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.     

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.     

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.     

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.     

Relationship between antral lymphocyte density and basal gastrin levels in patients with Helicobacter pylori infection

BACKGROUND: The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood. AIM: To evaluate whether antral lymphocyte density could play a role in this alteration. METHODS: A total of 12 patients with active duodenal ulcer and 10 with non-ulcer dyspepsia were enrolled upon detection of Helicobacter pylori infection at endoscopy Enrolled as controls were 7 matched dyspeptic patients without Helicobacter pylori infection. Biopsy specimens were collected for Helicobacter pylori and histological assessments, and for antral lymphocyte density assessment by a histomorphometric method. A blood sample was obtained from each patient to determine basal gastrin levels. All patients were controlled by a further endoscopy 4 weeks after the end of Helicobacter pylori treatment. RESULTS: Antral lymphocyte density (5,464 +/- 1,328 and 5,635 +/- 1,186 vs 2,267 +/- 557 lymphocytes/mm2; p<0.001 and p<0.001, respectively) and gastrin levels (66.7 +/- 14.1 and 60.4 +/- 21.7 vs 40.7 +/- 7.8 pg/dl; p=0.004 and p=0.02, respectively) were higher in duodenal ulcer and non-ulcer dyspepsia patients than in controls, while no significant differences emerged between duodenal ulcer and non-ulcer dyspepsia patients. There was a significant direct correlation between antral lymphocyte density and gastrin levels both in duodenal ulcer (r=0.77; p=0.003) and in non-ulcer dyspepsia (r=0.75; p=0.03) patients, while no correlation was found in controls [r=0.12; p=0.8). After treatment, this correlation persisted in 10 eradication failure patients (r=0.68; p=0.027), but disappeared in those successfully cured. CONCLUSIONS: These data suggest that lymphocyte density in the antral mucosa could play a role in the impaired gastrin production occurring in patients with Helicobacter pylori infection.     

Campylobacter pylori, duodenal ulcer, and gastric metaplasia: possible role of functional heterotopic tissue in ulcerogenesis.

Multiple pinch biopsies were taken from the duodenum and antrum of 137 subjects (46 active duodenal ulceration; 44 healed ulcers; 47 'normal'), and examined for the presence and grade of gastritis, gastric metaplasia, and Campylobacter pylori. These factors, as well as age, sex, cigarette, and anti-inflammatory agent intake were evaluated as possible risk factors for duodenal ulceration. Pentagastrin induced Congo Red staining of the duodenal bulb was performed in an additional 43 cases, to determine the presence of functioning parietal cells in the duodenum. Ninety eight per cent of patients with duodenal infection with C pylori had active or healed duodenal ulcers. Bacteria were confined to areas of gastric metaplasia which was always infiltrated with inflammatory cells. The metaplastic tissue was usually superficial in type, although patients had C pylori associated with heterotopic tissue: this has not been previously described. Congo Red staining of the duodenal bulb showed that functioning endogenous acid producing tissue could be found most often at the edges of duodenal ulcers, but also in non-ulcer subjects. Cigarette smoking, age, sex, and ingestion of non-steroidal anti-inflammatory agents were not to be found to be significant risk factors for duodenal ulceration. In contrast, the presence of duodenal infection with C pylori proved to be a strong risk factor for duodenal ulceration (RR = 51), together with gastric metaplasia (RR = 6.2), and antral C pylori infection (RR = 7.6). These data identify duodenal infection with C pylori as the strongest risk factor for development of duodenal ulceration. Our finding of endogenous acid production around the edges of duodenal ulcers suggests an active role for parietal cells in the duodenum. We postulate a synergistic role for duodenal C pylori and endogenous acid production in the development of duodenal ulceration.     

功能性消化不良是否需要根除幽门螺杆菌——支持的观点

幽门螺杆菌（H.pylori）阳性的功能性消化不良（FD）或非溃疡性消化不良（NUD）相当于有消化不良症状的慢性活动性胃炎，前者强调消化不良症状,后者则强调胃黏膜组织学改变。根除H.pylori可使部分患者的症状得到长期改善,胃黏膜活动性炎症消退，逆转或防止萎缩／肠化生的发展,预防胃癌和消化性溃疡，与其他治疗措施相比具有费用,疗效比优势。     

Antibody response to Helicobacter pylori CagA and heat-shock proteins in determining the risk of gastric cancer development

