Effect of Helicobacter pylori eradication on gastric metaplasia of the duodenum.

Helicobacter pylori associated duodenal ulcers occur in patches of gastric metaplasia. The pathogenesis of gastric metaplasia is unclear, but it has been produced in experimental animals by acute injury and has been shown to be present to a greater extent of H pylori positive subjects. This study aimed to discover if gastric metaplasia regressed with eradication of H pylori or healing of duodenal ulcers, or both. Thirty two duodenal ulcer patients with H pylori infection confirmed by biopsy urease test and by antral histological examination were studied. Patients were treated with triple therapy (deNol 240 mg twice daily, amoxycillin 500 mg three times daily, and metronidazole 400 mg three times daily) for two weeks after the first endoscopy and were subsequently re-endoscoped. Three duodenal bulb biopsy specimens were obtained per patient at each endoscopy. Biopsy sections were stained with haematoxylin and eosin to determine the severity of duodenitis, and with diastase periodic acid-Schiff/alcian blue to assess the extent of gastric metaplasia. Slides were assessed by two histopathologists unaware of treatment status. H pylori was eradicated in 63% of subjects and all ulcers were healed at follow up. The median extent of gastric metaplasia at the start of treatment and 6-18 months (median 10) after treatment was compared in the two groups. Gastric metaplasia declined in eradicators from 16% to 8% (p < 0.05) while in non-eradicators there was no significant change (25% initially and at follow up). A positive relation between extent of gastric metaplasia and duodenal inflammation score was present before treatment (r(s) = 0.74, p < 0.001) and was unchanged after treatment in the non-eradicator group (r(s) = 0.89, p < 0.001). In the eradicator group, however, the inflammation score had significantly declined (p < 0.02) and the close relation with gastric metaplasia was no longer present. These results suggest that H pylori itself is at least in part responsible for producing gastric metaplasia of the duodenum.     

Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer

BACKGROUND: The aim of this study was to determine whether the amount of Helicobacter pylori and the extent of gastric metaplasia in the duodenal mucosa play critical roles in the pathogenesis of duodenal ulcer. METHODS: Duodenal and gastric biopsy specimens were obtained from H. pylori-positive patients with duodenal ulcer, gastric ulcer or chronic gastritis. The extent of gastric metaplasia was evaluated histologically and endoscopically using the methylene blue test. In this study, we performed competitive polymerase chain reaction, a highly sensitive and quantitative method for determining the amount of H. pylori gastric and duodenal mucosa. The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in the three patient groups were compared. The correlation between the amount of H. pylori in the duodenum and gastric antrum and extent of gastric metaplasia were also determined. RESULTS: The prevalence and extent of gastric metaplasia and the amount of H. pylori in the duodenal bulb in patients with duodenal ulcer were much higher than in patients with gastric ulcer or chronic gastritis. A positive correlation was found between the amount of H. pylori in the duodenum and the extent of gastric bulb and that in the antrum. CONCLUSIONS: The findings of this study indicate that H. pylori colonization in the duodenal bulb may play a critically important role in the pathogenesis of duodenal ulcer and that the amount of H. pylori in the duodenal bulb may be related to the amount of H. pylori in the gastric antrum and the extent of gastric metaplasia in the duodenal bulb.     

Distribution and prevalence of Campylobacter pylori in the stomach

We investigated the distribution and prevalence of Campylobacter pylori in the stomach and duodenum. In this study, 500 biopsy specimens were obtained from 245 patients. In each case, biopsy specimens were taken from more than 2 sites. C. pylori was detected by culture, urease test and acridine-orange stain. C. pylori was not detected on the intestinal metaplasia, gastric cancer tissue and duodenal mucosa without gastric metaplasia. In 21% of cases, C. pylori was detected in only one site. Because of the patchy distribution of C. pylori, more than 2 biopsy specimens from different sites were needed to avoid sampling error. Detection rate of C. pylori was almost equal in antrum, angle and body as well as in male and female. H2 receptor antagonists did not affect the detection rate of C. pylori. According to the endoscopic diagnosis of the biopsied site, C. pylori was detected in 87% of gastric ulcer, 60% of duodenal ulcer (duodenal mucosa with gastric metaplasia), 73% of chronic gastritis and 62% of endoscopically normal gastric mucosa.     

