Eradication of Helicobacter pylori infection improved gastric mucosal atrophy and prevented progression of intestinal metaplasia,especially in the elderly population: A long‐term prospective cohort study

Background and Aims: It still remains controversial whether gastric mucosal atrophy and intestinal metaplasia are reversible after eradication of Helicobacter pylori infection. The aims of this study were to evaluate the histological changes in gastric mucosa after H. pylori eradication during long‐term follow‐up periods, and to verify the propriety of H. pylori eradication for the elderly population. Methods: Two hundred and forty‐one patients with H. pylori infection and 84 cases more than 60 years old were classified as the elderly group. The mean follow‐up period was 101 months. A series of endoscopic examinations with five‐point biopsies were performed before and every year after H. pylori eradication. We evaluated the histological grades according to the Updated Sydney System. Statistical analysis was performed using the Wilcoxon signed rank test and the Mann–Whitney U‐test, and P < 0.05 was considered to be statistically significant. Results: The atrophic grades improved only at the angle in the 5th year and at all points, except for the antrum, in the 10th year after H. pylori eradication. In the elderly group, the atrophic score improved in both the 5th and 10th year. However, improvement in the younger group was achieved only in the 10th year. The metaplastic score did not change in either the 5th or 10th year after H. pylori eradication in all patients. Conclusion: Eradication of H. pylori infection improved gastric atrophy and prevented the progression of intestinal metaplasia in the elderly population during the long‐term follow‐up periods. H. pylori eradication for the elderly population is effective.     

Correlation between serum pepsinogen levels and gastric mucosal histological findings before and after Helicobacter pylori eradication therapy

Background: Helicobacter pylori causes chronic gastritis and is also associated with many other gastrointestinal diseases. The incidence of gastric cancer is thought to vary according to the degree and topography of chronic gastritis. Histological findings of specimens obtained at endoscopy are therefore important. In the present study, we investigated the correlation between these histological findings and serum pepsinogen (PG) levels. Methods: Helicobacter pylori eradication therapy was conducted in 100 H. pylori‐positive patients. Endoscopies were performed prior to, and 2 months after, eradication therapy; gastric mucosal biopsies were taken from the antrum and corpus. Helicobacter pylori infection was diagnosed using the rapid urease test, culture and histology. Using the Updated Sydney System, histological findings of inflammation, activity, atrophy and intestinal metaplasia were each graded. Blood was taken on the same two occasions for determination of serum levels of PG I and II. Results: Levels of PG I were highest in association with antrum‐predominant gastritis (APG), followed in order by pangastritis (PAN) and corpus‐predominant gastritis (CPG), with a significant difference between APG and CPG. No correlations were seen between PG II levels and gastritis topography. Examination of the relationship between PG levels and histological findings revealed significant correlations between PG I levels after eradication atrophy and intestinal metaplasia in the gastric corpus. No significant correlations were seen between PG II levels and before or after eradication histological findings. Conclusion: Our results indicate that serum PG levels may be a useful indicator of before‐eradication gastritis topography and after‐eradication gastric atrophy in the gastric corpus.     

Kyoto global consensus report on Helicobacter pylori gastritis and its impact on Chinese clinical practice

The Kyoto global consensus report on Helicobacter pylori (H. pylori) gastritis has had a great effect on the field of H. pylori studies worldwide. For the first time H. pylori gastritis was defined entirely as an infectious disease and H. pylori‐associated dyspepsia as a new category of organic dyspepsia apart from functional dyspepsia, together with a proposed diagnostic algorithm. Accordingly, the report states that the eradication of H. pylori should be regarded as the first‐line treatment for dyspepsia. Moreover, H. pylori eradication before the development of pre‐neoplastic changes is recommended to reduce the risk of more serious complications of H. pylori gastritis. Despite the recommendations of this new global consensus, the task of transforming them into feasible and practical recommendations for individual countries will require them to become region‐specific, which requires further discussion.     

Helicobacter pylori infection induces a reversible expression of the CDX2 transcription factor protein in human gastric epithelium