OBJECTIVE: To investigate whether the systemic antibody response to Helicobacter pylori heat shock protein B can be considered, in addition to anti cytotoxin-associated protein [CagA) antibody determination, a further serological marker of increased risk of gastric cancer development. METHODS: A total of 98 Giemsa positive Helicobacter pylori patients (28 with gastric cancer, 30 with duodenal ulcer and 40 with nonulcer dyspepsia) were studied. Serum samples obtained from all patients were tested for IgG antibodies to CagA (116 kDa), VacA [89kDa) and heat skock protein B (54 kDa) antigens of Helicobacter pylori by the Western blot technique. RESULTS: 26/28 patients [(92.9% with gastric carcinoma, 29/30 patients [96.7%) with duodenal ulcer and 30/40 patients (75.0%) with non-ulcer dyspepsia were seropositive for CagA protein. The prevalence of serum IgG antibody to CagA in the cancer patients was not significantly higher than in duodenal ulcer and non-ulcer dyspepsia patients. The prevalence of antibodies to VacA was not significantly different between gastric carcinoma and non-ulcer dyspepsia patients. In contrast the prevalence of systemic antibodies to heat skock protein B was significantly higher in gastric cancer patients (78.6%) than in duodenal ulcer (36.7%, p=0.002) or nonulcer dyspepsia patients (52.5%, p=0.029). CONCLUSIONS: The detection of antibodies to heat shock protein B is proposed as an additional test which, in association with the determination of serum antibodies to CagA, could help in determining the risk of developing severe gastroduodenal disease, and gastric cancer, in particular.     

Ranitidine bismuth citrate or omeprazole-based triple therapy for Helicobacter pylori eradication in Helicobacter pylori- infected non-ulcer dyspepsia

AIM: To test the eradication rate of Helicobacter pylori by ranitidine bismuth citrate-based triple therapy, and evaluate the symptomatic response of Helicobacter pylori eradication therapy for non-ulcer dyspepsia. METHODS: A total of 59 consecutive Helicobacter pylori infected non-ulcer dyspepsia patients were randomly selected to receive either one of two triple therapy regimens, including metronidazole, amoxycillin plus ranitidine bismuth citrate (RAM group) or omeprazole (OAM group). To determine the success of eradication, patients underwent the 13C-urea breath test, 6 weeks and one year after treatment. The dyspeptic symptom scores were also assessed at the time of enrolment, 6 weeks and one year after treatment. RESULTS: Per-protocol and intention-to-treat eradication rates were 77.7% and 70% in RAM group and 83.8% and 68.9% in OAM group (p = non significant). At both the 6th week and at the first year after treatment, the mean symptom scores were lower than pre-treatment scores in the study population, regardless of whether treatment was successful or not. However, patients, whether eradicated successfully or not-eradicated, presented similar 6-week and 1-year scores. CONCLUSIONS: One-week RAM triple therapy, which is cheaper than the OAM regimen, is a relatively effective alternative regimen for Helicobacter pylori eradication in Taiwanese. Triple therapy for Helicobacter pylori eradication was not the whole management for the relief of dyspeptic symptoms of non-ulcer dyspepsia patients.     

Regression of duodenal gastric metaplasia in Helicobacter pylori positive patients with duodenal ulcer disease.

BACKGROUND: It is unclear whether the extent of duodenal gastric metaplasia is due to Helicobacter pylori and/or acid. AIMS: To investigate the role of Helicobacter pylori eradication in the regression of duodenal gastric metaplasia in patients with duodenal ulcer maintained in acid suppression conditions. METHODS:. Duodenal (anterior, superior inferior walls of first part of duodenum) and gastric antrum biopsies were obtained from 44 Helicobacter pylori positive duodenal ulcer patients. Helicobacter pylori infection was diagnosed by rapid urease test, histology and 13C-Urea Breath Test. Patients were treated with 20 mg omeprazole tid associated with 250 mg clarithromycin and 500 mg amoxycillin four times daily for 10 days and maintained with 20 mg omeprazole daily for 18 weeks. Control endoscopies were performed at 6 and 18 weeks after beginning treatment. RESULTS: Duodenal gastric metaplasia regression was observed in all (32/32) patients in whom Helicobacter pylori was eradicated, but in only 3 out of 6 patients in whom eradication was not achieved (p<0. 001). CONCLUSIONS:. The present results suggest that Helicobacter pylori eradication associated with prolonged acid suppression may represent a good therapeutic strategy to achieve duodenal gastric metaplasia regression and highlight the combined role of acid and Helicobacter pylori in the pathogenesis of duodenal gastric metaplasia.     