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum.

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.     

Helicobacter Pylori and Refractory Duodenal Ulcers: Cross-over Comparison of Continued Cimetidine with Cimetidine plus Antimicrobials

Objectives: To determine the distribution of Helicobacter pylori in the antral and duodenal mucosa of patients with duodenal ulcers refractory to 12 wk of treatment with cimetidine and to evaluate the effect of adding antimicrobial agents to cimetidine on the bealing of refractory duodenal ulcers. Methods: A randomized crossover comparison of continued 800 mg of cimetidine at night for 4 wk with cimetidine plus 500 mg of amoxycillin three times a day for the first 2 wk and 250 mg of metronidazole three times a day for the second 2 wk. H. pylori status in the gastric antral and duodenal mucosa was evaluated by histology and bacterial culture before and at the end of each treatment period. Results: Forty-eight patients were studied. Upon entry to the study, all patients had antral colonization with H. pylori . In the duodenum, active chronic duodenitis was present in 66%, duodenal gastric metaplasia in 33%, and H. pylori in 50%, similar proportions to patients with nonrefractory duodenal ulcers. Healing occurred in 70% (30 of 43) of patients during treatment with cimetidine plus antimicrobials but in only 21 % (6 of 28) during treatment with cimetidine alone ( P = 0.0003). In patients who received antimicrobials, neither clearance of H. pylori from the antrum (58% of patients) or duodenum (71% of colonized patients) nor eradication of H. pylori (33%) was significantly correlated with ulcer healing. Conclusions: The distribution of H. pylori in refractory duodenal ulcers is similar to nonrefractory ulcers, and the combination of amoxycillin and metronidazole with cimetidine increases the proportion of refractory duodenal ulcers, which heals.     

Geographic differences in the distribution of intestinal metaplasia in duodenal ulcer patients

OBJECTIVE: A strong correlation exists between atrophic gastritis and the intestinal type of gastric carcinoma. Duodenal ulcer disease characteristically has an antral predominant gastritis and a lower risk for gastric cancer. The aim of this study was to investigate the extent and distribution of intestinal metaplasia in duodenal ulcer in countries differing in gastric cancer incidence. METHODS: Topographically mapped gastric biopsy specimens (median 11) were obtained from patients with duodenal ulcer in four countries (Korea, Colombia, USA, and South Africa). Sections were stained with a triple stain and evaluated for Helicobacter pylori (H. pylori), active inflammation, and intestinal metaplasia. RESULTS: One hundred and sixty-five patients with duodenal ulcer were examined (29 from Korea, 52 from Colombia, 62 from the USA, and 22 from South Africa). The percentage of biopsies with intestinal metaplasia was significantly greater in Korean patients (86%) compared with that in other countries (50%) (p = 0.0004). Intestinal metaplasia was most prevalent in the antrum lesser curve and greater curve, and the body lesser curve. Intestinal metaplasia was present in the gastric corpus of 38% of duodenal ulcer patients from Korea compared with an average of 10% elsewhere (p = 0.018). No differences were observed in the density or distribution of H. pylori infection or in the degree of active gastritis between countries. CONCLUSIONS: Although antral predominant gastritis is the prevalent pattern of gastritis in duodenal ulcer, intestinal metaplasia in the gastric corpus may be found with geographic differences. These findings suggest that duodenal ulcer and gastric cancer are not mutually exclusive diseases but are rather ends of the spectrum of H. pylori infection.     

Gastric metaplasia and Helicobacter pylori infection.

