was higher in SSBE patients than in CIM patients (P < 0.01). H. pylori infection was correlated with antral intestinal metaplasia (P < 0.05),but not with reflux symptomatic,endoscopic,or histological markers of GERD in CIM patients. SSBE was correlated with reflux symptomatic and endoscopic esophagitis (P < 0.01),but not with H. pylori infection and antral intestinal metaplasia. CONCLUSION:Dysplasia risk is significantly greater in SSBE patients than in CIM patients. CIM is a manifestation of H. pylori-associated and multifocal atrophic gastritis,whereas SSBE may result from GERD.     

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.     

Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study

OBJECTIVE: Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. MATERIAL AND METHODS: Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58+/-12.6 years (mean+/-SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. RESULTS: Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). CONCLUSIONS: Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

Comparison of He/icobacter py/ori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylineosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Comparison of Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients

AIM: To compare Helicobacter pylori infection and gastric mucosal histological features of gastric ulcer patients with chronic gastritis patients in different age groups and from different biopsy sites. METHODS: The biopsy specimens were taken from the antrum, corpus and upper angulus of gastric ulcer and chronic gastritis patients. Giemsa staining, improved Toluidine-blue staining and H pylori-specific antibody immune staining were performed as appropriate for the histological diagnosis of H pylori infection. Hematoxylin-eosin staining was used for the histological diagnosis of activity of H pylori infection, mucosal inflammation, glandular atrophy and intestinal metaplasia and scored into four grades according to the Updated Sydney System. RESULTS: Total rate of H pylori infection, mucosal inflammation, activity of H pylori infection, glandular atrophy and intestinal metaplasia in 3 839 gastric ulcer patients (78.5%, 97.4%, 82.1%, 61.1% and 64.2%, respectively) were significantly higher than those in 4 102 chronic gastritis patients (55.0%, 90.3%, 56.2%, 36.8%, and 37.0%, respectively, P<0.05). The rate of H pylori colonization of chronic gastritis in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 33.3%, 41.7%, 53.6%, 57.3%, 50.7%, 43.5%, respectively; in corpus, it was 32.6%, 41.9%, 53.8%, 60.2%, 58.0%, 54.8%, respectively; in angulus, it was 32.4%, 42.1%, 51.6%, 54.5%, 49.7%, 43.5%, respectively. The rate of H pylori colonization of gastric ulcer in <30 years, 31-40 years, 41-50 years, 51-60 years, 61-70 years and >70 years age groups in antrum was 60.5%, 79.9%, 80.9%, 66.8%, 59.6%, 45.6%, respectively; in corpus, it was 59.7%, 79.6%, 83.6%, 80.1%, 70.6%, 59.1%, respectively; in angulus, it was 61.3%, 77.8%, 75.3%, 68.8%, 59.7%, 45.8%, respectively. The rate of H pylori colonization at antrum was similar to corpus and angulus in patients, below 50 years, with chronic gastritis and in patients, below 40 years, with gastric ulcer. In the other age- groups, the rate of H pylori colonization was highest in corpus, lower in antrum and lowest in angulus (all P<0.05). The rates of glandular atrophy and intestinal metaplasia were higher and earlier in H pylori-positive patients than those without H pylori infection (both P<0.01). In comparison of gastric ulcer patients with chronic gastritis patients, the rate of glandular atrophy and intestinal metaplasia was higher in H pylori-positive patients with gastric ulcer than in H pylori-positive patients with chronic gastritis (both P<0.01); the rate of glandular atrophy and intestinal metaplasia were also higher in H pylori-negative patients with gastric ulcer than in H pylori-negative patients with chronic gastritis (both P<0.01). Both glandular atrophy and intestinal metaplasia were much more commonly identified in the angulus than in the antrum, lowest in corpus (all P<0.01). CONCLUSION: Rate of H pylori infection, glandular atrophy and intestinal metaplasia in gastric ulcer were higher than in chronic gastritis in all-different age -groups. Distribution of H pylori colonization is pangastric in the younger patients. It is highest in corpus, lower in antrum and lowest in angulus in the older age groups. Progression of glandular atrophy and intestinal metaplasia seem to have a key role in the distribution of H pylori colonization. H pylori appears to be the most important risk factor for the development of glandular atrophy and intestinal metaplasia, but it is not the only risk.     