Seroprevalence of eight Helicobacter pylori antigens among 182 patients with peptic ulcer, MALT gastric lymphoma or non-ulcer dyspepsia. Higher rate of seroreactivity against CagA and 35-kDa antigens in patients with peptic ulcer originating from Europe and Africa.

BACKGROUND: It has been suggested that Helicobacter pylori may induce more or less severe gastroduodenal disease according to the strain virulence. DESIGN: We used Western blot to determine antigenic profiles associated with duodenal or gastric ulcer disease, MALT lymphoma and non-ulcer dyspepsia, and to identify geographical differences. METHODS: One hundred and eighty-two consecutive patients with H. pylori infection were studied. H. pylori infection was diagnosed by a rapid urease test or histological examination of gastric biopsy samples. Bacterial density and gastritis were assessed histologically by using the Sydney scoring system. Western blot was used to identify antibodies against eight antigens (CagA, VacA, urease A, heat shock protein B, and 19.5, 26.5, 30 and 35 kDa). Patients were questioned on their smoking habits and place of birth and childhood. RESULTS: There were 73 patients with duodenal ulcer, 30 with gastric ulcer, eight with erosive duodenitis, 17 with gastric MALT lymphoma and 54 with non-ulcer dyspepsia. Most (>85%) were seropositive for the heat shock protein B and 26.5-kDa antigens. The prevalence of the other antigens ranged from 45% (VacA) to 68% (urease B). The seroprevalence of CagA antigen was significantly higher (P < 0.01) in cases of gastroduodenal ulcer (84%) than non-ulcer dyspepsia (37%). Similarly, 35-kDa antigen reactivity was more frequent (P < 0.05) in duodenal ulcer patients (75%) than in those with non-ulcer dyspepsia (50%). The antigenic profiles associated with MALT gastric lymphoma and non-ulcer dyspepsia were similar. Multivariate analysis showed that only gastroduodenal ulcer was significantly associated with CagA. Gastroduodenal ulcer and a childhood spent in Africa were both associated with 35-kDa and combined CagA-35-kDa reactivity. CONCLUSIONS: This study confirms the strong seroprevalence of H. pylori CagA antigen and shows a high prevalence of the 35-kDa antigen in patients with gastroduodenal ulcer, especially those raised in Africa. There was no difference in the serological pattern between patients with non-ulcer dyspepsia and those with MALT lymphoma. Tests for antibodies to the CagA-35-kDa antigen combination might be used to select H. pylori-infected dyspeptic patients warranting treatment.     

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.     

Are twelve days of omeprazole, amoxicillin and clarithromycin better than six days for treating H. pylori infection in peptic ulcer and in non-ulcer dyspepsia?

BACKGROUND/AIMS: To evaluate whether omeprazole, amoxicillin and clarithromycin for 12 days is more effective for Helicobacter pylori eradication than the same regimen for only 6 days; and to verify whether these eradication regimens are more effective in peptic ulcer disease than in non-ulcer dyspepsia. METHODOLOGY: We studied 411 patients in whom a gastroscopy was carried out due to symptoms related to the upper gastrointestinal tract and who were diagnosed with duodenal ulcer (175 patients, 43%), gastric ulcer (42 patients, 10%), or non-ulcer dyspepsia (194 patients, 47%), and concomitant infection by H. pylori. At endoscopy, biopsies were obtained for rapid urease test, and a 13C-urea breath test was carried out. Urea breath test was repeated four weeks after completing eradication treatment with 1) omeprazole (20 mg b.i.d.), amoxicillin (1 g b.i.d.) and clarithromycin (500 mg b.i.d.) for six days (239 patients), or 2) the same regimen for 12 days (172 patients). RESULTS: H. pylori eradication was achieved in 73.6% (95% CI, 68-79%) of the patients treated during 6 days, and in 84.3% (79-90%) of those receiving 12 days of therapy (P < 0.01). The overall eradication rate with both regimens (6 plus 12 days), respectively in patients with duodenal ulcer, gastric ulcer and non-ulcer dyspepsia, was 84.6% (79-90%), 75.6% (61-86%), and 72.8% (67-79%) (P < 0.01 when comparing duodenal ulcer vs. non-ulcer dyspepsia). Twelve-day regimen was more effective than 6-day regimen only in non-ulcer dyspepsia (62% vs. 83%, P < 0.01), but not in duodenal or gastric ulcer. In the multivariate analysis the duration (6 vs. 12 days) of eradication therapy (odds ratio: 2.2; 1.3-3.7) and the type of disease (duodenal ulcer vs. non-ulcer dyspepsia; odds ratio: 2.3; 1.3-3.8) were the only variables which influenced on H. pylori eradication efficacy (chi 2 model, 17; P < 0.001). CONCLUSIONS: Efficacy with omeprazole-amoxicillin-clarithromycin regimen in patients with duodenal ulcer is higher than in those patients with non-ulcer dyspepsia. The increase of H. pylori eradication rate by 21% in our non-ulcer dyspepsia patients justifies the prolongation from 6 to 12 days of omeprazole-amoxicillin-clarithromycin therapy, whilst the increase of cure rates in duodenal or gastric ulcer patients with a 12-day therapy would not be cost-effective.     

