The histopathology of non-steroidal anti-inflammatory drug induced gastroduodenal damage: correlation with Helicobacter pylori, ulcers, and haemorrhagic events

AIMS: The spectrum of microscopic lesions resulting from the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), known as chemical gastritis, remains unclear, and the variable prevalence reported in different studies makes this issue a matter of lively debate. The aim of this study was to evaluate the prevalence and importance of chemical gastritis in patients regularly taking NSAIDs. Owing to the high prevalence of Helicobacter pylori infection, particularly in subjects over 60 years of age, and in view of a possible association with damage, the presence of H pylori infection in the same tissue sample was also determined in all patients. METHODS: One hundred and ninety seven subjects were enrolled, 118 of whom were receiving chronic treatment with NSAIDs and 79 of whom were controls, pair matched for age, sex, and clinical symptoms (ulcer-like dyspepsia or upper digestive tract haemorrhage). Antral biopsies taken during upper gastroduodenal endoscopy were assessed for chemical gastritis according to a modified version of Dixon's score, and for Helicobacter correlated chronic active gastritis, according to the updated Sydney system. RESULTS: Chemical gastritis was identified in 11 patients taking NSAIDs (9%) and in four controls (5%) (p < 0.05). Helicobacter pylori was detected in 53 patients taking NSAIDs (45%) and in 34 controls (43%). Patients taking NSAIDs had a significantly higher number of erosions and ulcers and worse endoscores than controls. The presence of H pylori did not appear to increase histological damage, ulcer prevalence, or haemorrhagic events. CONCLUSIONS: Chemical gastritis is present in a limited number of patients regularly taking NSAIDs, and is not strongly correlated with NSAID induced damage. In many cases of peptic ulcer or upper gastrointestinal bleeding in patients taking NSAIDs, the presence of chemical gastritis or H pylori infection cannot solely account for the development of mucosal damage.     

Can NSAID/ASA-induced erosions of the gastric mucosa be identified at histology?

Studies in animals have shown that NSAID/ASA-induced erosions have an ischaemic pathogenesis. We therefore studied the question of whether such erosions in human gastric biopsy material can be identified on the basis of the ischaemic necrosis. Histological sections prepared from forceps biopsy material obtained from 122 patients with erosions (at least three biopsy specimens from the erosion and two from antrum and corpus each) were classified by a pathologist blinded to the endoscopic findings and the medication used by the patients. NSAID/ASA erosions were diagnosed when a homogeneous eosinophilic ischaemic necrosis blending into the adjoining lamina propria presented. Helicobacter pylori (Hp)-induced erosions were diagnosed when, in the presence of Hp gastritis, erosive defects were covered with a non-homogeneous fibrinoid necrosis containing granulocytes and cell debris. Finally, the histological classification was compared with data on medication usage. The histological diagnosis was Hp-induced erosions in 59 patients, NSAID/ASA-induced erosions with no Hp gastritis in 23, and NSAID/ASA-induced erosions with concomitant Hp gastritis in 40. A comparison of this histological classification with the data provided by the referring physicians on patient medication revealed that 70% of the patients with histological diagnosis of NSAID/ASA-induced erosions in the absence of Hp gastritis, and 65% of those diagnosed to have NSAID/ASA-induced erosions and concomitant Hp gastritis, had been taking such drugs. Among the erosions diagnosed as H. pylori-induced, 81% of the patients were reported not to take such medication. The sensitivity of the diagnosis of NSAID/ASA-induced erosions was 72.9%, and specificity 79.6%. The results of the present study show that a high percentage of the NSAID/ASA-induced erosions of the gastric mucosa can indeed be correctly diagnosed at histology.     

Helicobacter pylori, gastritis, and peptic ulceration in the elderly.

