Helicobacter pylori associated antral gastritis in peptic ulcer disease patients and normal healthy population of kashmir, India

Aim: To study the association of Helicobacter pylori infection with chronic antral gastritis in peptic ulcer disease patients and healthy population of Kashmir.Methods: 50 peptic ulcer patients (duodenal ulcer = 46, gastric ulcer = 2 and combined duodenal and gastric ulcer = 2) and 30 asymptomatic healthy volunteers were included in this study. Peptic ulcer was diagnosed on endoscopic examination. 4-6 punch biopsies were taken from gastric antrum in all the individuals and in case of gastric ulcer an additional biopsy was taken from the edge of the ulcer to exclude its malignant nature. Helicobacter pylori (H. pylori) organism was diagnosed using three different test methods, viz. Histology (using Giemsa Stain), Microbiology (Gram Stain) and Biochemistry (using one minute Endoscopy Room Test). Histological diagnosis of H. pylori was taken as the "gold standard" for the presence of H. pylori organism. Histological diagnosis of gastritis was made using Hematoxylin and Eosin Stain and the gastritis was classified as active chronic gastritis and superficial chronic gastritis.Results: Out of 30 peptic ulcer disease patients with associated antral gastritis, 27 (90%) were positive for H. pylori on histological examination (13 superficial chronic gastritis and 14 active chronic gastritis) whereas out of 8 healthy volunteers with histological evidence of chronic antral gastritis, H. pylori was observed in 7 individuals (87.50%) (4 active chronic gastritis and 3 superficial chronic gastritis).Conclusion: A highly significant association between H. pylori infection with chronic antral gastritis both in peptic ulcer disease patients and healthy volunteers of Kashmir was found in this study. Association between H. pylori infection and chronic gastritis was 90% in peptic ulcer group and 87.50% in healthy population (P<0.005).     

老年人消化性溃疡与慢性萎缩性胃炎的相关性研究

目的研究老年人消化性溃疡与慢性萎缩性胃炎的相关性。方法对十二指肠溃疡（DU）、胃溃疡（GU）和复合性溃疡（CU）的老年患者胃窦、胃窦胃体交界处和胃体黏膜以及慢性胃炎（CG）患者胃窦黏膜活检标本进行组织学检查,统计各自胃黏膜的萎缩、肠化生、慢性炎症、活动性和幽门螺杆菌（Hp）感染的发生率。结果 DU患者胃窦、胃窦胃体交界处和胃体黏膜的萎缩发生率分别为54.0%、8.0%和16.0%,肠化生发生率分别为19.0%、6.0%和4.0%。其胃窦黏膜肠化生的发生率明显低于相应的GU、CU或CG者。3种消化性溃疡和CG患者均存在胃窦部慢性炎症,且老年消化性溃疡患者胃体部炎症的发生率较高,其胃炎活动性以胃窦部为主,且均较CG者高。结论老年人消化性溃疡均可有胃窦部灶性萎缩和肠化生发生,但DU胃窦黏膜肠化发生率最低,这可能是老年DU患者罹患胃癌危险性较低的原因之一。     

Incidence of Gastric Metaplasia and Helicobacter pylori Infection in Duodenal Bulb - With Specific Reference to Patients With Duodenal Ulcers

We determined the incidence of gastric metaplasia in the duodenal bulb of duodenal ulcer patients and the Helicobacter pylori (H. pylori) infection rate at sites with gastric metaplasia. Biopsy of the duodenal bulb showed the presence of gastric metaplasia in 61 of 86 patients (71%) overall and in 18 of 47 patients (38.3%) who had gastrectomy at an early gastric cancer. The histological diagnosis of H. pylori infection showed good agreement (83.3%) with the result of the rapid urease test, indicating that H. pylori occurs in regions with gastric metaplasia. This finding suggests that H. pylori infects gastric metaplasia in the duodenal bulb, causing mucosal injury, which is then transformed into duodenal ulcers. The exact mechanism by which gastric metaplasia is caused is unknown, but it is believed to occur in the transitional zone in the duodenal mucosa.     