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.     

Effect of non-steroidal anti-inflammatory drugs on gastric and duodenal prostaglandin concentrations in patients with Helicobacter pylori infection.

BACKGROUND/AIMS: Both Helicobacter pylori and non-steroidal anti-inflammatory drugs are reported to affect gastroduodenal prostaglandin synthesis. However, their influence on gastric mucosal prostaglandins remains unclear. The aim of this study was to investigate the influence of nonsteroidal anti-inflammatory drugs on mucosal prostaglandin synthesis in patients with Helicobacter pylori infection. METHODOLOGY: We enrolled 87 Helicobacter pylori-infected patients in this study (gastric ulcer: 33, duodenal ulcer: 41, and non-ulcer dyspepsia: 13). Of them, 27 patients received non-steroidal anti-inflammatory drugs. Endoscopy was performed and biospy specimens from gastric body, antrum and duodenal bulb were assessed for Helicobacter pylori and prostaglandin concentration. RESULTS: A significantly lower mucosal prostaglandin E2 level at gastric body (142.2 +/- 28.1 ng/mg vs. 222.0 +/- 12.4 ng/mg, mean +/- SEM) and antrum (131.3 +/- 26.4 ng/mg vs. 226.0 +/- 19.0 ng/mg) was noted in Helicobacter pylori-infected gastric ulcer patients with non-steroidal anti-inflammatory drugs ingestion than in that of patients without non-steroidal anti-inflammatory drugs ingestion (p < 0.05). Using a multivariate analysis, we found that non-steroidal anti-inflammatory drug was an independent variable affecting gastric and duodenal mucosal prostaglandin E2 synthesis in patients with Helicobacter pylori-infected gastric ulcer. CONCLUSIONS: Non-steroidal anti-inflammatory drugs decrease gastroduodenal mucosal prostaglandin E2 synthesis in gastric ulcer patients with Helicobacter pylori infection.     

Gastric metaplasia and duodenal ulcer disease in children infected by Helicobacter pylori.

BACKGROUND--Helicobacter pylori infection of the gastric mucosa is vital in the pathogenesis of duodenal ulcer disease. H pylori will only colonise gastric epithelium and its association with duodenal disease is therefore not easily explained. AIMS--To determine if gastric metaplasia in the duodenum increases the risk of duodenal ulcer disease in children infected with H pylori. PATIENTS--All children undergoing upper endoscopy over a 20 month period in a children's hospital in Ireland. METHODS--Two biopsy specimens were obtained from the antral mucosa and two from the first part of the duodenum. One antral biopsy specimen was used in a rapid urease test (Clo Test). Biopsy sections were stained with haematoxylin and eosin and also with cresyl violet for identification of H pylori. Periodic acid Schiff (PAS) stain was performed to identify areas of gastric metaplasia. RESULTS--Gastric and duodenal biopsy specimens were obtained from 148 patients (M:F 1:2:1). Twenty five children (17%) had H pylori positive gastritis. Thirty four children (23%) had gastric metaplasia in the duodenum. Nine per cent of children under the age of 8 years had gastric metaplasia compared with 38% in those 12 years of age or over (p < 0.005). Seven children had duodenal ulcer disease. Gastric metaplasia was present in six of seven (86%) children with duodenal ulcer disease compared with 28 of 141 (20%) without ulceration (p < 0.001). While both H pylori and gastric metaplasia were each significant risk factors for duodenal ulcer disease, the combined presence of both factors was associated with a pronounced increase in duodenal ulcer disease. Duodenal ulcer disease occurred in over 50% of children with both H pylori infection and gastric metaplasia. In contrast duodenal disease did not occur in children (0 of 100) when both were absent. CONCLUSION--The presence of gastric metaplasia in the duodenum is the major risk factor for duodenal ulcer disease in patients colonised by H pylori.     

