Relationship between pepsinogen I/II ratio and age or upper gastrointestinal diseases in Helicobacter pylori-positive and -negative subjects]

BACKGROUND/AIMS: Although previous reports suggested that pepsinogen (PG) I/II ratio was the index of gastric atrophy, PG I/II ratio was also related to other factors such as Helicobacter pylori (H. pylori) infection, various gastrointestinal diseases, and aging. The aim of this study was to evaluate the relationship between serum PG I/II ratio and age or upper gastro-intestinal diseases according to H. pylori infection status. METHODS: A total of 529 individuals (307 male; mean age, 57.2 years) were divided into 4 groups (94 gastric ulcers, 35 duodenal ulcers, 105 reflux esophagitis, and 295 atrophic gastritis) according to endoscopic diagnosis. H. pylori infection was determined by H. pylori IgG antibody (ELISA) and PG was measured by latex immunoassay. RESULTS: H. pylori infected patients showed markedly increased serum PG II levels (24.0+/-14.7 ng/mL vs. 13.8+/-16.6 ng/mL, p0.001) and low PG I/II ratio (3.9+/-2.0 vs. 6.0+/-2.5, p0.001) than non-infected subjects. In H. pylori infected patients, mean PG I/II ratios in the gastric ulcer and atrophic gastritis group were significantly lower than those of the duodenal ulcer and reflux esophagitis group (p0.001, ANOVA, Turkey's multiples comparison test). The mean ratio of open type atrophic gastritis was lower than that of close type atrophic gastritis (3.0+/-1.4 vs. 3.8+/-1.7, p0.005). PG I/II ratio gradually decreased with age in H. pylori-infected patients with atrophic gastritis (R(2)=0.9, p=0.005, linear regression analysis). CONCLUSION: Serum PG I/II ratio reflects H. pylori infection and gastric atrophy. In the presence of H. pylori infection, gastric atrophy progresses with age.     

Clinical Significance of Helicobacter pylori Seropositivity and Seronegativity in Asymptomatic Blood Donors

To determine the clinical significance ofHelicobacter pylori seropositivity and seronegativity inhealthy blood donors, we carried out a serologicalevaluation of Helicobacter pylori status and endoscopy in a healthy blood donors population. In all,1010 donors were screened for Helicobacter pylori by IgGELISA and assessed for pepsinogen I and gastrin levelsby RIA; 298 IgG seropositive and 61 seronegative subjects underwent endoscopy with biopsies. Of359, 165 were also tested for CagA by western blotting.Of the 298 IgG seropositives, 274 were shown to beinfected on biopsy testing. Endoscopy revealed 70 peptic ulcers, 41 cases of erosive duodenitis,and two gastric cancers. In all 105 seropositive donorswere tested for CagA and 69 were CagA positive [34/58gastritis (58.6%), 24/35 duodenal ulcer (68.6%) and 11/12 gastric ulcer (91.6%)].Histologically active/chronic gastritis was associatedwith CagA: 88.4% vs 50% (CagA seropositive vsseronegative). Of the 61 IgG seronegatives, 59 werenegative on biopsy testing. At endoscopy three had duodenitis. Ofthe 60/61 IgG seronegatives tested for CagA, one had amoderate reaction. Duodenal ulcer donors showed higherpepsinogen I levels than donors without duodenal ulcers (97.7 g/ml vs 80.9 g/mlrespectively). Screening for Helicobacter pylori andanti-CagA seropositivity and pepsinogen I can identifyindividuals likely to have gastroduodenal pathology evenin the absence of symptoms.     