Ulcers and gastritis

This article reviews recently published literature regarding ulcers and gastritis. Although endoscopy is the most useful procedure for diagnosis in the upper gastrointestinal tract, complications do occur, and procedure-related costs are significant. The appropriate indication for endoscopy has recently been debated. Helicobacter pylori is known to be an important pathogen involved in gastric and duodenal inflammation. Peptic ulcer disease and severe gastric mucosal injury are caused by virulent strains, and many reports have focused on CagA. Follow-up studies on surveillance endoscopy in patients with peptic ulcer or gastritis report that patients with atrophic gastritis and intestinal metaplasia are at significantly higher risk for gastric cancer. H. pylori eradication sometimes causes gastroduodenal erosion and reflux esophagitis, and the mechanisms involved have been revealed. Proton-pump inhibitors are useful in the treatment of ulcers caused by nonsteroidal anti-inflammatory drugs (NSAIDs), reflux esophagitis, and for preventing rebleeding after endoscopic hemostasis, but the effect of long-term acid suppression on the gastric mucosa is still a matter of debate. H. pylori infection and NSAID intake are both risk factors for peptic ulcer disease, and are important aspects in this field.     

Ulcers and gastritis

This article reviews recently published reports on ulcers and gastritis. Helicobacter pylori is known to be an important pathogen involved in gastroduodenal inflammation and peptic ulcers. Conventional endoscopy is of limited usefulness in the evaluation of gastritis, but magnifying endoscopy is evidently helpful in the diagnosis of chronic atrophic gastritis, intestinal metaplasia, and H. pylori infection. A significant reduction in the incidence of refractory ulcers and the prevalence of H. pylori infection in patients with peptic ulcer disease followed the introduction of H. pylori eradication treatment. Chronic H. pylori infection is associated with gastric cancer, and the effect of H. pylori eradication on the prevention of gastric cancer is an important issue that is still a matter of controversy. Endoscopic hemostasis and intravenous proton-pump inhibitor (PPI) infusion represent a widely accepted approach to the treatment of peptic ulcer bleeding. In clinical practice, it is important to prevent recurrent bleeding and to treat patients who do not respond to endoscopic therapy or PPI treatment. Laparoscopic repair for peptic ulcer perforations, with postoperative eradication treatment, has gradually met with acceptance in patients with H. pylori infection. H. pylori infection and its treatment continue to be interesting problems in this field.     

The effect of Helicobacter pylori eradication on duodenal gastric metaplasia

We investigated the incidence of duodenal gastric metaplasia and its response to Helicobacter pylori eradication in patients with duodenal ulcer or erosive duodenitis. Gastric and duodenal biopsies were taken from patients with endoscopically detected H. pylori positive duodenal ulcer or erosive duodenitis, and the presence and extent of duodenal gastric metaplasia was recorded. Patients were given omeprazole 20 mg twice daily for 2 weeks, and amoxicillin 1 g and clarithromycin 500 mg twice daily for 10 days, and then ranitidine for a further 8 weeks. Biopsies were repeated 6 months after the start of treatment. Duodenal gastric metaplasia was initially present in 22 patients (52%) and was more frequent in ulcer patients than in duodenitis patients, but not significantly so (69% versus 45%). After treatment, H. pylori was eradicated in 68% of duodenal gastric metaplasia patients and the duodenum was normal endoscopically in 85% of these patients. Duodenal gastric metaplasia was improved or eliminated in 12/15 H. pylori eradicators (80%) and in 5/7 H. pylori non-eradicators (71%), a non-significant difference. The improvement in duodenal gastric metaplasia appeared to be independent of H. pylori eradication.     

Pathogenesis of gastric and duodenal ulcer in the elderly

In the elderly, H. pylori infection and nonsteroidal anti-inflammatory drug(NSAID) use are most important risk factors for peptic ulcer disease. It is now recognized that, in patients with H. pylori infection, nonatrophic antral-predominant gastritis results in increased acid secretion, which is seen in duodenal ulcer patients, whereas corpus-predominant gastritis and pangastritis result in decreased acid secretion, that are seen in patients with proximal gastric ulcer and gastric cancer. These physiological changes are considered to be related to disease outcome. On the other hand, NSAIDs induced gastrointestinal toxicity is primarily due to the inhibition of mucosal prostaglandin synthesis in the gastric mucosa, which subsequently impairs the gastric cytoprotective factors. These two factors may independently, or even synergistically, cause the development of peptic ulcer disease in the elderly.     

