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

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

消化不良病人胃窦胃体内镜表现及病理对比研究

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

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.     

The effect of eradication therapy on histological changes in the gastric mucosa in patients with non-ulcer dyspepsia and Helicobacter pylori infection. Prospective randomized intervention study.

BACKGROUND/AIMS: Eradication therapy results in the control of gastritis. Little is known about its influence on changes in the topographic distribution and regression of specific mucosal alterations in patients with dyspepsia. Our previous study has shown the complex pathological changes in the cardia, corpus and antrum in patients with Helicobacter pylori (H. pylori) infection and NUD. To determine the effect of eradication therapy on the development of histological changes in the lower esophagus, cardia, corpus and antrum in patients with nonulcerous dyspepsia, 3 and 6 months after therapy. METHODOLOGY: Two hundred and fifty-one consecutive patients with dyspepsia (the presence of ulcer and stomach malignancy was ruled out) and H. pylori infection were followed up in a prospective study. Every patient underwent endoscopic examination with eight biopsies taken (antrum, corpus, cardia and lower esophagus) before, and 3 and 6 months after eradication therapy (Pantoprazole 40 mg daily, Amoxycilline 1000 mg b.i.d., Clarithromycine 500 mg b.i.d.). The biopsies were stained by (H&E) and Giemsa's staining modified for H. pylori detection. The inflammation, its activity, H. pylori and other mucosal alterations were investigated semi-quantitatively and assessed according to the Sydney system. RESULTS: In the cardia, corpus and antrum, significant decrease in chronic inflammation, and H. pylori activity (p<0.001) was found. Atrophy was insignificantly higher in the cardia (p<0.05), whereas in the corpus (p<0.05) and antrum (p<0.001) it was lower. Intestinal metaplasia remained unchanged in the cardia and in the antrum; in the corpus an insignificant decrease was found. The number of patients with foveolar hyperplasia in the cardia was higher, but this increase was not significant, in contrast to the corpus (p<0.01) and antrum (p<0.05). This was especially the case between the first and the second visit. Regression of lymphoid follicles was significant in the cardia (p<0.001) and in the antrum (p<0.01), whereas their quantity in the corpus was unchanged. In the corpus and antrum, a significant increase of chemical gastropathy between the second and third visit (p<0.001) was found. The same applied for hemorrhages found in the esophagus papillae (p<0.001). CONCLUSIONS: Eradication therapy was closely associated with a significant decrease of inflammation activity and H. pylori infection. Chronic inflammation, mucosal atrophy and intestinal metaplasia persisted, even though their intensity was decreased, and signs of chemical gastropathy with hemorrhages in the esophageal papillae were found.     

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.     

The prevalence of Helicobacter pylori in nonulcer dyspepsia. Importance of stratification according to age

Helicobacter pylori (formerly Campylobacter pylori) is causally related to active antral gastritis and is highly associated with duodenal and gastric ulcers. However, the relationship of H pylori to nonulcer dyspepsia is less clear. We determined the presence of H pylori in unselected patients who were undergoing upper gastrointestinal tract endoscopy, and we found a prevalence of 37% in 110 patients with nonulcer dyspepsia that was similar to previous data. Patients with nonulcer dyspepsia who had H pylori were found to be significantly older than patients with nonulcer dyspepsia who did not have H pylori. In addition, when stratified according to age, we detected an increased prevalence of H pylori in patients with nonulcer dyspepsia with increasing age, similar to that reported for asymptomatic control populations. This finding casts doubt as to the causal role of H pylori for most patients with nonulcer dyspepsia and stresses the importance of considering epidemiologic factors, such as age, when evaluating the role of H pylori in specific disease states.     

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.     

Comparison of clinical, serological and histological findings between non-ulcer dyspepsia patients with and without Helicobacter pylori infection