Prevalence of Peptic Ulcer in Dyspeptic Patients and the Influence of Age,Sex, and <Emphasis Type="Italic">Helicobacter pylori</Emphasis> Infection

We investigated the prevalence of peptic ulcer in dyspeptic patients in China to analyze the influence of age, sex, and Helicobacter pylori (H. pylori) infection. The results showed that the prevalence of gastric and duodenal ulcer increased with age. In patients under 60 years old, the prevalence of duodenal and gastric ulcers in females was markedly lower than that in males, especially the prevalence of duodenal ulcer. The prevalence of duodenal ulcer and gastric ulcer in H. pylori-infected patients was markedly higher than in patients without H. pylori infection. In the patients under 60 years old, sex differences were still seen in both H. pylori-positive and H. pylori-negative patients. The prevalence of gastric and duodenal ulcers was markedly increased with age in both H. pylori-positive and H. pylori-negative patients. Multivariate logistic regression analysis showed that age, male sex, and H. pylori infection were three independent risk factors for gastric and duodenal ulcers.     

Helicobacter pylori, non-steroidal anti-inflammatory drugs and smoking in risk pattern of gastroduodenal ulcers

BACKGROUND: Helicobacter pylori, NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. METHODS: 5967 dyspeptic patients underwent 13C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. RESULTS: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. CONCLUSIONS: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).     

Herpes simplex virus type 1 in peptic ulcer disease： An inverse association with Helicobacterpylori

AIM: To assess the frequency of herpes simplex virus type I in upper gastrointestinal tract ulcers and normal mucosa with the modern and better assays and also with a larger number of well characterized patients and controls and its relationship to Helicobacter pylori(H pylori). METHODS: Biopsy specimens from 90 patients (34 with gastric ulcer of the prepyloric area and 56 with duodenal ulcer) were evaluated. Biopsies from 50 patients with endoscopically healthy mucosa were considered as the control group. The method used to identify herpes simplex virus-1 (HSV-1) was polymerase chain reaction. H pylori was detected by the CLO-test and by histological method. RESULTS: Herpes simplex virus-1 was detected in 28 of 90 patients with peptic ulcer (31%) [11 of 34 patients with gastric ulcer (32.4%) and 17 of 56 with duodenal ulcer (30.4%)] exclusively close to the ulcerous lesion. All control group samples were negative for HSV-1. The likelihood of H pylori negativity among peptic ulcer patients was significantly higher in HSV-1 positive cases than in HSV-1 negative cases (P = 0.009). Gastric ulcer patients with HSV-1 positivity were strongly associated with an increased possibility of Helicobacter pylori negativity compared to duodenal ulcer patients (P = 0.010). CONCLUSION: HSV-1 is frequent in upper gastrointestinal tract ulcers but not in normal gastric and duodenal mucosa. There is an inverse association between HSV-1 and H pylori infection.     

Helicobacter pylori,Non-steroidal Anti-inflammatory Drugs and Smoking in Risk Pattern of Gastroduodenal Ulcers

Background: Helicobacter pylori , NSAID and cigarette smoking are major risk factors for gastroduodenal ulcers. However, the results of studies on the interaction between these factors on ulcerogenesis are controversial. This study was designed to examine the association between gastroduodenal ulcers and H. pylori infection, NSAID use, smoking and age. Methods: 5967 dyspeptic patients underwent 13 C-urea breath test (UBT) and upper endoscopy, while age and dyspeptic symptoms were reported. Results: Out of 5967 patients, 31.8% were ulcerated; 9.2% had gastric, 17.2% duodenal and 5.4% both gastric and duodenal ulcers. H. pylori was found in 72.5% of gastric ulcer patients, in 83.6% of duodenal ulcer patients, in 76.9% of gastroduodenal ulcer patients and in 64.8% of dyspeptic patients. The gastric, duodenal and gastroduodenal ulcers were related to H. pylori significantly and the respective ORs were: 1.44, 2.77 and 1.81. NSAID alone was used by 6.2%-12.7% of ulcer patients, tending to raise only the risk of gastric ulcer but reducing that of duodenal and gastroduodenal ulcers. The H. pylori prevalence was significantly higher in smokers (76%) than in non-smokers (67%) and the ulcer risk was also significantly higher in smokers than in non-smokers. About 20% of ulcers were 'idiopathic', i.e. without NSAID and H. pylori and the ratio of these ulcers to all ulcers significantly increased during the 5 years of the study. Conclusions: Based on multivariable logistic regression analysis we conclude that: 1) H. pylori infection, NSAID use, smoking and age play major roles in the pathogenesis of peptic ulcerations; 2) there is a negative interaction between H. pylori and NSAID on duodenal ulcers, suggesting that H. pylori reduces the development of these ulcers in NSAID users, and 3) about 20% of peptic ulcers in the Polish population are unrelated to H. pylori and NSAID use (idiopathic ulcers).     