Campylobacter gastritis and associated disorders

Our review of evidence that Campylobacter pylori is an important factor in gastritis, peptic ulcer disease, and "nonulcer dyspepsia" suggests that C pylori is the most common cause of chronic active gastritis. The association between C pylori gastritis and duodenal ulcer, which approaches 100%, leads to the suggestion that this infection plays an important role in the pathogenesis of duodenal ulcer. Evidence supporting a central role in the pathogenesis of gastric ulcer and nonulcer dyspepsia is less compelling.     

Scope and consequences of peptic ulcer disease. How important is asymptomatic Helicobacter pylori infection?

H pylori infection is so common as to seem ubiquitous in many areas of the world. Transmission is believed to be primarily person to person. The pathogen invariably damages the gastric mucosa, resulting in both structural and functional abnormalities. It causes histologic gastritis and is critical in the pathogenesis of the gastritis-associated diseases, namely, gastric ulcer, duodenal ulcer, gastric adenocarcinoma, and primary gastric lymphoma. Elimination of the infection results in healing of gastritis and cure of peptic ulcer disease.     

Esophagitis, gastritis and duodenitis provoked by cure of Helicobacter pylori infection

It has been recently reported that curing Helicobacter pylori (H. pylori) infection may provoke reflux esophagitis. We studied the effect of cure of H. pylori infection on the development of disorders of the upper gastrointestinal (UGI) tract. The estimated incidence of reflux esophagitis, gastric erosions and duodenal erosions after cure of infection was 8.9%, 32.8% and 8.9%. The incidences of reflux esophagitis, gastric erosions and duodenal erosions were 10.0%, 30.0% and 6.7% in patients with gastric ulcer, 2.8%, 36.1% and 27.8% in those with duodenal ulcer and 9.2%, 30.3% and 1.3% in those with atrophic gastritis. Therefore, patients whose H. pylori infection has been cured should carefully be investigated by endoscopy for H. pylori-associated disease.     

长春地区慢性胃病患者幽门螺杆菌感染状况调查

目的通过对本地区慢性胃病患者幽门螺杆菌（H.pylori）感染状况调查,了解本地区流行病学特点,为进一步阐明其与慢性胃病发生发展的关系提供理论依据。方法采用ELISA方法测定血清H.pyloriIgG抗体及CagA抗体;采取胃粘膜活检组织进行快速尿素酶试验,调查H.pylori感染情况,分析其与各种疾病的关系。结果1180例慢性胃病患者H.pylori感染率为67.11%,复合性溃疡、十二指肠溃疡、胃溃疡及慢性萎缩性胃炎感染率分别为90.9%、84.57%、83.96%和80.24%。与慢性浅表性胃炎相比差异有显著性。消化性溃疡、慢性萎缩性胃炎、胃癌和胃息肉患者血清Hp-CagA抗体的阳性率明显高于慢性浅表性胃炎（P〈0.05）。结论本地区慢性胃病患者H.pylori感染率高与多数地区的普通人群,H.pylori感染者尤其是CagA阳性者,更易发生慢性萎缩性胃炎、消化性溃疡及胃癌。     

Helicobacter pylori as a new paradigm in the pathogenesis of upper GI diseases

Discovery of H. pylori from human gastric mucosa have induced an evolution in the concepts of upper GI diseases, especially in those of gastritis, peptic ulcer and gastric cancer. A new classification of gastritis, Sydney system and updated Sydney system, are proposed and commonly used in worldwide. Eradication treatment against H. pylori infection can completely improve the histologic gastritis, which is defined by the infiltration of inflammatory cells. In gastric and duodenal ulceration, the eradication of H. pylori accelerates the ulcer healing without acid suppression, and prevents the ulcer recurrence without any maintenance therapy. These accumulating data suggest that H. pylori could have an etiologic relation to ulcer diseases, because these are a kind of intervention study on etiology. Thus, in ulcer diseases, H. pylori is proven to play an etiologic role. On the basis of these studies, a new treatment strategy is proposed in upper GI diseases. This is a new paradigm on upper GI diseases.     