BACKGROUND AND AIMS: The role of Helicobacter pylori (H. pylori) infection in non-ulcer dyspepsia (NUD) remains controversial. This study investigates the clinical, serological and histological differences between patients with H. pylori-positive and -negative NUD. METHODS: One hundred and eighty consecutive patients with NUD were enrolled from January to December 1998. The severity of symptoms was evaluated by the Tucci's scoring system. The histological changes of gastric mucosa were assessed according to the Updated Sydney System, and a fasting blood sample was obtained to test the serum gastrin and pepsinogen I levels. RESULTS: The H. pylori-positive NUD patients were notably older than H. pylori-negative NUD patients (48.2 +/- 15.9 vs 39.8 +/- 15.7 years, P= 0.001). There were no differences in other clinical factors between the two NUD groups. The serum pepsinogen I levels were considerably higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (78.9 +/- 42.2 vs 61.5 +/- 43.3 ng/mL, P<0.01). However, no significant differences in serum gastrin levels were discovered between the two groups. The antrum histological scores for chronic inflammation, acute inflammation, gland atrophy and lymphoid follicles were higher in H. pylori-positive NUD patients than in H. pylori-negative NUD patients (2.09 vs 1.01, P<0.001; 1.22 vs 0.36, P<0.001; 0.76 vs 0.36, P<0.01; 0.33 vs 0.13, P<0.01, respectively). CONCLUSIONS: The present study discovered marked differences in age, serum pepsinogen I levels, histological grades of acute inflammation, chronic inflammation, gland atrophy and lymphoid tissue formation between H. pylori-positive and H. pylori-negative NUD patients. Further investigation of the clinical prognosis of the two groups of patients is necessary.     

Chronic Helicobacter pylori infection in a population in southern Sweden analysed by histopathology, immunoblot and ELISA serology

BACKGROUND: Many individuals are infected with the bacterium Helicobacter pylori. Some develop ulcers or mucosal atrophy. AIMS: To correlate the histological characteristics of the H. pylori -induced gastritis to the immunoblot pattern of the H. pylori infection and to compare the presence of H. pylori bacteria in tissue specimens with ELISA serology and immunoblot analysis. METHODS: One hundred and sixty-six consecutive patients were referred to gastroscopy. Forty patients were excluded for various reasons and 126 were included in the study. RESULTS: Twenty-three patients had ulcerations and 25 erosions. Ninety-two (73%) had a chronic gastritis and in 90 (71%) it involved both the antrum and corpus. Ninety-one (72%), of whom 96% had a chronic gastritis, had visible bacteria in the tissue specimens, used as the 'gold standard' for the detection of infection. In patients with chronic gastritis 65 (70%) had positive H. pylori ELISA serology, 27 (30%) had negative H. pylori ELISA, while 76 (83%) had a positive immunoblot pattern. The ELISA positive patients had more advanced chronic gastritis but a lower frequency of metaplasia and atrophy. Acute inflammatory activity in the chronic gastritis had a high immunoreactivity to 120 kDa (CagA) protein and was significantly correlated to antibody reactivity to proteins in the 53-65 kDa range (heat shock proteins) and to a 43 kDa subunit. Metaplasia and atrophy in antrum was associated with a 62 kDa protein band. CONCLUSION: Almost all H. pylori-infected patients had a pangastritis, visible in both antrum and corpus. Acute inflammatory activity in the chronic gastritis and the presence of metaplasia and atrophy in antrum were associated with a specific immunoblot pattern, indicating infection with more virulent strains. Immunoblot analysis had a better sensitivity than ELISA H. pylori serology.     

Helicobacterpylori infection and gastropathy： A comparison between Indonesian and Japanese patients

AIM: To compare the effects of Helicobacter pylori ( H pylori) infection on gastropathy between Indonesian and Japanese patients.METHODS: Biopsy specimens were obtained during upper gastrointestinal endoscopy from 167 subjects (125 Indonesians and 42 Japanese) with uninvestigated symptoms of dyspepsia. The specimens were analyzed for the presence of H pylori using urease analysis, histopathology, and cell culture. The grade and activity of gastritis was assessed using the updated Sydney system.RESULTS: The percentages of Indonesian and Japanese patients who were H pylori-positive at the antrum or body of the stomach were similar (68% and 59.5%, respectively; P = 0.316). Of those who were H pylori-positive, more Japanese patients than Indonesian patients had high levels of polymorphonuclear cells ( P = 0.001), mononuclear cells ( P = 0.013), glandular atrophy ( P = 0.000), and intestinal metaplasia ( P = 0.011) in both the antrum and body of the stomach.CONCLUSION: The grade of gastritis and prevalence of mucosal atrophy and intestinal metaplasia were higher in Japanese patients. The difference between Indonesian and Japanese patients was significant.     