AIMS: To determine the histopathological types of gastritis, presence of H pylori, and of peptic ulceration in patients aged 70 and over, compared with younger adults. METHODS: Gastric antral and corpus biopsy specimens from 112 elderly patients were classified and graded histologically according to the Sydney system. Details of recent antibiotic and non-steroidal anti-inflammatory drug use were recorded. Eighty four of the patients were positive for H pylori IgG antibodies and parietal cell antibodies. The results were compared with those from a series of 124 adult patients aged under 60. RESULTS: H pylori were visible at histological examination in only 57 of 87 (65.5%) elderly patients with chronic gastritis (excluding "special forms") compared with 72 of 79 (91.1%) of the younger patients with gastritis (p < 0.0002). Severe atrophy of the corpus mucosa was significantly associated with absence of H pylori (p < 0.002), and was present in eight of 30 elderly patients with helicobacter negative gastritis. Other explanations for absence of H pylori include recent antibiotic intake, more intestinal metaplasia, and lower bacterial load in elderly patients (p < 0.05). Autoimmune gastritis and NSAID use did not seem to be relevant. Serodiagnosis showed reduced sensitivity (81%) in patients who were helicobacter positive histologically, but was positive in 14 of 23 (61%) with H pylori negative gastritis histologically, suggesting either current infection that had been missed or previous infection. Peptic ulceration was significantly associated with NSAID use, but not with H pylori in the elderly. CONCLUSIONS: The spectrum of gastritis is different in the elderly, compared with younger adults, due to a significant group with chronic gastritis who are H pylori negative on histological examination. NSAID use, but not demonstration of H pylori (at histological examination) is associated with peptic ulceration in the elderly.     

Helicobacter pylori infection and chronic gastritis in gastric cancer.

AIMS: To investigate the prevalence of Helicobacter pylori associated chronic gastritis in patients with gastric cancer. METHODS: Serum IgG antibodies for H pylori were determined in 54 consecutive patients with gastric carcinoma. The prevalence of H pylori in gastric mucosa was also examined histologically (modified Giemsa) in 32 patients from whom adequate biopsy specimens of the antrum and corpus were available. Thirty five patients with gastrointestinal tumours outside the stomach and 48 with non-gastrointestinal malignancies served as controls. RESULTS: Of the 54 patients, 38 (70%) had H pylori antibodies (IgG) in their serum (three additional patients had H pylori antibodies IgA, class specific but not IgG specific). This prevalence was significantly higher (p less than 0.05) than that (49%) in the 35 controls. No differences in prevalence of H pylori antibodies were found between gastric cancer cases of intestinal (IGCA) or diffuse (DGCA) type, both these types showing H pylori antibodies (IgG) in 71% of the patients. In the subgroup of 32 subjects, five patients had normal gastric mucosa and four showed corpus limited atrophy ("pernicious anaemia type" atrophy of type A). All of these nine patients had no evidence of current or previous H pylori infection in serum (no IgG antibodies) or in tissue sections (negative Giemsa staining). The remaining 23 patients had antral or pangastritis, and all had evidence of current or previous H pylori infection. CONCLUSIONS: H pylori associated chronic gastritis was the associated disease in 75% of the patients with gastric cancer occurring equally often in both IGCA and DGCA groups. About 25% of cases seem to have a normal stomach or severe corpus limited atrophy, neither of which showed evidence of concomitant H pylori infection.     

Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons

We estimated the prevalences of Helicobacter pylori (formerly called Campylobacter pylori) infection and histologic gastritis in 113 asymptomatic persons, using endoscopic biopsy of the gastric antrum and corpus. Unsuspected lesions, mainly mucosal erosions, were revealed at endoscopy in 16 subjects (14 percent). Gastritis was found in 42 subjects (37 percent), of whom 36 (32 percent of the total) were found to be infected with H. pylori on the basis of hematoxylin-eosin staining. H. pylori was not found in any of the 71 subjects with normal histologic features. Gastritis and H. pylori were noted in both the antrum and corpus in 75 percent of those infected (n = 27). The prevalence of H. pylori infection increased from 10 percent (2 of 20 subjects) in those between the ages of 18 and 29, to 47 percent (7 of 15) in those between the ages of 60 and 69, but the effect of age did not reach statistical significance. The prevalence of gastritis increased significantly with advancing age. Stepwise logistic regression analysis revealed that the relative risk for H. pylori infection associated with recent (within six months) antibiotic use was 5.8 (95 percent confidence interval, 1.5 to 22.1), whereas the relative risk was 6.5 (95 percent confidence interval, 1.4 to 29.2) for those who had never used bismuth compounds. We conclude that histologic gastritis and H. pylori infection commonly occur in the stomach of apparently normal persons and increase in prevalence with advancing age. All the subjects with H. pylori infection had gastritis, suggesting a possible etiologic role for the bacterium in the histologic lesion.     

Chemical gastritis and Helicobacter pylori related gastritis in patients receiving non-steroidal anti-inflammatory drugs: comparison and correlation with peptic ulceration.