Ulcer and gastritis

As in previous years, developments in the field of ulcers and gastritis have been dominated by new findings related to Helicobacter pylori. With the decrease in the frequency of H. pylori infection, the relative proportion of non-H. pylori ulcers has increased. Attempts to reduce the endoscopy workload by H. pylori or CagA screening have not been successful, and are probably ill-advised. It has become increasingly clear that curing H. pylori infection will not automatically lead to complete relief of symptoms in patients with duodenal ulcer disease. Post-therapy confirmation of cure will probably become the norm. Studies comparing omeprazole to misoprostol or ranitidine for nonsteroidal anti-inflammatory drug (NSAID) ulcer prevention in true NSAID ulcers have shown that omeprazole is equal to full-dose misoprostol for ulcer healing and to the lowest useful dose of misoprostol for ulcer prevention. H2-receptor antagonists cannot be recommended for NSAID ulcer healing or prevention. Elimination of H. pylori increases the prevalence of gastroesophageal reflux disease in a population in such a way that superficially, there appears to be a choice between more gastroesophageal reflux disease or multifocal atrophic gastritis. The risk of developing adenocarcinoma of the esophagogastric junction is many times (10-fold to 60-fold) less than the risk of developing gastric cancer from CagA-positive H. pylori infection with multifocal atrophic gastritis - the "protective" lesion.     

Peptic ulcer pathophysiology

Despite extensive research, the etiology of peptic ulcer disease remains unclear. Given the multiple processes that control acid and pepsin secretion and defense and repair of the gastroduodenal mucosa, it is likely that the cause of ulceration differs between individuals. Acid and pepsin appear to be necessary but not sufficient ingredients in the ulcerative process. It is clear that the majority of gastric ulcers and a substantial number of duodenal ulcers do not have increased gastric acid secretion. Recent research has focused more on protection and repair of the stomach and duodenum. NSAIDs cause a significant number of gastric and duodenal ulcers; this is probably due to inhibition of prostaglandin production with loss of its protective effects. In the absence of NSAIDs and gastrinoma, it appears that most gastric ulcers and all duodenal ulcers occur in the setting of H. pylori infection. Evidence is mounting in support of H. pylori as a necessary ingredient in the ulcerative process, similar to acid and pepsin. It is not known whether the bacteria or the accompanying inflammation is the more important factor in the pathophysiology. Although the pathophysiology of gastric ulcer and duodenal ulcer is similar, there are clearly differences between the two groups. Duodenal ulcer is typified by H. pylori infection and duodenitis and in many cases impaired duodenal bicarbonate secretion in the face of moderate increases in acid and peptic activity. These facts suggest the following process: increased peptic activity coupled with decreased duodenal buffering capacity may lead to increased mucosal injury and result in gastric metaplasia. In the presence of antral H. pylori, the gastric metaplasia can become colonized and inflamed. The inflammation or the infection itself then disrupts the process of mucosal defense or regeneration resulting in ulceration. A cycle of further injury and increased inflammation with loss of the framework for regeneration may then cause a chronic ulcer. Gastric ulcer often occurs with decreased acid-peptic activity, suggesting that mucosal defensive impairments are more important. The combination of inflammation, protective deficiencies, and moderate amounts of acid and pepsin may be enough to induce ulceration. Many questions remain in understanding the pathophysiology of peptic ulcer disease. The physiology and pathophysiology of mucosal regeneration and the mechanisms by which H. pylori and inflammation disrupt normal gastroduodenal function will be fruitful areas of future investigation.     

Geographical Pathology of Helicobacter pylori Infection: Is There More than One Gastritis?

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection.

This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.     

Helicobacter pylori: aggressor or innocent bystander?

Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries. Although the reservoir is uncertain, water or food transmission seems likely. There is sufficient evidence to assign an etiologic role to the bacteria in the causation of type B antral gastritis. H. pylori is found in areas of gastric metaplasia within the duodenum and is associated with duodenitis. Although acute infection leads to hypochlorhydria, chronic colonization has little effect on acid secretion. Studies have thus far failed to establish a convincing relationship between H. pylori and nonulcer dyspepsia, although the bacteria may play a role in selected patients. H. pylori is found in association with most idiopathic gastric and duodenal ulcers, but it is unclear as to whether the bacteria plays a causative or permissive role. The organism has a predilection for intercellular spaces and the mucous layer, thus affording relative isolation from luminally active antibiotics. Monotherapy with bismuth preparations transiently eliminates the bacteria, but recolonization is rapid, probably due to regrowth of sequestered organisms. A combination of metronidazole, bismuth, and tetracycline (or amoxicillin) affords the best eradication rate, but the potential side effects of this program should be considered. The present therapy of duodenal ulcer disease is effective and without significant risk. Treatment of H. pylori should be reserved for those patients who relapse on adequate maintenance therapy. If a safe and effective antibiotic becomes available, more frequent testing and earlier treatment intervention may become more attractive. H. pylori is probably an "innocent bystander" for most patients, but the bacteria may sufficiently impair the defenses of the antral and duodenal mucosa to facilitate the development and relapse of ulcer disease in subsets of patients.     