Objective. The homeobox gene CDX2 is implicated in the appearance of intestinal metaplasia in Helicobacter pylori gastritis. The aim of this study was to investigate whether CDX2 expression in gastric mucosa occurs before the appearance of overt intestinal metaplasia in H. pylori gastritis, and whether or not this expression is reversible. Material and methods. CDX2 was studied by immunohistochemistry in a cohort of 38 patients with H. pylori gastritis before and after eradication (mean follow-up 6.3 years) of H. pylori. A cohort of 49 individuals with healthy stomachs was analysed as a control. Results. In the control group no immunostaining of CDX2 in the epithelial cells of the gastric body was found, while in 57% of the cases a mild, aberrant nuclear immunostaining of CDX2 in the non-metaplastic epithelial cells in antrum, designated as “positive staining of single cells” (PSSC), was found. In H. pylori gastritis, the PSSC was seen in antrum and corpus in 100% and 26% of the cases, respectively. The prevalence of antral PSSC was significantly increased (on average by 4-fold) in H. pylori gastritis as compared with controls. After eradication of H. pylori, the prevalence of PSSC decreased significantly in antrum but not in corpus. Conclusions. Expression of CDX2 at low intensity is common in the epithelium of normal antrum, and this expression is enhanced in H. pylori gastritis. Expression of CDX2 is reversible at least in antrum after eradication of H. pylori infection.     

Reduced relapse rate in duodenal ulcer disease leads to normalization of psychological distress: twelve‐year follow‐up

Background: The aim of this study was to elucidate the relationship between duodenal ulcer (DU) disease and psychological symptoms. Methods: Sixty‐four Helicobacter pylori‐positive patients with frequently relapsing DUs (patient group 1) were compared with 78 control subjects without dyspepsia, starting 2 years before and ending 10 years after eradication of H. pylori. Seven non‐relapsing and untreated patients (patient group 2) were also followed‐up. Results: The relapse rate was reduced from 100% per year in the two years before anti‐H. pylori treatment to 0.3% per year after treatment in patient group 1. The reinfection rate was 0.7% per year. Anxiety and neuroticism were high at inclusion, but had normalized at the 10‐year follow‐up in relapse‐free patients. There was no increase of gastro‐oesophageal reflux symptoms during the 10 years after H. pylori eradication. Conclusions: Normalization of anxiety and neuroticism following cure of DU disease supports the view that the increased anxiety and neuroticism are consequences, and not causes, of the disease.     

Comparison of the improvement in gastric mucosal tissue after Helicobacter pylori eradication between young and elderly people

Background and study aimsHelicobacter pylori (H. pylori) infection has been clearly shown to be a cause of gastric cancer, and the incidence of gastric cancer has been shown to decrease with eradication. However, few reports have described the utility of eradication therapy in elderly people. Thus, an investigation focusing on how much actual histological improvement is obtained with eradication therapy in elderly people was conducted.Patients and methodsThis was a retrospective study conducted using medical information of patients diagnosed with H. pylori-associated gastritis and who underwent eradication therapy. The histological improvement was assessed based on changes in the atrophy and intestinal metaplasia scores of the Updated Sydney system from before to after eradication. We investigated the rates of histological improvement in atrophy and intestinal metaplasia one year after and long term more than five years after H. pylori eradication in an elderly group and a younger group.ResultsThis study included 221 patients (elderly group 123, younger group 98). In histological atrophy, higher rates of improvement were seen in the corpus than in the antrum, and the rates of cure in the antrum were lower in elderly group than in younger group (p = 0.0282). With regard to intestinal metaplasia, the rates of improvement in the antrum were lower in elderly group than in younger. In long term observation, although the rates of cure in the antrum were lower in elderly, improvements were seen in atrophy scores in most of the patients and intestinal metaplasia scores in about half of patients.ConclusionThough there is more obvious improvement in the gastric mucosa when H. pylori eradication therapy is performed at a young age, some mucosal improvement can be expected in about half of patients after eradication, even in elderly people.     

Nodular gastritis in adults is caused by Helicobacter pylori infection

A close relationship exists between nodular gastritis and Helicobacter pylori infection in children. The pathogenesis and optimal management of nodular gastritis in adults, however, are unclear. This study describes the clinicopathologic features of nodular gastritis in adults and correlates treatment with outcome. Of 97,262 adult patients who underwent endoscopy, 187 (0.19%) were diagnosed with nodular gastritis, 151 (81%) of whom had dyspepsia. Nodular gastritis predominantly affects young women (49 men and 138 women, mean age, 32.6 years). All 134 patients tested for Helicobacter pylori infection were infected, and 65/66 (98%) had inflammation of both the antrum and the corpus. Twenty-five (13%) had associated lesions (peptic ulcers or cancer). Dyspepsia improved after eradication of Helicobacter pylori infection, but did not improve spontaneously. Nodular gastritis in adults is caused by Helicobacter pylori infection and shows a predilection for females and young adults. Helicobacter pylori eradication decreases symptoms and reduces the risk of peptic ulcers and possibly gastric cancer.     

Helicobacter pylori eradication in the healing of atrophic gastritis: A one-year prospective study

Objective. Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. Material and methods. Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58±12.6 years (mean±SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. Results. Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). Conclusions. Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.     