Effect of lifestyle, smoking, and diet on development of intestinal metaplasia in H. pylori-positive subjects

OBJECTIVES: This study aimed to evaluate the influence of environmental and sociodemographic factors and the effect of smoking, alcohol, and dietary habits on the risk of gastric intestinal metaplasia (IM) in Helicobacter pylori-infected subjects. METHODS: The investigation was based on 2598 consecutive volunteer blood donors tested for the presence of antibodies against H. pylori from March 1995 to March 1997. Endoscopy with multiple biopsies was offered to all H. pylori-positive, symptomatic subjects. The presence or absence of IM was diagnosed by gastric biopsies. A serologically H. pylori-positive subject with gastric IM was defined as a case, whereas serologically H. pylori-positive subjects without IM were used as controls. All patients answered a detailed questionnaire collecting sociodemographic characteristics and smoking, alcohol drinking, and dietary habits. Odds ratios (ORs) and their 95% CIs were estimated by unconditional logistic regression, including terms for age and sex, to assess the association between the data collected and IM. RESULTS: Three hundred forty-four subjects with serological H. pylori infection and upper-GI symptoms underwent GI endoscopy, during which biopsies were taken for histological diagnosis. Histology revealed metaplasia in 74 subjects (21.5%). Incomplete IM was found in 37.8% of these cases. No significant associations were found between IM and anthropometric or sociodemographic factors. There was a significant association between age and IM (chi2 for trend, 6.67; p value, 0.009). Current smokers of over 20 cigarettes per day had a 4-fold risk of IM (OR, 4.75, 95% CI, 1.33-16.99). A 2-fold increased risk was found for high butter consumers (OR, 2.17; 95% CI, 1.14-4.11). No significant specific associations were found between the variables studied and complete or incomplete IM. CONCLUSIONS: This study found that smoking and high butter consumption may increase the risk of having gastric IM in H. pylori-positive subjects.     

Intestinal metaplasia: evolution after Helicobacter pylori eradication and influence in the success of eradicating therapy.

INTRODUCTION: intestinal metaplasia associated with Helicobacter pylori infection is a stage of the temporal sequence of histological lesions gradually induced by this microorganism. It is considered a preneoplastic lesion and its regression after eradication is controversial. AIM: to assess the evolution of intestinal metaplasia after eradication and to investigate whether metaplasia is a factor that contributes to successful treatment. MATERIAL AND METHODS: four hundred Helicobacter pylori positive patients were studied. Eradicating therapy was administered and endoscopic biopsies of gastric antrum and body were taken before and after eradication. Among other histological data, the presence of intestinal metaplasia was assessed. RESULTS: of all patients successfully treated, biopsies were taken before and after eradication in 268 of them: 71 (26,5%) had metaplasia before and 50 (18,7%) after eradication. A significant difference was observed in the outcome (p = 0,036) of the first eradicating treatment between the group without initial metaplasia (72,7%) and the group with initial metaplasia (61.2%). DISCUSSION: Helicobacter pylori eradication can revert intestinal metaplasia in some patients. On the other hand, the first treatment could be less successful in patients with intestinal metaplasia.     

Endoscopic patterns of gastric mucosa and its clinicopathological significance

AIM: To explore the correlation of magnifying endoscopic patterns and histopathology, Helicobacter pylori (H pylori)infection of the gastric mucosa. METHODS: Gastric mucosal patterns in 140 patients with chronic gastritis were studied using Olympus GIF-Q240Z magnifying endoscope. Histopathological examination, rapid urease test and Warrthin-Starry staining were taken with biopsy samples from the magnified sites of stomach. The magnifying endoscopic patterns were compared with histopathological results and Hpyloridetection. RESULTS: The pit patterns of gastric mucosa were classified as types A (round spot), B (short rod), C (branched), D (reticular) and E (villus). The detection rate of chronic atrophic gastritis (CAG) by magnifying endoscopy was 94.3 % (33/35), which was significantly higher than that by routine endoscopy (22.9 %, 8/35) (P&lt;0.01). The pit patterns of 31 cases of intestinal metaplasia (IM) appeared as type E in 18 cases (58.1%), type D in 8 cases (25.8 %) and type C in 5 cases (16.1%). Fourteen out of 18 patients (77.8 %) with complete type (type I) of IM appeared as type E of pit patterns, whereas only 4 of 13 (30.8 %) patients with incomplete type (typesⅡ and Ⅲ) of IM appeared as type E (P&lt;0.05). Collecting venules in the anterior of lower part of gastric corpus were subgrouped into types R (regular), I (irregular) and D (disappeared). Hpyloriinfection was found in 12.2%(9/74),60%(9/15) and 84.3%(43/51) cases in these types respectively. Hpyloriinfection rate in type R was significantly lower than that in other two types (P&lt;0.01). CONCLUSION: Magnifying endoscopy may have an obvious value in diagnosing chronic atrophic gastritis, intestinal metaplasia and Hpy/oriinfection.     