Helicobacter pylori infection induces duodenitis and superficial duodenal ulcer in Mongolian gerbils

BACKGROUND: There is no direct evidence for an animal model of Helicobacter pylori induced duodenal ulcer. AIM: In this study we evaluated the roles of bacterial strain and age of experimental animals in induction of duodenitis and duodenal ulcer in Mongolian gerbils after H pylori infection. METHODS: Specific pathogen free Mongolian gerbils were inoculated orally with three bacterial strains (H pylori ATCC 43504, TN2GF4, and K-6, a clinical isolate from a patient with gastric cancer in our clinic). These strains have both the cagA gene and VacA. Five week old gerbils were used to emulate prematurity infection and 14 week old animals were used as mature test subjects. Animals were observed for 12 weeks after inoculation. Interleukin 8 (IL-8) production in gastric epithelial cells (MKN74) after coculture with the H pylori strains was measured by ELISA. RESULTS: Gastritis and gastric ulcers were found in all gerbils infected with the three strains. However, duodenitis and gastric metaplasia were seen more frequently in gerbils infected with TN2GF4 and K-6 strains than in the ATCC 43504 infected or control groups (p<0.05). Superficial duodenal ulcers with severe duodenitis and gastric metaplasia were found in two gerbils inoculated at 14 weeks with the TN2GF4 strain but none at five weeks. The TN2GF4 strain stimulated significantly higher levels of IL-8 than ATCC 43504 and K6 strains (p=0.0039). CONCLUSIONS: When injected into adult Mongolian gerbils, a specific strain (TN2GF4) of H pylori can induce duodenitis with gastric metaplasia and superficial duodenal ulcers. Induction of duodenal ulcer in an animal model fulfills the requirements of Koch's postulates for establishing a role for H pylori as a causative agent.     

Helicobacter pylori and risk of ulcer bleeding among users of nonsteroidal anti-inflammatory drugs: a case-control study.

BACKGROUND & AIMS: Peptic ulcer complications related to use of nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most common serious adverse drug reactions. Whether Helicobacter pylori infection potentiates this gastrointestinal toxicity of NSAIDs is still unresolved. In this study, we investigated the role of H. pylori as a cause of bleeding peptic ulcer among NSAID users. METHODS: A case-control study of current users (n = 132) of NSAIDs (including acetylsalicylic acid), admitted because of bleeding peptic ulcer, was performed. Controls were 136 NSAID users without gastrointestinal complications. H. pylori was diagnosed by either increased levels of serum immunoglobulin G or by 13C-urea breath test. RESULTS: Fifty-eight (44%) case subjects had a bleeding gastric ulcer, 54 (41%) had a bleeding duodenal ulcer, 12 (9%) had both gastric and duodenal ulcers, and 8 (6%) had hemorrhagic gastritis. H. pylori was present in 75 (57%) cases compared with 59 (43%) controls. The adjusted odds ratio of bleeding peptic ulcer among NSAID users associated with H. pylori infection was 1.81 (95% confidence interval, 1.02-3.21). H. pylori accounted for approximately 24% of bleeding peptic ulcers among elderly NSAID users. CONCLUSIONS: NSAID users infected with H. pylori have an almost twofold increased risk of bleeding peptic ulcer compared with NSAID users without H. pylori.     

Effect of Helicobacter pylori infection on 24 hour intragastric acidity in patients with gastritis and duodenal ulcer.