Histopathological profile of gastritis in adult patients seen at a referral hospital in Kenya

AIM： To conduct a detailed histological study of gastritis in adult patients attending an endoscopy clinic at a Kenyan teaching and referral hospital.
METHODS： Biopsy specimens from consecutive patients were examined and graded according to the Updated Sydney System for H pylori infection, chronic inflammation, neutrophil activity, glandular atrophy and intestinal metaplasia. Also documented were gastric tissue eosinophil counts and presence of lymphoid follicles.
RESULTS： The rate of the graded variables, in the antrum and corpus respectively, were as follows： H pylori infection （91%, 86%）, chronic inflammation （98%, 93%）, neutrophil activity （91%, 86%）, glandular atrophy （57%, 15%） and intestinal metaplasia （11%, 2%）. Lymphoid follicles were noted in 11% of cases. Duodenal and gastric ulcers were documented in 32% and 2% respectively. The mean eosinophil count was 5.9 ±0.74 eosinophils/ HPF and 9.58 ± 0.93 eosinophils/HPF in the corpus and antrum respectively. Significant association was found between the degree of H pylori colonisation with chronic inflammation, neutrophil activity and antral glandular atrophy. Biopsies from the antrum and corpus showed significant histopathological discordance for all the graded variables. H pylori negative cases were associated with recent antibiotic use.
CONCLUSION： The study the chief cause of gastritis reaffirms that H pylori is in this environment. The majority of patients show a moderate to high degree of inflammation but a low degree of glandular atrophy and intestinal metaplasia. The study shows that interrelationships between the histological variables in this African population are similar to those found in other populations worldwide including non-African populations.     

Endoscopic [13C]-urea breath test for quantification of Helicobacter pylori infection

BACKGROUND: We previously developed a new diagnostic method for Helicobacter pylori infection and called it the endoscopic [13C]-urea breath test (EUBT). Here we evaluate the relationship between the EUBT results and the histological findings. METHODS: The EUBT was performed on 137 patients with gastroduodenal diseases. After the collection of a baseline breath sample, gastroduodenal endoscopy was performed. Twenty milliliters of 0.05% phenol red solution containing 100 mg of [13C]-urea was sprayed over the entire gastric mucosa under endoscopic observation. A breath sample was collected 15 min after spraying. The content of 13CO2 in the breath samples was measured by ratio mass spectrometry. Two biopsy specimens each from the antrum and the middle corpus were obtained for culture and histology. Helicobacter pylori colonization, activity, inflammation, atrophy and intestinal metaplasia were classified on a four-point scale according to the Updated Sydney System. RESULTS: We found positive correlations between the EUBT values and the H. pylori colonization and activity score in the antrum and corpus, and negative correlations between the EUBT values and the atrophy and intestinal metaplasia scores in the corpus. CONCLUSIONS: The EUBT can be an indicator of the intragastric bacterial load and the histological findings for H. pylori.     

Improvement in atrophic gastritis and intestinal metaplasia in patients in whom Helicobacter pylori was eradicated

BACKGROUND: Glandular atrophy and intestinal metaplasia are precancerous lesions; whether Helicobacter pylori eradication affects these lesions is controversial. OBJECTIVE: To determine whether H. pylori eradication is associated with improvement in glandular atrophy and intestinal metaplasia after at least 1 year. DESIGN: Single-blind, uncontrolled prospective trial. SETTING: Academic gastroenterology clinic in Japan. PATIENTS: 163 consecutive patients with dyspepsia and H. pylori infection. INTERVENTION: One-week course of a proton-pump inhibitor and antibiotic therapy. MEASUREMENTS: Endoscopic examination with antral and corporal biopsy was done before treatment and at 1 to 3 and 12 to 15 months after treatment. Gastritis, atrophy, and metaplasia were graded according to the updated Sydney System. RESULTS: In the 115 patients in whom H. pylori was eradicated, inflammation and mean neutrophil activity had decreased by 1 to 3 months, and both glandular atrophy in the corpus and intestinal metaplasia in the antrum had decreased by 12 to 15 months. Glandular atrophy in the corpus improved in 34 (89%) of 38 patients with atrophy before treatment, and intestinal metaplasia in the antrum improved in 28 (61%) of 46 patients who had metaplasia at baseline. In the 48 patients in whom eradication was unsuccessful, no significant histologic changes were observed. CONCLUSION: In the year after successful H. pylori eradication, precancerous lesions improved in most patients.     