AIMS: To evaluate the prevalence and significance of chemical gastritis, in comparison with gastritis related to Helicobacter pylori in patients receiving non-steroidal anti inflammatory drugs (NSAIDs). METHODS: Two hundred and eighteen patients were studied, 174 of whom were taking NSAIDs. Chemical gastritis was defined as the presence of foveolar hyperplasia, muscle fibres in the lamina propria, oedema and vasodilation, in the absence of a chronic inflammatory cell infiltrate. RESULTS: Chemical gastritis was found in 46 (26%) patients taking NSAIDs, and three (7%) in subjects not taking these drugs (p less than 0.01). H pylori was detected in 56 (32%) subjects taking NSAIDs compared with 22 (50%) not taking these agents (p less than 0.02). Ulcers were found in 16 out of 72 patients (22%) taking NSAIDs and without H pylori infection or chemical gastritis compared with 27 out of 56 (48%) with H pylori related gastritis (p less than 0.01), and 25 out of 46 (54%) with chemical gastritis (p less than 0.01). CONCLUSIONS: Peptic ulcers associated with the use of NSAIDs seem to occur more commonly in patients with chemical gastritis or H pylori infection. Patients taking NSAIDs also seem to have a greater prevalence of chemical gastritis but a lower prevalence of H pylori than those not taking these drugs.     

Prevalence of Campylobacter pylori as demonstrated by histology or CLO-test in different types of gastritis. A study in 5 clinically predefined groups of patients

The prevalence of Campylobacter pylori infection as detected by histology was studied in 5 predefined groups of patients. The associated histologic and endoscopic findings were registered. Validity of CLO-test was tested against the histologic detection. The following groups of patients were studied: A) Non-ulcer dyspepsia (defined by one or all of three symptoms: heartburn, nausea/inappetence, halitosis/belching) B) control group (no specific symptoms, no ulcer, no history of gastric surgery) C) Duodenal ulcer D) Gastric ulcer E) Billroth I or II resection of the stomach. 200 patients were recruited for group A-C, in group D 134 patients and in group E 113 patients were studied. A mean prevalence of 60% was observed. Prevalence was highest in patients with duodenal ulcer (86%). In group D a prevalence of 65%, in A and E a prevalence of 54%, and in B of 40% were seen. The overall test sensitivity of the CLO-test compared against the histologic detection rate was 75%, the specificity 81%. Sensitivity was reduced in group A (69%) and E (53%) and in patients with inactive chronic gastritis (67%). In all groups patients with active forms of gastritis showed the highest prevalence of C. pylori infection. The specificity of the CLO-test was reduced in patients with duodenal ulcer (46%) and gastric ulcer (48%). Decreased specificity observed after therapy with histamin receptor (H2) blockers may explain this finding. The relationship of C. pylori infection with active types of gastritis or gastro-duodenal ulcer hints at a causal relation but is no definite proof of its etiologic role. The validity of the CLO-test seems questionable in patients with gastroduodenal ulcer or operated stomach.     

Giardia lamblia trophozoites in gastric biopsies

To assess the prevalence of gastric giardiasis in gastric biopsies of patients with carcinoma stomach and in patients taking treatment for duodenal ulcer. Gastric biopsy specimens from 54 patients of carcinoma stomach and 100 antral biopsies from patients taking treatment for duodenal ulcer were included in the study. Sections were stained with haematoxylin and eosin, methylene blue and May Grunwald-Giemsa stains and examined for presence of Giardia lamblia trophozoites. Eight out of 54 (14.9%) biopsies of gastric carcinoma patients harboured trophozoites of Giardia lamblia. Associated H. pylori infection was present in all biopsies (8/8; 100%). Atrophy and intestinal metaplasia was present in 62.5% (5/8) and 25% (2/8) cases respectively. Sections from seven out of 35 patients (20%) taking treatment for duodenal ulcer showed presence of G. lamblia. H. pylori infection, gastritis and atrophy were found in 85.7% (6/7), 71.4% (5/7) and 28.6% (2/7) cases respectively. First gastric biopsy in these patients was negative for G. lamblia but 2nd and 3rd biopsies were positive. A careful search for G. lamblia trophozoites should be made while examining the gastric biopsies, especially in patients with carcinoma stomach, intestinal metaplasia, atrophic gastritis and those taking treatment for duodenal ulcer. This may help in indirect diagnosis of clinically unsuspected cases of intestinal giardiasis and may explain persistence of vague upper gastrointestinal tract (UGIT) symptoms despite clearance of H. pylori in patients on anti-ulcer therapy.     