Helicobacter pylori status, gastric histology, and 24 hour acidity were studied in 35 gastritis patients, 21 duodenal ulcer patients, and 14 subjects with normal gastric mucosa. H pylori was identified in 21 of 35 patients with chronic active gastritis and in 19 of 21 duodenal ulcer patients, but in none of those with normal gastric mucosa. Mean scores of activity of gastritis were similar in H pylori positive gastritis and duodenal ulcer patients, but were significantly lower in H pylori negative gastritis patients (2.1 (0.8) and 2.3 (0.9) v 1.4 (0.7); p < 0.01, respectively). Median 24 hour hydrogen ion activity (interquartile range) was 21 (8.9-38.0) mmol/l in normal subjects and 23 (11.2-49.0) mmol/l, 19 (7.1-33.1) mmol/l, 44 (25.1-63.1) mmol/l, and 36 (31.6-39.8) mmol/l respectively in gastritis and duodenal ulcer patients with and without H pylori infection. During all predefined time periods, intragastric acidity was significantly higher in patients with H pylori positive duodenal ulcers compared with gastritis patients and normal subjects. However, there was no significant difference in intragastric acidity between the H pylori positive and negative gastritis patients. These results suggest that most of the subjects with chronic H pylori infection have normal gastric acidity.     

Ideology of Helicobacter pylori prevalence in peptic ulcer disease in an inner-city minority population

GOALS AND BACKGROUND: The prevalence of Helicobacter pylori infection among patients with peptic ulcer disease has been reported to range from 61 to 94%. Recent studies show a reduction in the prevalence of H. pylori infection in patients with peptic ulcer disease. This study was conducted to determine the prevalence of H. pylori infection in peptic ulcer disease in an inner-city hospital in Washington, DC. METHODS: Medical records of all patients who had undergone upper gastrointestinal endoscopy from July 1997 through June 1999 were reviewed. All patients who had gastric ulcer and/or duodenal ulcer on upper gastrointestinal endoscopy were studied. Demographic characteristics, history of nonsteroidal antiinflammatory drug ingestion, alcohol consumption, and associated diseases were studied. H. pylori was considered to be present if CLOtest and/or histopathology were positive for H. pylori. Patients with negative pathology for H. pylori or negative pathology and CLOtest were considered negative for H. pylori. RESULTS: One-hundred fifty-six patients were found to have gastric and/or duodenal ulcers. Fifty-one ulcer patients did not meet the inclusion criteria and were excluded. Among the 105 patients who were included in the study, gastric ulcers were found in 48 patients (45.7%), duodenal ulcers were found in 46 patients (43.8%), and both gastric and duodenal ulcers were found in 11 patients (10.5%). H. pylori was present in 66.7% of gastric ulcer patients and in 69.5% of duodenal ulcer patients. Antral histology and CLOtest were in agreement 96% of the time. CONCLUSIONS: At the District of Columbia General Hospital, an inner-city hospital serving predominantly an African-American community, the prevalence of H. pylori in ulcer patients compares similarly to other more recent studies that have found a decreased prevalence of this bacterial infection in ulcer patients. This suggests that the treatment of H. pylori in minority patients is reducing the proportion of ulcers due to this bacterium, as has been seen with the majority population.     

Role of Helicobacter pylori in ulcer healing and recurrence of gastric and duodenal ulcers in longterm NSAID users. Response to omeprazole dual therapy.