Duodenal and antral mucosal biopsy specimens were obtained from 139 patients with dyspeptic complaints to study the prevalence and extent of gastric metaplasia in the duodenal bulb in relation to Helicobacter pylori (H pylori) infection and duodenal ulcer disease. On logistic regression, the presence and extent of gastric metaplasia was not significantly associated with H pylori infection. The prevalence of gastric metaplasia, however, was found to be higher in patients with current or past evidence of duodenal ulcer disease in comparison with subjects with functional dyspepsia (p = 0.01). A follow up study on 22 patients before and at least one year after eradication of H pylori showed that the mean extent of gastric metaplasia did not change significantly after eradication and did not differ when compared with 21 patients with persisting infection. It is concluded that the unchanged gastric acid output after eradication of H pylori is a more important factor in the development of gastric metaplasia than the H pylori related inflammatory process.     

Link betweenHelicobacter pylori-associated gastritis and duodenal ulcer

We examined the interrelationships among the degree of fundic mucosal atrophy, the prevalence ofHelicobacter pylori in the gastric antrum, the gastric juice, and the duodenum with and without gastric metaplasia, in 20 duodenal ulcer patients and 20 non-duodenal ulcer patients. The detection rates ofH. pylori in the antrum, the gastric juice, and the duodenum were significantly higher in duodenal ulcer patients (80%, 65%, and 60%) than in non-duodenal ulcer subjects (50%, 20%, and 5%). The frequency ofH. pylori was significantly lower in the gastric juice (30%) and the duodenum (10%) in non-duodenal ulcer patients with antralH. pylori, compared with those in duodenal ulcer patients with antralH. pylori. All of seven patients with both gastric metaplasia andH. pylori infection in the duodenum had duodenal ulcer, whereas only 1 of 14 patients without either gastric metaplasia orH. pylori infection in the duodenum had duodenal ulcer. There was normal or mild atrophic mucosa in the fundus of duodenal ulcer patients withH. pylori in the antrum, whereas moderate or severe atrophic mucosa in non-duodenal ulcer patients withH. pylori gastritis. These results suggest that the preserved fundic mucosa, gastric metaplasia in the duodenum, and a greater load ofH. pylori to the duodenum through the gastric juice may be prerequisites for the formation of duodenal ulcers.     

Gastric metaplasia and chronic inflammation at the duodenal bulb mucosa

BACKGROUND: Chronic inflammation and gastric metaplasia are often observed in biopsy specimens from the duodenal bulb of Heliobacter pylori positive patients with duodenal ulcer disease (DU). AIMS: We set out to investigate the prevalence of these lesions and their associations with other gastric and duodenal histopathological lesions. PATIENTS: A total of 1255 consecutive patients who underwent upper gastrointestinal endoscopy were recruited into the present study. METHODS: Two biopsy specimens were obtained from each of the following sites: duodenal bulb, gastric antrum, gastric body, and distal to the superior duodenal angle. These specimens were stained with hematoxylin-eosin, alcian blue periodic acid Schiff (pH 2.5) and modified Giemsa (Heliobacter pylori infection was determined only by histology). RESULTS: The mean age of the study population was 57 years, and male:female ratio 1:1.6. Overall, 235 (19%) had gastric metaplasia and/or chronic inflammation in the duodenal bulb mucosa, and H. pylori organisms could be found in 17 (1%). In univariate analyses, gastric metaplasia and/or chronic duodenal bulb inflammation positively associated with male sex (p = 0.046), Heliobacter pylori-positive chronic gastritis (p = 0.033), villous atrophy of distal duodenal mucosa, i.e., coeliac disease (p < 0.001), duodenal ulcer (p < 0.001), and duodenal bulb deformity and scarring in endoscopy (p < 0.001), but not with age (p = 0.7) nor use of nonsteroidal anti-inflammatory drugs (p = 0.055). Multivariate analysis revealed that independent risk factors for gastric metaplasia and chronic inflammation in duodenal bulb were duodenal Heliobacter pylori infection (odds ratio 1.6, 95% confidence interval CI 1.1-2.1), and villous atrophy of the distal duodenal mucosa (odds ratio 12.7, 95% CI 4.4-36.5), while chronic atrophic gastritis was protective against them (odds ratio 0.5, 95% CI 0.3-0.8). CONCLUSIONS: In addition to Heliobacter pylori infection, duodenal bulb gastric metaplasia and chronic inflammation may result from predisposition to toxic dietary components in gluten-sensitive subjects.     