Predictors of Mortality in Patients Admitted to Hospital for Acute Upper Gastrointestinal Hemorrhage

Background: Although the ‘test‐and‐treat’ strategy is suggested as first‐line therapy for uninvestigated dyspepsia, no large‐scale studies in a real‐life setting are available. Methods: 1552 dyspeptic patients aged between 25 and 60 with no alarm symptoms were recruited to the study. After screening with a ¹³ C‐urea breath test, they were randomized into three treatment arms: Helicobacter pylori‐positive either to eradication therapy with OAM (omeprazole, amoxycillin and metronidazole) (Hp+/erad) or omeprazole 20?mg daily (Hp+/ome) for 10 days, whereas H. pylori‐negative patients (Hp?/ome) were treated with 20?mg omeprazole for 10 days. Gastrointestinal symptoms were registered at baseline at 1 and 2 years on the Gastrointestinal Symptom Rating Scale (GSRS) and quality of life with the Psychological General Well‐Being index (PGWB). Additional visits, referrals for and number of endoscopies and their findings were registered during the 2 years' follow‐up. Results: Of the 1552 patients, 583 were H. pylori‐positive (37.6%), and 288 of these were randomized for omeprazole and 295 to OAM. The Hp?/ome group had fewer general practitioner (GP) contacts (P?H. pylori‐positive groups. Eradication therapy significantly improved general well‐being and reduced upper gastrointestinal symptoms: abdominal pain (P?=?0.0001), heartburn (P?=?0.0061), acid regurgitation (P?=?0.003), hunger pain (P?=?0.009), especially in Hp+/erad. Peptic ulcer was found in 6.2%, 1.0%, 0.2% in Hp+/ome, Hp?+/erad and Hp?/ome, respectively (P?=?0.0007). Only 3 patients (1.0%) developed peptic ulcers in Hp?+/erad, all eradication failures. Conclusions: In uninvestigated dyspepsia, a negative test result for H. pylori reduces the number of GP contacts and endoscopy referrals compared to H. pylori‐positive regardless of eradication therapy. Applied in real life, the test‐and‐treat strategy failed to reduce the number of endoscopies, but significantly reduced peptic ulcer disease and improved dyspeptic symptoms and quality of life.     

Relevance of VacA and mucosal pathological changes in Chinese patients with upper gastrointestinal diseases before and after Helicobacter pylori eradication

OBJECTIVE: To investigate the influence of VacA activity on gastric mucosa prior to and after Helicobacter pylori eradication in Chinese patients with peptic ulcers and chronic gastritis. METHODS: Seventy‐four dyspeptic patients with H. pylori infection were enrolled. The status of H. pylori infection was evaluated by culture and histo­pathology before and 4?6 weeks after H. pylori eradication therapy. Histological specimens were examined and graded semiquantitatively according to the updated Sydney classification. RESULTS: Helicobacter pylori with VacA was found in 59 of 74 patients (80%), and its prevalence in patients with peptic ulcers and chronic gastritis was similar. Helicobacter pylori eradication rates in patients with VacA⁺ and VacA^? strains were similar. Before eradication, the degrees of acute or chronic inflammation, epithelial damage, atrophy, intestinal metaplasia (IM) and the number of lymphoid follicles were similar in patients with VacA⁺ and VacA^?H. pylori. Four to 6 weeks after the eradication of H. pylori infection, the degrees of acute and chronic inflammation, and epithelial damage in the antrum decreased significantly, particularly in patients with VacA⁺H. pylori (P < 0.0001). The number of lymphoid follicles in the antrum also decreased more in patients with VacA⁺H. pylori than in those with VacA^?H. pylori (P= 0.051). However, there was no difference in the extent of atrophy and IM between these two groups. CONCLUSIONS: There is no specific correlation between VacA⁺/VacA^?H. pylori strains and mucosal clinicopathological features in Chinese patients with upper gastrointestinal diseases before and after eradication therapy. Successful eradication of H. pylori infection does not improve atrophic and IM lesions of the gastric mucosa.     