BACKGROUND: The relation between Helicobacter pylori infection and non-steroidal anti-inflammatory drug (NSAID)-associated peptic ulcers remains unclear; in particular, it is not known whether H pylori plays a part in the healing and recurrence of these ulcers. AIMS: To evaluate prospectively in a consecutive series of arthritis patients receiving longterm NSAID treatment the prevalence of peptic ulcer as well as the effect of H pylori eradication on the healing and recurrence of gastric and duodenal ulcer found. PATIENTS: Some 278 consecutive patients underwent gastroscopy with multiple biopsies of the gastric antrum and corpus for histological examination and rapid urease test. One hundred peptic ulcers (59 gastric ulcers, 39 duodenal ulcers, and two gastric ulcers concomitant with a duodenal ulcer) were found. Seventy per cent of these ulcers were H pylori positive. METHODS: According to their H pylori status, ulcer patients were randomised to one of the following treatments: H pylori negative ulcers received omeprazole 20 mg twice daily for four to eight weeks, whereas H pylori positive lesions were treated with omeprazole 20 mg twice daily plus amoxycillin 1 g twice daily (the second of these for the first two weeks) or omeprazole alone for four to eight weeks while continuing NSAID therapy. Patients with healed ulcers were endoscopically followed up for six months after stopping antiulcer therapy while continuing NSAIDs. RESULTS: Endoscopic healing rates for gastric and duodenal ulcers in the three different groups were similar both at four and eight weeks. H pylori eradication did not influence healing, which occurred in 14 of 20 (70%) of patients in whom H pylori was eradicated, compared with 14 of 17 (82%) of patients with persistent infection. Cumulative recurrence rates at six months did not statistically differ among the three different groups (27% in H pylori negative, 46% in H pylori positive, and 31% in those where H pylori was eradicated during the healing phase), although a numerical trend in favour of a higher recurrence rate in infected patients was evident. CONCLUSIONS: H pylori eradication does not confer any significant advantage on the healing of gastric and duodenal ulcers associated with longterm NSAID use. It remains to be established with certainty whether eradication may be helpful in the reduction of recurrence in a specific subset of NSAID associated ulcer.     

Duodenal erosions after eradication of Helicobacter pylori infection

BACKGROUND: There is interest in the development of GERD after Helicobacter pylori eradication. In contrast, the development of duodenal erosions after therapy has received scant attention. Patients were examined after eradication of H pylori infection to determine the frequency of post-therapy duodenal erosions (primary outcome) and whether there was a relation between development of duodenal and esophageal erosions. Additionally, factors were searched for that would identify patients at increased risk for duodenal erosions. METHODS: A single-center, endoscopist-blinded, observational study was conducted of 196 patients in whom H pylori was eradicated. The presence of esophageal or duodenal erosions was evaluated 4 weeks and 6 months after eradication. Serum gastrin and pepsinogen I (PG I) and II (PG II) levels were also determined for 83 patients entering the study during its final year. RESULTS: Multiple small duodenal erosions developed in 8.6% of patients after H pylori eradication and were more common in patients with pre-eradication duodenal ulcer (27.8%) compared with those with gastric ulcer (6.7%) or atrophic gastritis (1.4%) (p < 0.05). Duodenal erosions were associated with high levels of PG I before and after eradication. The frequency of duodenal erosions decreased over time (3.1% by 6 months). CONCLUSION: Duodenal erosions occur after H pylori eradication and appear to be related to duodenal ulcer and increased PG I levels, both of which are associated with increased acid secretion. Measurement of PG I may help to identify patients who have duodenal erosions develop after H pylori therapy for studies of the pathogenesis of these lesions.     

胃十二指肠疾病幽门螺杆菌检出的意义

目的:研究幽门螺杆菌(Hp)与消化性溃疡及慢性胃炎致病的关系。方法:因胃十二指肠疾病而做胃镜的患者,采取胃粘膜进行组织快速检菌,一分钟尿素酶(1min UT)试验和血清间接免疫荧光法进行检菌分析。结果:对5000例胃及十二指肠疾病Hp的组织检出率为88.1％。1min UT阳性率为62.9％,两种检菌法有显著差异(P<0.01)。十二指肠溃疡Hp检出为96.0％,胃癌和萎缩性胃炎Hp感染率为50.0％和59.2％,而1min UT只有41.5％阳性率。结论:胃癌和萎缩性胃炎均有粘膜层萎缩,腺体减少、粘液分泌功能降低,Hp茵不能适应强酸环境下生存。十二指肠溃疡和慢性胃炎多伴引起幽门口水肿和幽门变型,胃排空减缓。是导致Hp茵高检出率的重要因素。     