十二指肠粘膜胃上皮化生的诊断及临床意义

目的：探讨十二指肠粘膜胃上皮化生的诊断及临床意义。方法：对58例经胃镜检查确诊的十二指肠球部溃疡患者行十二指肠美蓝染色,于不染区或着色区取材作病理检查和快速尿素酶试验。结果：58例患者中,26例于溃疡附近出现斑片状粉红色不染区,13例出现白色不染区,19例着蓝色,三者的胃上皮化生检出率分别为80．8％（21／26）,15．4％（2／13）和10．5％（2／19）,粉红色不染区的胃上皮化生检出率明显高于着色区（P＜0．01）,25例检出胃上皮化生者中22例幽门螺杆菌（H.pylori)阳性（88．0％）,33例无胃上皮化生者中4例H.pylori阳性（12．1％）,前者的阳性率显著高于后者（P＜0．01）,结论：十二指肠美蓝染色用于辨别十二指肠胃上皮化生效果较好,对针对性取材及[观察十二指肠球部溃疡患者胃上皮化生的动态变化有指导意义。     

Abnormal clearance of exogenous acid and increased acid sensitivity of the proximal duodenum in dyspeptic patients

BACKGROUND & AIMS: Although acid is likely to play a role in the genesis of symptoms in dyspeptic patients, most studies have failed to show an increase in gastric acid secretion. The aim of this study was to investigate clearance of acid from the duodenum and its relationship with symptoms in patients with functional dyspepsia. METHODS: Twelve patients and 10 healthy volunteers were studied using an assembly allowing recording of pressures and pH. Acid and saline were infused intraduodenally during phase II and postprandially. Sensations were scored before and 1 and 5 minutes after each infusion. RESULTS: After acid infusion in the fasting period, a greater increase in acidity in the duodenal bulb (P = 0.007) and fewer duodenal pressure waves (P = 0.002) were observed in dyspeptic patients. No significant differences in the time with pH < 4 and duodenal motor activity were observed in the postprandial period. Acid infusion reproducibly increased the sensation of nausea in patients (P < 0.001) but not in the controls. Saline infusion had no effect on upper gastrointestinal sensations. CONCLUSIONS: In fasting dyspeptic patients, clearance of exogenous acid from the duodenal bulb and duodenal motor activity are decreased. The duodenal bulb in dyspeptic patients is hypersensitive to acid infusion, which induces the nausea.     

Deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer： A correlated study

AIM: To investigate the correlation among the presence and degree of gastric metaplasia of duodenal regenerating mucosa, the deformity of bulb and the recurrence of duodenal ulcer. METHODS: A total of 99 patients with duodenal ulcer were treated with H2-antagonist with or without antimicrobial therapy. All patients received follow-up endoscopic examinations 6 wk after treatment. When the ulcer(s) were noted to be healed, two biopsies were taken from the ulcer scar for histological study of gastric metaplasia, and 4 biopsies were taken from antrum for Helicobacter pylori (H pylori) study. Out of these cases, 44 received further follow-up endoscopic examinations after 3,6 and 12 mo respectively for studying the recurrence rate of duodenal ulcers. The correlation among ulcer recurrence, degree of gastric metaplasia of regenerating mucosa, bulbar deformity, and colonization of H pylori in the stomach was then studied. RESULTS: The results showed that there was a strong correlation between the deformity of duodenal bulb and the degree of gastric metaplasia of regenerating duodenal mucosa. The recurrence rate of duodenal ulcer had a significant difference between patients with and without H pylori colonization in the stomach (P<0.001). The greater the degree of gastric metaplasia of duodenal regenerating mucosa, the higher the recurrence rate of duodenal ulcer (P= 0.021). The more deformed the duodenal bulb, the higher the incidence of recurrence of duodenal ulcer (P = 0.03). CONCLUSION: There is a correlation among deformity of duodenal bulb, gastric metaplasia of duodenal regenerating mucosa and recurrence of duodenal ulcer. A more severely deformed duodenal bulb is closely related to a greater extent of gastric metaplasia. Both factors contribute to the recurrence of duodenal ulcer.