Prolonged use of proton pump inhibitors, CagA status, and the outcome of Helicobacter pylori gastritis

GOALS AND BACKGROUND: To assess whether prolonged use of proton pump inhibitors (PPIs) in patients infected with Helicobacter pylori has adverse effects on gastritis. STUDY: We studied 34 H. pylori-positive individuals with reflux esophagitis, Barrett esophagus, or nonulcer dyspepsia. Half of them were on maintenance treatment with PPIs (mean, 8 years) and half were not.H. pylori and CagA status were tested serologically. Gastric biopsies were classified histopathologically by the updated Sydney classification. RESULTS: Proton pump inhibitors in H. pylori gastritis are associated with significantly less antral inflammation and lower H. pylori density, regardless of CagA status. There was a tendency toward more antral atrophy in patients with the CagA strain who were undergoing maintenance treatment with PPIs (p = 0.08), but there was an opposite tendency in CagA-negative individuals (p = 0.08). Intestinal metaplasia was seen more frequently in CagA-positive, treated individuals (p = 0.028). CONCLUSIONS: These findings support the hypothesis that CagA status is important in the progression to atrophy and that maintenance treatment with PPIs accelerate this progression, while reducing inflammatory infiltration.     

Implications of anti-parietal cell antibodies and anti-Helicobacter pylori antibodies in histological gastritis and patient outcome

AIM: To develop a serum or histological marker for early discovery of gastric atrophy or intestinal metaplasia. METHODS: This study enrolled 44 patients with gastric adenocarcinoma, 52 patients with duodenal ulcer, 14 patients with gastric ulcer and 42 consecutive healthy adults as controls. Each patient received an endoscopy and five biopsy samples were obtained. The degrees of histological parameters of gastritis were categorized following the Updated Sydney System. Anti-parietal cell antibodies (APCA) and anti-Helicobacter pylori (H pylori) antibodies (AHPA) were analyzed by immunoassays. H pylori infection was diagnosed by rapid urease test and histological examination. RESULTS: Patients with gastric cancer and gastric ulcer are significantly older than healthy subjects, while also displaying higher frequency of APCA than healthy controls. Patients with positive APCA showed higher scores in gastric atrophy and intestinal metaplasia of corpus than patients with negative APCA. Patients with positive AHPA had higher scores in gastric atrophy, intestinal metaplasia, and gastric inflammation of antrum than those patients with negative AHPA. Elderly patients had greater prevalence rates of APCA. Following multivariant logistic regression analysis, the only significant risk factor for antral atrophy is positive AHPA, while that for corpus atrophy is positive APCA. CONCLUSION: The existence of positive APCA correlates with glandular atrophy in corpus and the presence of positive AHPA correlates with glandular atrophy in antrum. The existence of serum APCA and AHPA betokens glandular atrophy and requires further examination for gastric cancer.     

Is nonulcer dyspepsia related to Helicobacter pylori infection?

Dyspepsia, defined as pain or discomfort centered in the upper abdomen, is a common clinical problem. A variety of underlying disease states may result in dyspepsia, but commonly, diagnostic investigation will show no identifiable pathology, and the patient is diagnosed with nonulcer dyspepsia. Numerous hypothesis have been suggested as to the cause of symptoms in patients with nonulcer dyspepsia, including perturbations of gastroduodenal motility, hypersensitivity to physiologic stimuli including acid, and the effect(s) of infection within the gastric mucosa by Helicobacter pylori. Some epidemiological studies have suggested that patients with nonulcer dyspepsia may have a slightly higher prevalence of H. pylori infection. However, association does not prove causation. Causation of nonulcer dyspepsia by H. pylori could best be documented by resolution of symptoms following eradication of the infection. Early intervention studies indicated that there was a beneficial effect on symptoms of nonulcer dyspepsia with H. pylori eradication, but most of these studies had serious methodological flaws. In the last few years there have been a number of well-designed studies investigating the effect of H. pylori eradication on symptoms in patients with nonulcer dyspepsia. The results of these studies are inconsistent, but suggest that there is little, if any benefit from treatment. This case-based article on nonulcer dyspepsia discusses these studies in detail and provides a possible explanation for the differences in outcomes.     

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.     