Effect of Helicobacter pylori eradication on bulbitis and duodenal gastric metaplasia

BACKGROUND/AIMS: Duodenal gastric metaplasia seems to be linked to infection by Helicobacter pylori, to the extent of acid secretion and to bulbitis. An investigation was made of the relationship between bulbitis and duodenal gastric metaplasia, or whether bulbitis can arise along with duodenal gastric metaplasia after Helicobacter pylori eradication in an average of six years. METHODOLOGY: We compared 22 patients with duodenal ulcers [male/female 16/6; (mean age+/-SD) 55+/-12 years] Helicobacter pylori-negative after eradication, with 23 Helicobacter pylori-positive patients free from active duodenal ulcers [male/female 17/6; (mean age+/-SD) 59+/-12 years]. RESULTS: The bulbitis score was found to be lower in the Helicobacter pylori-negative than in the Helicobacter pylori-positive group (p=0.02). The duodenal gastric metaplasia score in the Helicobacter pylori-negative was higher than in the Helicobacter pylori-positive group (p=0.001). We failed to find any relationship between the presence of bulbitis and duodenal gastric metaplasia. We found a non-significant inverse correlation between the presence of duodenal gastric metaplasia and chronic body gastritis (p=0.07). CONCLUSIONS: Bulbitis and duodenal gastric metaplasia may depend on different causal factors not related to Helicobacter pylori infection. The extension of duodenal gastric metaplasia with time following recovery from peptic ulcer disease may represent a mucosal protection factor against acid.     

Acid Secretion and Serum Gastrin in Normal Subjects and Patients with Duodenal Ulcer: The Role of Helicobacter pylori

Objectives : To compare gastric secretory function in patients with duodenal ulcer and in healthy volunteers with and without Helicobacter pylori infection. Methods : Basal acid output, peak acid output, meal-stimulated acid output, fasting and meal-stimulated serum gastrin concentrations were measured in 136 healthy volunteers (63 H. pylori positive. 73 H. pylori negative) and 52 duodenal ulcer patients, all but one of whom were H. pylori positive. Results : By multivariate linear regression analysis. H. pylori infection was a significant negative predictor of basal acid output and a positive predictor of fasting and meal-stimulated gastrin concentrations. When compared to truly normal ( i.e., H. pylori -negative) control subjects, duodenal ulcer patients had elevated basal acid output, peak acid output, fasting and meal-stimulated gastrin concentrations. Conclusions : Our results show that in patients with duodenal ulcer disease, hypergastrinemia is largely related to gastric H. pylori infection, whereas acid by persecretion is due to factors other than H. pylori .     

Usefulness of proton pump inhibitor (PPI) maintenance therapy for patients with H. pylori-negative recurrent peptic ulcer after eradication therapy for H. pylori: pathophysiological characteristics of H. pylori-negative recurrent ulcer scars and beyond acid suppression by PPI