Prevalence of Helicobacter pylori infection and related gastroduodenal lesions in spouses of Helicobacter pylori positive patients with duodenal ulcer.

BACKGROUND: To date, very few studies have evaluated the risk of infection among spouses of Helicobacter pylori positive patients and their results are conflicting. AIM: To assess the seroprevalence of H pylori infection in spouse of H pylori positive patients with duodenal ulcer as compared with age and sex matched volunteer blood donors, as well as the frequency of endoscopic gastroduodenal lesions in these spouses, according to the presence or absence of gastrointestinal complaints. METHODS: Some 124 spouses (48% males) of patients with duodenal ulcer consecutively seen over a 10 month period were studied. They were all screened for serum IgG anti-H pylori antibodies and asked to complete a questionnaire with particular reference to the presence of chronic or recurrent dyspepsia. Upper gastrointestinal tract endoscopy with antral and corpus biopsy specimens taken for histological examination and urease rapid test was offered to all seropositive spouses. Volunteer blood donors (248), living in Milan and matched for age, sex, north-south origins, and socioeconomic status to the cases, were used as controls. RESULTS: Spouses of patients with duodenal ulcer had a significantly higher seroprevalence of H pylori infection than controls (71% v 58%, p < 0.05); 30 of 88 (34%) H pylori positive spouses complained of dyspeptic symptoms compared with only four of 34 (12%) seronegative spouses (p < 0.02). At endoscopy, H pylori infection was confirmed in 48 of 49 (98%) seropositive spouses. The endoscopic findings in those spouses showed active duodenal ulcer in eight (17%), duodenal scar and cap deformity in two (4%), active gastric ulcer in two (4%), erosive duodenitis in three (6%), antral erosions in two (4%), antral erosions plus duodenitis in one, and peptic oesophagitis in another patient. The prevalence of major endoscopic lesions was significantly higher in symptomatic spouses than in those who had never been symptomatic. CONCLUSIONS: These findings show that being the spouse of an H pylori positive patient with duodenal ulcer may increase the risk of H pylori colonisation and perhaps of peptic ulcer disease, and raises questions as to whether serological screening of cohabiting partners of H pylori positive patients with duodenal ulcer may be indicated.     

Pathophysiology of duodenal ulcer disease

: Before the discovery of Helicobacter pylori infection some 12 years ago, three major disturbances in gastric physiology had been identified in patients with duodenal ulcer disease. These abnormalities were: impaired acid inhibition of gastrin release from the antral mucosa, increased basal and stimulated acid secretion by the body of the stomach and increased acid load in the duodenum. Some of these abnormalities in gastric function can now be explained by the effects of H. pylori infection. The increased release of gastrin by the antral mucosa in duodenal ulcer patients, for example, can be entirely explained by the effects of this organism. Other abnormalities, however, appear to have a genetic basis or may be due to environmental factors. Much work has been conducted on the relationship between H. pylori and the development of duodenal ulcer disease, and this paper aims to review recent studies in the field and to give an overview of the latest understanding of the pathophysiology of this disease.     

Duodenal histology, ulceration, and Helicobacter pylori in the presence or absence of non-steroidal anti-inflammatory drugs.