Morphologic features of the gastric mucosa in systemic lupus erythematosus and antiphospholipid syndrome

Morphology of gastric mucosa is characterized in the presence of Helicobacter pylori (HP) and Herpes viruses (HSV-1 and CMV). A total of 85 patients were examined (20 patients with primary APS and 65 with SLE). Chronic active gastritis was revealed in 85% patients with APS and 96% with SLE. 60% patients with APS and 45% with SLE had mucosal erosions. HP was detected in 70-87% of cases. Mixed infection of the gastric mucosa was observed in all the groups which was significantly associated with increased fibroblast and plasma cell number in the tunica propria. Tissue eosinophilia of the antral part of the stomach was observed in 39% of SLE patients. Glucocorticoid therapy was not associated with erosions and was combined with vascular thrombosis of gastric mucosa.     

Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease

From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P <.001) and epithelial degeneration (P =.004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non-Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and nonsteroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. HUM PATHOL 32:264-273. This is a US Government work. There are no restrictions on its use.     

Histological findings in gastric mucosa in patients treated with non-steroidal anti-inflammatory drugs.

AIMS--To identify distinguishing and general histological features related to the use of non-steroidal anti-inflammatory drugs (NSAID). METHODS--Slides from gastric antral biopsies of 50 patients with osteoarthritis taking NSAID were compared with slides from antral biopsies of 50 control cases matched for age, sex, and race. Semithin sections stained with toluidine blue were used. RESULTS--Chronic gastritis was seen in 76% of the patients taking NSAID and in 58% of the control cases; active inflammation was detected in 10% of the NSAID treated patients and in 24% of the control cases, and it appeared closely related with Helicobacter pylori infection. Some histological features common to all slides of patients taking NSAID were recognised. These consisted of focal erosions of the gastric epithelium and macroerosions, and they seemed to represent successive steps of a process of "desquamation". CONCLUSIONS--Some distinguishing morphological aspects appeared prominent; it is suggested that these may be related to the pathogenesis of NSAID linked peptic ulceration. On the other hand, epithelial damage due to NSAID appears very different from that due to Helicobacter pylori, another important factor involved in the aetiopathogenesis of peptic disease.     

Association of Helicobacter pylori with gastritis and peptic ulcer diseases

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.     

Serum pepsinogen I and II concentrations and IgG antibody to Helicobacter pylori in dyspeptic patients.

AIMS--To investigate the association between histologically confirmed gastritis, carriage of Helicobacter pylori and pepsinogen (PG) I and PG II concentrations. METHODS--Prospective study of 81 dyspeptic patients undergoing upper gastrointestinal endoscopy was made. The extent of gastric mucosal inflammation and the presence of H pylori was determined, and serology to evaluate PG I and II concentrations and IgG titres to H pylori was carried out. RESULTS--The presence of H pylori was strongly correlated with high IgG antibody titres to H pylori and gastritis. Patients who were H pylori positive had significantly higher PG I and PG II concentrations and a significantly lower PG I:PG II ratio than patients who were negative for H pylori. In 13 patients with duodenal ulcer and H pylori positive gastritis serum PG I concentrations were significantly higher than in H pylori positive patients without duodenal ulcer. Significant correlations were found between the age of patients and serum PG II, the PG I:PG II ratio, IgG antibodies to H pylori, the severity of body gastritis and H pylori infection, and between the degree of gastritis in the body of the stomach and the PG II concentration. CONCLUSIONS--Serum PG I and II concentrations, together with a fall in the PG I:PG II ratio, could be used as predictors of H pylori infection as well as serum IgG antibody response to H pylori.     

幽门螺杆菌感染与老年人上消化道疾病关系的临床研究

目的通过长期随访临床观察幽门螺杆菌（Helicobcter pylori,Hp）相关胃炎易继发消化性溃疡和胃癌。Hp感染率有随着年龄增长而升高的趋势,阐明Hp与老人上消化道疾病的关系。方法620例均为门诊和住院患者,按年龄分为老年组≥60岁272例,其中男180例,女92例,中位年龄65岁;青壮年组〈60岁348例,其中男213例,女135例,中位年龄36岁。上消化道疾病诊断：患者在电子胃镜下肉眼观察其胃和十二指肠粘膜,并在病变部位取材活检,送病理检查,以确定疾病性质（诊断）。Hp检测方法：采用^14C尿素呼气试验方法。患者于胃镜检查结束后或在上午空腹时接受试验。结果620例患者中Hp阳性371例,阳性率60%。其中老年组Hp阳性率为66.2%（180/272）,明显高于青壮年的54.9%（191/348）,差异有统计学意义（P〈0.01）。老年组慢性胃炎和胃溃疡Hp阳性率为66.4%及75.6%,均高于青壮年组的43.9%和41.0%,差异有统计学意义（P〈0.01）。老年组胃溃疡及胃癌患病率高于青壮年组差异有统计学意义（P〈0.05或〈0.01）。结论通过研究提示Hp感染在老年慢性胃炎和胃溃疡发病学上,具有比青壮年更大的重要性。同时,支持年龄与Hp成正相关的观点,说明Hp感染与上消化道疾病的发病关系密切。     