BACKGROUND/AIMS: Problems after Helicobacter pylori (Hp) eradication therapy include recurrence of Hp-negative peptic ulcers. We investigated the pathophysiological characteristics of Hp-negative recurrent ulcer scars, and performed proton pump inhibitor (PPI) maintenance therapy as a new therapy for prevention of recurrence in patients with Hp-negative recurrence after Hp eradication and investigated its usefulness. METHODOLOGY: The subjects were 21 patients with Hp-negative recurrent peptic ulcers after Hp eradication (gastric ulcer: 19, duodenal ulcer: 2) and 25 patients with non-recurrent ulcers (gastric ulcer: 20, duodenal ulcer: 5). The mucosa from the ulcer scar lesion was endoscopically obtained from patients, and HE staining, CD68 immunohistochemical staining, and investigation of the mucosal expression levels of TNF-alpha and IFN-gamma were performed by ELISA. Patients with recurrence after eradication were divided into two groups at the time of ulcer scar after the first treatment, and received maintenance therapy: the intermittent treatment group that received lansoprazole (LPZ), 30 mg/day, on two days on weekends (gastric ulcer: 9, duodenal ulcer: 1) and the ranitidine (RAN) 150 mg/day daily treatment group (gastric ulcer: 8, duodenal ulcer: 1). RESULTS: Infiltration of CD68-positive inflammatory cells was observed in the lamina propria mucosae over the epithelial layer in ulcer scars of the Hp-negative recurrent ulcer group compared with the non-recurrent ulcer group, and TNF-alpha and IFN-gamma significantly increased (27.22+/-6.23 pg/mg, 52.12+/-5.41 pg/mg vs. 4.23+/-2.14 pg/mg, 7.11+/-3.06 pg/mg, P<0.001). In the RAN maintenance therapy group, the ulcer recurred within 10 months in all patients, while the ulcer recurred in only one patient in the intermittent LPZ treatment group. CONCLUSIONS: These results suggested that the pathophysiological characteristic of Hp-negative recurrent ulcer scar lesions after eradication was infiltration of inflammatory cells, mainly monocytes/macrophages, in the lamina propria mucosae over the epithelial layer, and this may be a key factor in ulcer recurrence. Furthermore, intermittent PPI therapy using LPZ may be a useful maintenance therapy for prevention of recurrence in these cases.     

Mucosal expression and luminal release of epidermal and transforming growth factors in patients with duodenal ulcer before and after eradication of Helicobacter pylori.

BACKGROUND: Epidermal growth factor (EGF) and transforming growth factor-alpha (TGF alpha) are potent gastric acid inhibitors and stimuli of mucosal growth and protection but their involvement in Helicobacter pylori associated duodenal ulcer has been little examined. AIM: To assess gastric acid secretion, plasma gastrin concentrations, mucosal content of EGF and TGF alpha, and mucosal expression of these peptides and their receptor (EGFr) as well as salivary and gastric luminal release of EGF under basal conditions and after pentagastrin stimulation in 10 healthy subjects and in 25 H pylori positive patients with duodenal ulcer before and after two weeks of triple anti-H pylori therapy and four weeks after the termination of this therapy. RESULTS: Pentagastrin stimulation caused a significant increase in salivary and gastric release of EGF both in healthy controls and patients with duodenal ulcers but in the patients, the eradication of H pylori resulted in several fold higher gastric luminal (but not salivary) EGF release than before the anti-H pylori therapy. Mucosal contents of immunoreactive EGF and TGF alpha and mucosal expression of EGF, TGF alpha, and EGFr in H pylori positive patients with duodenal ulcer were significantly higher than those in healthy H pylori negative controls and this increase persisted after eradication of H pylori. Basal plasma gastrin was significantly reduced after two weeks of triple therapy and four weeks after the H pylori eradication all ulcers were completely healed. CONCLUSIONS: (1) H pylori infection in patients with duodenal ulcer was accompanied by enhanced plasma gastrin and increased mucosal content and expression of TGF alpha, EGF, and EGFr; (2) H pylori eradication resulted in ulcer healing, reduction in plasma gastrin, and enhancement of gastric (but not salivary) luminal release of EGF, particularly after pentagastrin stimulation; and (3) enhanced mucosal content and expression of TGF alpha, EGF, and EGFr and increased luminal release of EGF may contribute to ulcer healing after eradication of H pylori.     

Biopsy specimen acquisition in patients with newly diagnosed peptic ulcer disease as determined from a national endoscopic database