Helicobacter pylori eradication dramatically improves inflammation in the gastric cardia

OBJECTIVES: Inflammation of the gastric cardia, i.e., "carditis," has been associated with Helicobacter pylori (H. pylori) infection; however, some investigators believe carditis to be a histological marker for gastroesophageal reflux disease. The aim of this study was to investigate the role of H. pylori eradication on the grade of carditis scored according to the updated Sydney classification. METHODS: Consecutive patients presenting for upper endoscopy underwent systematic gastric biopsies (eight antral, 12 corpus, and four cardia). Patients with H. pylori infection and carditis were identified and followed prospectively before and after H. pylori treatment. At pretreatment and, on average, 2 yr after eradication of H. pylori, the degree of inflammation in the gastric cardia and H. pylori status were blindly assessed by a single pathologist. RESULTS: A total of 31 patients with H. pylori infection and carditis were identified. The mean age was 70 yr (range: 37-81 yr); all were male. Four were African-American and 27 were Caucasian. All patients were treated with standard anti-H. pylori therapy, including a proton pump inhibitor in combination with two antibiotics for 2 wk. Eradication of H. pylori was successful in 23 patients (group I), whereas eight patients had persistent infection (group II). Patients were followed after eradication therapy for a mean of 23.2 months (range: 6-48 months). After eradication therapy, there was a significant decrease (p < 0.0001) in the carditis scores (activity and inflammation scores) in group I, whereas the scores remained unchanged in group II patients. In both groups, there were no significant changes in the degree of intestinal metaplasia or atrophy. There were four patients with intestinal metaplasia, and one with atrophy. CONCLUSIONS: There is a dramatic improvement in the degree of inflammation and activity scores in the gastric cardia of patients with successful H. pylori eradication compared to those with persistent infection. By fulfilling one of Koch's postulates (i.e., improvement in the disease after cure of the possible etiological organism), these data support H. pylori as being the etiological agent for carditis in this group of patients.     

Nonsteroidal anti-inflammatory drug use does not affect short-term endoscopic and histologic outcomes after Helicobacter pylori eradication in patients with rheumatoid arthritis

We evaluated the effects of the use of nonsteroidal anti-inflammatory drugs (NSAIDs) on endoscopic and histological findings in patients with rheumatoid arthritis (RA) before and after the eradication of Helicobacter pylori infection. Helicobacter pylori (H. pylori) eradication using lansoprazole 30 mg, amoxicillin 750 mg, and clarithromycin 200 mg twice daily for 1 week was conducted in 44 patients (mean age: 56.5 years) with RA. Using the updated Sydney system, endoscopic and histological findings of the greater curvature of the antrum, the greater curvature of the upper corpus, and the lesser curvature of the lower corpus were compared before and after eradication, for a mean follow-up period of 3.5 months. Overall, H. pylori eradication was successful in 32 patients (72.7%). Of these 32 patients, 23 were NSAID users. In the successful eradication group, (1) there was no significant change on endoscopic findings, including gastric erythema and erosion in all three regions irrespective of NSAIDs use; (2) of 17 active ulcers before eradication in NSAIDs users, all healed except for one duodenal ulcer that persisted, where one patient newly developed a gastric ulcer, one developed erosive duodenitis, and two developed reflux esophagitis, all in NSAID users; (3) neutrophil infiltration and chronic inflammation were significantly improved in all three regions after H. pylori eradication irrespective of use of NSAIDs, while atrophic change and intestinal metaplasia did not change. In the eradication failure group; (1) there was no significant change on endoscopic and histological findings in the three regions; (2) two of three ulcers present before eradication on NSAID users persisted even after eradication, and no new cases of gastric ulcer or erosive duodenitis occurred. In conclusion, over a mean follow-up period of 3.5 months, use of NSAIDs in Japanese patients with RA did not impair the healing process of gastric and duodenal ulcers nor did it affect the endoscopic and histological improvements associated with H. pylori eradication.     