Gastrospirillum hominis and Helicobacter pylori infection in Thai individuals: Comparison of histopathological changes of gastric mucosa

The presence of Helicobacter pylori (H. pylori ) in the stomach is closely associated with histological signs of chronic active gastritis and peptic ulcer. Another spiral organism named Gastrospirillum hominis (G. hominis ) has led to further interest in the bacterial pathogenesis of gastritis. Due to the low prevalence of G. hominis , it is difficult to evaluate its biological behavior. Recently 16 cases of G. h ominis-associated gastritis were found in 257 Thai individuals, which made it possible to study the biological characteristics of G. hominis and its relationship with gastric mucosal inflammation. The results showed that H. pylori and G. hominis could be easily observed in the lower third of the mucous layer and in the mucosa of the gastric pits by means of toluidlne blue staining. Both bacteria immunostained positive. Helicobacter pylori were usually in the shape of curved bacillary while G. hominis often appeared in spiral configuration. In 257 cases of Thai subjects, 169 cases were found to be H. pylori positive, the detection rate was 65.7%, and 16 cases were G. hominis positive, with a 6.2% detection rate. In G. hominis infection, 43.6% of cases had normal gastric mucosa. Superficial, erosive and atrophlc gastritis cases were 13.2, 10.9 and 12.5%, respectively. Mucosal inflammation was usually severe in H. pylori , but neutrophil polymorph infiltration was often mild and focal in G. hominis Infection. Although no G. hominis infection with carcinoma was shown in our cases, the occurrence of mucosal atrophy, metaplasia and dysplasia was higher in both bacterial infections compared with H. pylori- and G. hominis -negative cases. It is suggested that G. hominis may be partly responsible for the mucosal inflammation and some malignant-associated lesions.     

Helicobacter heilmannii infection: clinical, endoscopic and histopathological features in Japanese patients

Gastric biopsy materials of 4074 consecutive Japanese patients undergoing esophagogastroduodenoscopy were reviewed, along with those of 15 patients with Helicobacter heilmannii infection (11, chronic gastritis; four, mucosa-associated lymphoid tissue (MALT) lymphoma). In four patients with H. heilmannii infection, the materials were examined by transmission electronmicroscopy. Urea breath test (three patients) and antibody test (five patients) were performed in patients with H. heilmannii infection. In two patients with MALT lymphoma, H. heilmannii was eradicated. The prevalence of H. heilmannii was 0.1% in the consecutive series. In chronic gastritis, the gastric mucosa was endoscopically normal (13.3%), had erythema (33.3%), or had erosions (53.3%); histologically, it showed no epithelial change, mild mononuclear cell infiltration, and slight and focal neutrophil infiltration; Helicobacter heilmannii was positive with anti-H. pylori antibody, and was detected in the mucous gel layer and in foveolae. In MALT lymphoma, the gastric mucosa was coarsely granular with enlarged mucosal folds without ulcers (two cases), with small ulcers (one case), or with multiple erosions (one case). Urea breath test and antibody test were both negative. Eradication of H. heilmannii resulted in remission of MALT lymphoma. Helicobacter heilmannii infection is therefore uncommon in Japanese adults, but is associated with chronic gastritis and gastric MALT lymphoma.     

Prevalence of H. pylori in patients with gastric cancer

The present study was taken with an aim to assess the prevalence of H. pylori in patients with gastric carcinoma and correlate it with gross appearance and histological type. Endoscopic biopsies from 54 patients with gastric carcinoma and 50 age and sex matched controls were taken after thorough upper gastrointestinal examination. Gross appearance of the tumour was noted and two biopsies each from the site of malignancy and from normal appearing areas were taken. Sections were stained with Haematoxylin & Eosin and Loeffler's methylene blue for histopathological details and presence of H. pylori. Prevalence of H. pylori in controls was slightly higher than the patients group (80% Vs 78%). Ulcerated type of gross appearance had maximum prevalence of H. pylori (88%). Prevalence of H. pylori was more in diffuse type of gastric cancer than intestinal type (86% Vs 68%). A significant association between H. pylori and grades of gastritis was noted (P < 0.01) in controls as well as in patient group but it failed to show a significant association with tumour grades, intestinal metaplasia, site of the tumour and age of the patients. So, it can be inferred that prevalence of H. pylori infection is not directly associated with pathogenesis of gastric cancer but it may act as a co-carcinogen by damaging the mucosa and thereby making it more susceptible to effects of carcinogen.     