Association between the IgG subclass response, inflammation and disease status in Helicobacter pylori infection

BACKGROUND: In many viral, bacterial and parasitic infections the Immunoglobulin G (IgG) subclass response has been shown to correlate with severity of inflammation and disease outcome. The aim of the present study was to investigate the association between the IgG subclass response to Helicobacter pylori infection and disease and inflammation. METHODS: Eighty-three symptomatic patients undergoing endoscopic examination were included in the study. Upon endoscopic examination, the presence of ulceration was noted and biopsy specimens were collected from the gastric antrum, body and transitional zone. Blood was also collected from each patient. Gastric biopsy sections were graded using the Sydney system. H. pylori specific IgG, IgG1, IgG2, IgG3 and IgG4 were measured by ELISA. The IgG subclass was also examined retrospectively in sera collected from 20 patients previously proven to have duodenal ulcer (DU). RESULTS: The results of histological examination and IgG serology showed 35 subjects to be H. pylori negative and 48 to be H. pylori positive. Of the 48 H. pylori positive subjects, 25 were diagnosed with functional dyspepsia (FD), 14 with current DU and 9 with evidence of past DU. Significantly higher levels of IgG2 antibodies were found in patients with DU as compared with patients with FD (P < 0.01). In addition, significantly higher IgG3 subclass antibody levels were associated with chronic inflammatory cells in the body (P < 0.05) and active inflammatory cells in the transitional zone (P < 0.01). A significantly increased level of IgG1 antibodies was associated with lower levels of colonization in the gastric antrum. CONCLUSION: The results of this study suggest that the IgG subclass response in subjects infected with H. pylori may be a marker of DU disease as well as increased levels of inflammation.     

Endoscopy-based Kyoto classification score of gastritis related to pathological topography of neutrophil activity

BACKGROUND Endoscopy-based Kyoto classification for gastritis and pathological topographic distribution of neutrophil infiltration are correlated with gastric cancer risk.AIM To investigate the association between Kyoto classification and the topographic distribution of neutrophil activity.METHODS Kyoto classification score, ranging from 0 to 8, consisted of atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness. Neutrophil activity was scored according to the updated Sydney System using biopsy samples obtained from the greater curvature of the corpus and the antrum. The participants were divided into four categories, inactive stomach, antrumpredominant gastritis, pangastritis, and corpus-predominant gastritis, based on the topographic distribution of neutrophil activity. Effects of sex, age, body mass index, drinking habit, smoking habit, family history of gastric cancer, serum Helicobacter pylori(H. pylori) antibody, and Kyoto score on topography of neutrophil infiltration were analyzed.RESULTS A total of 327 patients(comprising 50.7% women, with an average age of 50.2 years) were enrolled in this study. H. pylori infection rate was 82.9% with a mean Kyoto score of 4.63. The Kyoto score was associated with the topographic distribution of neutrophil activity. Kyoto scores were significantly higher in the order of inactive stomach, antrum-predominant gastritis, pangastritis, and corpuspredominant gastritis(3.05, 4.57, 5.21, and 5.96, respectively). Each individual score of endoscopic findings(i.e., atrophy, intestinal metaplasia, enlarged folds, nodularity, and diffuse redness) was correlated with the topographic distribution of neutrophil activity. On multivariate analysis, the Kyoto score, age, and serum H. pylori antibody were independently associated with the topographic distribution of neutrophil activity.CONCLUSION The Kyoto classification score was associated with the topographic distribution of neutrophil activity.     

Antral nodularity identifies children infected with Helicobacter pylori with higher grades of gastric inflammation

BACKGROUND: The endoscopic pattern of antral nodularity is a peculiar finding in children with Helicobacter pylori infection. The aim of this study was to determine whether this finding is related to more severe gastritis. METHODS: One hundred seventy-four consecutive children (median age 8.7 years) referred for gastroscopy were studied. Biopsy specimens from the antrum and body of the stomach were taken to assess H pylori status, gastritis score, and lymphoid follicles. Clinical diagnosis, major symptoms and endoscopic findings were recorded. RESULTS: Eighty-four (48%) children (median age 10.5 years) had evidence of H pylori infection. The endoscopic pattern of antral nodularity was found only in children infected with H pylori (34/84, 40.5% vs. 0/90, 0%, p < 0.0001% 100% specificity, 40.5% sensitivity). Among all children infected with H pylori, the gastritis score was higher (p < 0.0001) in those with antral nodularity (n = 34) than in those without (n = 50). Completely normal gastric mucosal histology was never found in children infected with H pylori with antral nodularity. The presence and number of lymphoid follicles was strongly related to the finding of antral nodularity (p < 0.01). CONCLUSIONS: The endoscopic pattern of antral nodularity identifies children with H pylori infection, severe gastritis, and increased lymphoid follicles.