Nonsteroidal anti-inflammatory drug use does not affect short-term endoscopic and histologic outcomes after Helicobacter pylori eradication in patients with rheumatoid arthritis

Abstract

We evaluated the effects of the use of nonsteroidal anti-inflammatory drugs (NSAIDs) on endoscopic and histological findings in patients with rheumatoid arthritis (RA) before and after the eradication of Helicobacter pylori infection. Helicobacter pylori (H. pylori) eradication using lansoprazole 30?mg, amoxicillin 750?mg, and clarithromycin 200?mg twice daily for 1 week was conducted in 44 patients (mean age: 56.5 years) with RA. Using the updated Sydney system, endoscopic and histological findings of the greater curvature of the antrum, the greater curvature of the upper corpus, and the lesser curvature of the lower corpus were compared before and after eradication, for a mean follow-up period of 3.5 months. Overall, H. pylori eradication was successful in 32 patients (72.7%). Of these 32 patients, 23 were NSAID users. In the successful eradication group, (1) there was no significant change on endoscopic findings, including gastric erythema and erosion in all three regions irrespective of NSAIDs use; (2) of 17 active ulcers before eradication in NSAIDs users, all healed except for one duodenal ulcer that persisted, where one patient newly developed a gastric ulcer, one developed erosive duodenitis, and two developed reflux esophagitis, all in NSAID users; (3) neutrophil infiltration and chronic inflammation were significantly improved in all three regions after H. pylori eradication irrespective of use of NSAIDs, while atrophic change and intestinal metaplasia did not change. In the eradication failure group; (1) there was no significant change on endoscopic and histological findings in the three regions; (2) two of three ulcers present before eradication on NSAID users persisted even after eradication, and no new cases of gastric ulcer or erosive duodenitis occurred. In conclusion, over a mean follow-up period of 3.5 months, use of NSAIDs in Japanese patients with RA did not impair the healing process of gastric and duodenal ulcers nor did it affect the endoscopic and histological improvements associated with H. pylori eradication.     

Helicobacter pylori infection influences tumor growth of human gastric carcinomas

BACKGROUND: Helicobacter pylori infection is considered a risk factor for gastric carcinoma. However, the effect of eradication therapy in gastric carcinoma patients is not well known. The aim of this study was to investigate the relationship between H. pylori infection and tumor growth of gastric carcinoma. METHODS: Fifty-one patients with gastric carcinoma participated in the study. Thirty-three were H. pylori-positive, 6 were H. pylori-negative, and 12 were diagnosed with gastric carcinoma after eradication of H. pylori. To investigate tumor growth of gastric carcinoma, cell proliferation and angiogenesis of the tumors were evaluated by immunohistochemical techniques using Ki-67 and CD34. RESULTS: The Ki-67 labeling index was 47.9 +/- 2.6 (mean +/- s) in the H. pylori-positive group, 38.1 +/- 3.6 in the H. pylori-eradicated group, and 22.2 +/- 5.5 in the H. pylori-negative group. It was significantly lower in the H. pylori-eradicated and H. pylori-negative groups than in the H. pylori-positive one, and a significant difference was also found between the H. pylori-positive and H. pylori-eradicated groups. The microvessel counts were 62.5 +/- 3.0, 50.2 +/- 4.0, and 66.0 +/- 9.8 in the positive, eradicated, and negative groups, respectively. A significant difference was found between the H. pylori-positive and H. pylori-eradicated groups. CONCLUSION: Our results suggest that H. pylori infection is associated with cell proliferation, and its eradication may influence tumor vascularity of gastric carcinoma. Therefore, H. pylori eradication therapy may contribute to the suppression of tumor growth.