Duodenitis and gastric metaplasia, which is often colonised by Helicobacter pylori (H pylori), are increasingly recognised for their importance in the pathogenesis of duodenal ulcers. The situation is not clear in patients receiving non-steroidal anti-inflammatory drugs (NSAIDs), who have a higher risk of peptic ulceration. The aim of this study was to identify the duodenal histological abnormalities in the presence or absence of NSAIDs, H pylori, and duodenal ulceration. Endoscopic duodenal biopsy specimens were taken from healthy looking mucosa of 172 patients (74 took NSAIDs, and 98 did not). Duodenitis was graded according to the degree of neutrophilic and plasma cell infiltration, villus height, Brunner's gland prolapse, and gastric metaplasia. The activity of duodenitis was dependent on the neutrophilic infiltration. A global score covering all the above factors was constructed, and H pylori in both the stomach and duodenum, was also assessed. The results showed that duodenitis with varying degrees of neutrophilic infiltration and gastric metaplasia was found in 20 patients (27%) taking NSAIDs, compared with 56 patients (57%) not taking NSAIDs (chi 2 = 16.24, p < 0.001). This degree of duodenitis was also found in 20 of 25 patients (80%) with duodenal ulcers, regardless of NSAID intake (chi 2 = 15.38, p < 0.001). Gastric metaplasia was identified in 20 patients (27%) receiving NSAIDs and 38 (39%) not receiving NSAIDs. Duodenal H pylori was only seen in patients with gastric metaplasia 10 (50%) receiving NSAIDs, and 34 (89%) not receiving NSAIDs. H pylori positive gastritis, and the combination of active duodenitis and gastric metaplasia were independent predictors of duodenal ulceration. It is concluded that active duodenitis is less common in patients taking NSAIDs but is strongly associated with gastric metaplasia, H pylori positive gastritis, and duodenal ulceration. These findings are relevant to the pathogenesis and treatment of duodenal ulcers in patients taking NSAIDs.     

Gastric metaplasia in the duodenal bulb shows increased mucosal interleukin-8 activity in Helicobacter pylori-positive duodenal ulcer patients

BACKGROUND: Although increased levels of interleukin (IL)-8 are known to be associated with infiltration of neutrophils in the gastric mucosa with Helicobacter pylori infection, no study has investigated the relationship between local IL-8 levels and neutrophil infiltration in the duodenal mucosa of patients with duodenal ulcer (DU). METHODS: Duodenal mucosal biopsy specimens with and without gastric metaplasia (GM) were obtained from patients with DU and controls with an endoscopic methylene blue (MB) staining method. Levels of IL-8 secreted in the organ cultures of biopsy specimens were measured with an enzyme-linked immunosorbent assay. The number of myeloperoxidase-positive neutrophils infiltrating the lamina propria was determined in immunohistochemically stained tissue sections. RESULTS: Histologic assessment showed that there was a strong correlation between the absence of endoscopic MB staining and the extent of GM. The levels of IL-8 in both duodenal and antral mucosal tissues were significantly higher in patients with H. pylori infection than in those without infection. In patients with DU the duodenal mucosal tissues with GM (MB-unstained mucosa) showed significantly higher levels of IL-8 than those without GM (MB-stained mucosa) or the antral mucosa. The number of neutrophils showed similar variations among DU and control patients with a positive correlation with IL-8 activity. The levels of IL-8 and the number of neutrophils decreased after H. pylori eradication in both duodenal and antral mucosal tissues, and these changes were more remarkable in the duodenal mucosal tissues with GM. CONCLUSIONS: Increased IL-8 activity in the duodenal mucosa with GM may be important for ulcerogenesis in H. pylori-positive DU patients.     