Prevalence of lymphoid follicles and aggregates in Helicobacter pylori gastritis in antral and body mucosa.

AIMS--To evaluate the prevalence of lymphoid follicles and aggregates in the antral and body mucosa in Helicobacter pylori gastritis and to assess if there were correlations with ulcers in the duodenum, pylorus, or stomach, and with chronic antral erosions. METHODS--Patients (n = 2692) with histologically confirmed H pylori antral gastritis were investigated. These comprised five groups: those with duodenal ulcers; those with pyloric ulcers; those with gastric ulcers; those with chronic erosions; and those with no associated lesions. In 1446 cases at least two additional biopsy specimens from the oxyntic mucosa were available. RESULTS--Lymphoid follicles and aggregates were found in 53.8% of cases in the antral mucosa compared with 14.8% in the oxyntic mucosa (p < 0.001). The various diseases showed significant differences in terms of the prevalence of follicles and aggregates: The highest numbers in the antral mucosa as well as the lowest in the oxyntic mucosa were found in patients with duodenal ulcers (60.5% and 9.2%, respectively). The highest numbers of follicles and aggregates in the oxyntic mucosa occurred in patients with gastric ulcers. CONCLUSIONS--The detection of lymphoid follicles and aggregates in oxyntic mucosa and the higher prevalence in antral mucosa fits well with the distribution of primary gastric lymphomas. This adds further weight to the notion that the development of follicles and aggregates, triggered by H pylori, might be an early precursor to gastric lymphoma. The differences between the groups investigated might be due to different strains of H pylori or differences in the respective sizes of antral and oxyntic mucosa.     

High prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic Hispanics.

In this study, we estimated the prevalence of Helicobacter pylori infection and histologic gastritis in 58 asymptomatic Hispanic adult volunteers (mean age, 41 years; 59% male) by endoscopic biopsy of the upper gastrointestinal tract. Forty-six subjects (79%) were found to harbor H. pylori in gastric biopsies, and all had histologic gastritis. Four other subjects were found to have gastritis in the absence of H. pylori. Similar prevalences of H. pylori and gastritis were noted in all age groups and also in American-born and immigrant Hispanics. Biopsy data and serologic studies of H. pylori antibodies correlated well. We conclude that H. pylori infection is an almost universal finding in the gastric mucosa of asymptomatic adult Hispanics, regardless of age. The clinical significance of these findings is unknown, but we speculate that H. pylori and its associated gastritis could have a role in the high incidence of gastric carcinoma in Hispanic populations.     

Association of Helicobacter pylori-dependent gastritis with gastric carcinomas in young Japanese patients: histopathological comparison of diffuse and intestinal type cancer cases

AIMS: The causal relationship of H. pylori gastric colonization with gastric cancer development has not as yet been fully elucidated. The prevalence of H. pylori infection increases with age in the asymptomatic population in Japan, and reaches a high plateau in those older than 40 years. The objective of this study was to assess the link between H. pylori and gastric carcinomas in patients younger than 40 years. METHODS AND RESULTS: Detection of H. pylori and assessment of background mucosa based on the Sydney system was performed histopathologically for 40 Japanese gastric cancer cases younger than 40 years and compared with 40 age- and sex-matched controls. H. pylori infection in gastric mucosa was detected significantly more frequently (P < 0.001) in patients with cancer (29/40; 72.5%) than in controls (11/40; 27.5%). Additionally, by histopathological comparison between intestinal (18 cases) and diffuse (70 cases) types of young gastric cancer patients, mucosal atrophy and intestinal metaplasia were found to coexist with acute and chronic inflammation in the background mucosa of both intestinal and diffuse types, being significantly more prevalent than in young controls. CONCLUSIONS: As well as the high prevalence of H. pylori in young subjects with gastric cancer, it is clear that persistent infection induces mucosal damage, resulting in atrophy and intestinal metaplasia. Thus, acute/chronic gastritis could play an essential role in the early development of neoplasia in the stomach.