高清胃镜观察胃黏膜形态预测幽门螺杆菌感染的探索*

目的通过高清胃镜观察、归纳幽门螺杆菌(Hp)感染时胃黏膜形态改变以预测Hp感染结果,从而探讨高清胃镜直接诊断Hp感染的临床价值。方法纳入2016年10月-2017年1月在深圳市龙岗区第二人民医院同时进行胃镜检查和13C-尿素呼气试验的连续性500例受检者,以高清胃镜在白光下直接观察胃黏膜形态,根据所见形态特点预测是否存在Hp感染,并与13C-尿素呼气试验结果进行比对,比较两者结果符合率。结果胃体、胃底黏膜充血或出血;胃黏膜水肿;胃底、胃体黏膜可见较多黏液;中度以上黏膜萎缩;黏膜肠上皮化生;十二指肠球部溃疡可能成为胃镜预测Hp感染阳性的特征点。胃体可见规则集合静脉(RAC);胃黏膜有光泽,无萎缩;胃底或胃体息肉;胃窦或胃体小弯的放射性充血可能成为胃镜预测Hp感染阴性的特征点。胃镜预测Hp感染的敏感性为90.1%,特异性为70.4%;阳性预测值为71.0%,阴性预测值为89.9%,总体符合率79.2%。结论高清胃镜直接观察胃黏膜形态表现可有效预测Hp感染情况,可在临床上进一步推广验证。     

Helicobacter pylori: controversies and an approach to management

Helicobacter pylori (formerly, Campylobacter pylori) is a gram-negative, spiral-shaped bacterium with a strong affinity for gastric-type epithelium. Convincing evidence indicates that H. pylori plays an etiologic role in the development of chronic, nonspecific gastritis, and it may play an important role in the pathogenesis of duodenal ulcer disease. An etiologic role for this organism in chronic gastric ulceration, nonulcer dyspepsia, and gastric carcinoma is not established. Whereas the diagnosis of H. pylori infection is relatively straightforward, the questions of when and how to treat the infection do not have established answers. A high rate of recrudescence follows most currently used therapeutic interventions. Until the pathogenicity of H. pylori in clinical disease is further supported and additional treatment trials have been completed, a conservative management approach is recommended.     

Guidelines in the management of Helicobacter pylori infection in Japan--in comparison with the guidelines published in other countries

Helicobacter pylori(H. pylori) is a causative agent for chronic gastritis and is an important risk factor for peptic ulcers, gastric carcinomas, and gastric MALT lymphomas. In 2000, the Japanese Society for Helicobacter Research published a guideline on the diagnosis and treatment of H. pylori infection for physicians in routine medical practice. In this guideline, H. pylori eradication therapy is recommended in gastric or duodenal ulcer patients. H. pylori eradication is also recommended in gastric MALT lymphoma patients but the guideline says it should be done at specialist institutions. Considering the high prevalence of gastric carcinomas in Japan. H. pylori eradication for the prevention of gastric carcinomas should be discussed urgently.     

The role of Helicobacter pylori in gastroduodenal disease.

Peptic ulcers are the result of a wide variety of factors, with H. pylori probably being one of the more significant. H. pylori has been most strongly associated with gastritis and duodenal ulcer disease. The relationship of H. pylori to gastric ulcers is less substantial. The eradication of H. pylori can be achieved in the majority of patients with triple antibiotic therapy. However, resistance to metronidazole occurs readily. Eradication of H. pylori can change the course of duodenal ulcer disease by decreasing recurrence rate from 80% to zero. Nonetheless, treatment for H. pylori should only be done in randomized trials at the current time because of the lack of completely effective therapy and the high risks of side effects. The mechanism by which H. pylori influences duodenal ulcer recurrence is unclear. Pathogenic mechanisms of the organism also need to be further elucidated.