Gastric Metaplasia in the Duodenal Bulb Shows Increased Mucosal Interleukin-8 Activity in Helicobacter pylori-Positive Duodenal Ulcer Patients

Background: Although increased levels of interleukin (IL)-8 are known to be associated with infiltration of neutrophils in the gastric mucosa with Helicobacter pylori infection, no study has investigated the relationship between local IL-8 levels and neutrophil infiltration in the duodenal mucosa of patients with duodenal ulcer (DU). Methods: Duodenal mucosal biopsy specimens with and without gastric metaplasia (GM) were obtained from patients with DU and controls with an endoscopic methylene blue (MB) staining method. Levels of IL-8 secreted in the organ cultures of biopsy specimens were measured with an enzyme-linked immunosorbent assay. The number of myeloperoxidase-positive neutrophils infiltrating the lamina propria was determined in immunohistochemically stained tissue sections. Results: Histologic assessment showed that there was a strong correlation between the absence of endoscopic MB staining and the extent of GM. The levels of IL-8 in both duodenal and antral mucosal tissues were significantly higher in patients with H. pylori infection than in those without infection. In patients with DU the duodenal mucosal tissues with GM (MB-unstained mucosa) showed significantly higher levels of IL-8 than those without GM (MB-stained mucosa) or the antral mucosa. The number of neutrophils showed similar variations among DU and control patients with a positive correlation with IL-8 activity. The levels of IL-8 and the number of neutrophils decreased after H. pylori eradication in both duodenal and antral mucosal tissues, and these changes were more remarkable in the duodenal mucosal tissues with GM. Conclusions: Increased IL-8 activity in the duodenal mucosa with GM may be important for ulcerogenesis in H. pylori-positive DU patients.     

Relation between gastric acid output, Helicobacter pylori, and gastric metaplasia in the duodenal bulb.

BACKGROUND: Factors that determine gastric metaplasia in the duodenal bulb are ill defined. It is more common and extensive in the presence of high acid output and possibly in the presence of Helicobacter pylori. However, no quantitative relation between acid output and the extent of gastric metaplasia has been demonstrated and its relation to H pylori is uncertain. AIM: To determine the relation between H pylori infection and acid output and the presence and extent of gastric metaplasia in the duodenal bulb. subjects: H pylori positive and negative patients with duodenal ulcer and healthy controls were studied. METHODS: Quadrantic duodenal bulb biopsy specimens were taken and the presence and extent of gastric metaplasia determined using a computer enhanced image intensifier. Basal and stimulated acid outputs were measured. RESULTS: gastric metaplasia was significantly (p < 0.05 more common and significantly (p < 0.05) greater in extent in patients with duodenal ulcer than in controls. Neither the prevalence or extent of gastric metaplasia was affected by H pylori status. There were significant (p < 0.01) direct correlations between acid output and extent of gastric metaplasia. CONCLUSIONS: Prevalence and extent of gastric metaplasia are not related to H pylori in controls, or in patients with duodenal ulcer. Rather, high acid response to gastrin may be more important.     

Helicobacter pylori infection, gastric metaplasia in the duodenum and the relationship with ulcer recurrence

OBJECTIVE: To study the prevalence of Helicobacter pylori (H. pylori) infection and gastric metaplasia (GM) in the duodenum a large group of patients with duodenal ulcer was evaluated to determine whether these factors are related to the number of ulcer recurrences. METHODS: Three hundred and seven patients diagnosed by endoscopy as having active duodenal ulcers were studied. At endoscopy, all patients had gastric biopsies taken for histology, the rapid urease test and culture. Three duodenal biopsies were also taken and processed for histology (haematoxylin & eosin, Giemsa, Warthin-Starry, and PAS stain). RESULTS: GM and H. pylori in the duodenum was identified in 73% (68-78%) and 66% (60-71%) of the cases, respectively. All patients with H. pylori in the duodenum also had GM at this location, while areas with GM but without H. pylori were described. The kappa statistic for concordance between GM and H. pylori at the duodenum was 0.82. The prevalence of GM and H. pylori, depending on the number of ulcer recurrences, was: 1st episode, 34% and 27%, respectively; 2nd episode, 84% and 80%; and > or = 3rd episode, 90% and 79% (P < 0.001 when comparing 1st vs 2nd or > or = 3rd episode). In the multivariate analysis, age and number of ulcer recurrences correlated both with GM and with H. pylori in the duodenum. Chronic duodenitis was demonstrated in all duodenal biopsies, 87% being active chronic duodenitis. H. pylori in the duodenum was more frequent in patients with active duodenitis (73%) than in those with inactive duodenitis (13%) (P < 0.001). CONCLUSIONS: Patients with recurrent ulcer disease have a higher prevalence of both GM and H. pylori infection in the duodenum, suggesting that these two factors are related with the chronicity and recurrence of duodenal ulcer disease. H. pylori infection in the duodenum always appears in areas of GM, although GM is not necessarily colonized by the organism. H. pylori infection cannot be excluded based only on the results of duodenal biopsies, as false negative results at this area are frequent.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Factors associated with Helicobacter pylori infection by a cagA-positive strain in children