BACKGROUND: Eradication of Helicobacter pylori infection decreases peptic ulcer recurrence. Therefore, assessment of Helicobacter pylori status is recommended for patients with newly diagnosed peptic ulcer disease. METHODS: Data obtained from the Clinical Outcomes Research Initiative's national endoscopic database were analyzed to characterize the acquisition of biopsy specimens in patients with a non-bleeding gastric or duodenal ulcer newly diagnosed by EGD. RESULTS: Between January 2000 and June 2003, 8299 patients underwent EGD with identification of non-bleeding peptic ulcer disease in the stomach (5390) or the duodenum (2909). Overall, biopsy specimens were obtained from the gastric or duodenal ulcer in 5578 (67%) of these patients. Multivariate analysis identified male gender (odds ratio [OR] 0.75, 95% confidence interval (CI) [0.66-0.85] vs. female), age greater than 75 years (OR 0.67, 95% CI [0.57-0.77] vs. age <55 years), ulcer location (OR 0.53, 95% CI [0.48-0.59] for duodenal vs. gastric ulcers) and endoscopy setting (OR 0.35, 95% CI [0.31-0.39] for academic vs. community; OR 0.36, 95% CI [0.32-0.41] for Veterans Affairs medical centers vs. community) as independent predictors for the acquisition of biopsy specimens (p < 0.001 for all). CONCLUSIONS: The findings of this study suggest that there is variation in the rates of biopsy specimen acquisition among patients with ulcers who may be at risk for Helicobacter pylori infection. Given the established benefit of Helicobacter pylori eradication, further study is needed to determine whether physicians are diagnosing and treating Helicobacter pylori infection adequately in patients with peptic ulcer.     

Clinical relevance of Helicobacter pylori CagA-positive strains: gastroduodenal peptic lesions marker.

OBJECTIVES: peptic ulcer is characterized by its recurrent nature, which necessitates maintenance treatment in most patients. But this natural history can be changed in patients with peptic ulcer associated to Helicobacter pylori, as shown by the low rates of recurrence and decreased hemorrhagic recidivism associated with this infection. Whether CagA or VacA strains are associated with a greater risk of peptic ulcer is controversial. This study was designed to examine endoscopic findings and their relation with H. pylori phenotype (CagA or VacA). METHODS: 106 selected dyspeptic patients underwent upper gastrointestinal tract endoscopic examination between September 1996 and May 1997 [69 with H. pylori (Hp) and 37 without this infection]. Endoscopic findings were classified as gastric ulcer (GU), duodenal ulcer (DU), gastric erosions (GE), duodenitis (Du), chronic gastritis (CG) and normal mucosa (NM). Hp phenotype was analyzed with a western blot test. RESULTS: 75% of H. pylori strains were CagA-positive and 54.2% were VacA-positive. 82.4% of the cases of DU were associated with a CagA+ phenotype, but the association was not statistically significant. Otherwise 100% of gastric ulcers were associated with CagA+ strains (p < 0.005). VacA phenotype was not associated with any particular endoscopic finding. Peptic ulcer (DU or GU) was also associated with the CagA+ phenotype (p < 0.05). CONCLUSIONS: the CagA+ H. pylori phenotype seems to be a peptic lesion marker, but was more frequently related with GU than with DU in our sample of Spanish patients.     

Attributable Risk of H. pylori in Peptic Ulcer Disease

Recent reports in the United States have found that fewer peptic ulcers are due to Helicobacter pylori than previously believed. The aim of this study is to determine if the declining prevalence of H. pylori infection in the general population can account for the apparent increase in the frequency of non-H. pylori ulcers. A total of 396 patients with peptic ulcer or ulcer scar were enrolled in this study. The pre-1950 population consisted of 149 patients with gastric ulcers and with 44 duodenal ulcers. The post-1950 population consisted of 96 patients with gastric ulcers and 107 with duodenal ulcers. The frequency of H. pylori-negative gastric ulcers was 5.4% in patients born before 1950 and 4.2% in patients born after 1950, and the frequency of H. pylori-negative duodenal ulcers was 0% and 1.9%, respectively. There are no statistical differences between the two populations in gastric and duodenal ulcers. H. pylori seropositivity was 74.9% in asymptomatic volunteers born before 1950 and 20.7% in those born after 1950 (P < 0.01) in the general population. The attributable risk of H. pylori infection in peptic ulcer diseases was not affected by the prevalence of H. pylori infection in the general population in Japan. This suggests that the apparent increase in frequency of non-H. pylori ulcers in the United States is not simply due to the declining prevalence of infection. Other explanations for non-H. pylori ulcers should be sought.