Although infection with a cagA-positive Helicobacter pylori strain is considered a risk factor for the development of duodenal peptic ulcer in adults, this association has not been demonstrated in children. The presence of cagA was investigated by polymerase chain reaction in H. pylori strains isolated from 27 children with duodenal ulcer and 53 without duodenal ulcer. All patients (100%) with duodenal ulcer and 33 (62.3%) without ulcer were colonized by a cagA-positive strain (P=.00007). A cagA-positive status was also associated with a more marked macroscopic gastritis, with a greater inflammatory infiltrate of both mononuclear and polymorphonuclear cells in the antral and oxyntic gastric mucosae and degenerative and regenerative changes of the gastric mucosa. Increased cagA positivity was also associated with increased age, but no association between cagA-positive status and sex was observed.     

Enhanced gastric nitric oxide synthase activity in duodenal ulcer patients.

Nitric oxide, the product of nitric oxide synthase in inflammatory cells, may have a role in tissue injury through its oxidative metabolism. Nitric oxide may have a role in the pathogenesis of duodenal ulcer and may be one of the mechanisms responsible for the association between gastric infection with Helicobacter pylori and peptic disease. In this study, calcium independent nitric oxide synthase activity was detected in human gastric mucosa suggesting expression of the inducible isoform. In 17 duodenal ulcer patients gastric antral and fundic nitric oxide synthase activity was found to be two and 1.5-fold respectively higher than its activity in the antrum and fundus of 14 normal subjects (p < 0.05). H pylori was detected in the antrum of 15 of 17 duodenal ulcer patients and only in 7 of 14 of the control subjects. Antral nitric oxide synthase activity in H pylori positive duodenal ulcer patients was twofold higher than in H pylori positive normal subjects (p < 0.05). In duodenal ulcer patients antral and fundic nitric oxide synthase activity resumed normal values after induction of ulcer healing with ranitidine. Eradication of H pylori did not further affect gastric nitric oxide synthase activity. These findings suggest that in duodenal ulcer patients stimulated gastric mucosal nitric oxide synthase activity, though independent of the H pylori state, may contribute to the pathogenesis of the disease.     

Helicobacter pylori and chronic active inflammation of the duodenum and stomach in duodenal ulcer patients treated with ranitidine, misoprostol, or an acid-neutralizing agent

Biopsy specimens from the stomach and duodenum of 45 duodenal ulcer patients treated with ranitidine, misoprostol, or an antacid were examined. During 4 weeks of treatment the duodenal ulcer healed in 31 patients. The treatment regimens showed no significant effect on the amount of Helicobacter-like structures (HLS) or the presence of active inflammation, either in the stomach or in the duodenum. All patients had chronic active antral gastritis before and after treatment. HLS were found histologically in 91.7% of all antral specimens, in 94.2% of the gastric corpus specimens, in 15.9% of the duodenal bulb specimens, and in 0.9% from the lower duodenal knee. The frequency of chronic active gastritis was clearly lower in the gastric corpus than in the antrum, whereas the occurrence of HLS was about the same. This may indicate a higher resistance of the gastric corpus mucosa to H. pylori.