Comparison of Gastric Histology Among Swedish and Japanese Patients with Peptic Ulcer and Helicobacter pylori Infection

Background: The natural course of Helicobacter pylori gastritis may vary between different ethnic groups. Gastric histopathology and the occurrence of H. pylori organisms in the stomach were investigated in healed duodenal (DU) and gastric (GU) ulcer patients recruited in Sweden (S) and Japan (J) in an identical trial. Methods: In 203 patients (JGU?=?39, JDU?=?55, SDU?=?109), various morphological gastritis variables and H. pylori were assessed from biopsy specimens obtained using a specific sampling protocol and interpreted according to guidelines of the updated Sydney grading system. Results: The ratio of GU:DU was observed to be very different between the recruited Japanese (39:55) and Swedish (0:109) patients. A comparison of data from SDU and JDU showed that the prevalence of H. pylori infection and the antral predominant gastritis demonstrated by both SDU and JDU were essentially identical. A comparison of data from JDU and JGU demonstrated a greater prevalence of H. pylori infection in the antrum, but not corpus, of JDU compared to JGU patients. The prevalence of atrophy and intestinal metaplasia was higher in both the antrum and corpus of JGU compared to JDU in all patients. Conclusions: The site specified biopsy methodology and standardized interpretation criteria utilized in this study clearly show that the histotopographic profile of Swedish and Japanese DU patients is essentially the same.     

Helicobacter pylori Infection,Pattern of Gastritis,and Symptoms in Erosive and Nonerosive Gastroesophageal Reflux Disease

Background: The aim of this study was to evaluate the prevalence of Helicobacter pylori infection and the characteristics of gastritis and symptoms of patients with erosive and nonerosive gastroesophageal reflux disease (GERD). Methods: We studied 202 consecutive patients with a diagnosis of GERD (symptoms score and endoscopy): group A (n = 110), erosive GERD; group B (n = 92), nonerosive GERD; 200 patients with upper abdominal complaints without abnormalities at endoscopy (functional dyspepsia, group C); and 200 asymptomatic controls tested for H. pylori serum antibody (group D). Antral and body biopsy specimens were taken for histology and the rapid urease test in groups A, B, and C. Results: The prevalence of H. pylori infection was higher in groups B and C (62% and 55%, respectively) than in A and D (36% and 40%) (P &lt; 0.05). In positive patients H. pylori colonization and gastritis grade scores in the gastric body were higher in nonerosive than in erosive GERD and functional dyspepsia (P &lt; 0.05). No differences in H. pylori colonization or gastritis grades were found in the antrum. Fifty-nine patients with nonerosive GERD (64%) and 42 with erosive GERD (38%) showed other dyspeptic symptoms associated with reflux symptoms (P &lt; 0.05). Conclusions: H. pylori prevalence is higher in patients with nonerosive GERD than in normal subjects and in patients with erosive GERD and similar to that of patients with dyspepsia. Patients with nonerosive GERD often show dyspeptic symptoms and higher H. pylori colonization and inflammation grades in the proximal stomach. Our data support the hypothesis that in GERD H. pylori gastritis may, on the one hand, protect against the development of esophageal erosions and, on the other, contribute to the esophageal hypersensitivity to acid which is a feature of GERD.     

GASTRIC CANCER DETECTED AFTER HELICOBACTER PYLORI ERADICATION

Background: Helicobacter pylori is associated with progression to gastric cancer. However, it is still unclear whether eradication therapy can prevent the development of gastric cancer. Methods: Subjects were 242 patients in whom success in eradication of Helicobacter pylori had been continuous for more than 3 years. Clinical, endoscopic and histological findings were compared retrospectively between those who developed gastric cancer (cancer group) and those who did not (non‐cancer group). Clinical features of each cancer case were also evaluated. Results: Gastric cancer was found in six of the 242 subjects (2.5%) during a mean follow‐up period of 4.6 years (range: 3.0–7.0). The mean age of the cancer group tended to be higher than that of the non‐cancer group. Endoscopy revealed a more severe grade of gastric corpus atrophy in the cancer group, and histological findings showed that the degree of intestinal metaplasia in the upper corpus was higher in the cancer group. Four of the six cancers were located in the gastric antrum. All were early cancers and five were of 0‐IIc type endoscopically. All were intestinal type histologically. Conclusions: Gastric cancer was discovered at a rate of 2.5% during the mean follow‐up period of 4.6 years after H. pylori eradication. Careful endoscopic follow up is necessary even after successful eradication, especially in cases characterized by an endoscopically high grade of gastric atrophy and pathologically severe intestinal metaplasia at the upper corpus.     

Correlation of serum pepsinogens and gastrin-17 with atrophic gastritis in gastroesophageal reflux patients: a matched-pairs study

Background and Aim: An algorithm (GastroPanel) for the non‐invasive diagnosis of atrophic gastritis has been previously proposed, based on serum pepsinogen‐I, gastrin‐17, and Helicobacter pylori (H. pylori) antibodies. The aim of the present study was to evaluate whether serum markers correlate with and predict gastric atrophy in gastroesophageal reflux disease (GERD) patients. Methods: The baseline data of the prospective ProGERD study, a study on the long‐term course of GERD (n = 6215 patients), served to select patients with atrophic gastritis diagnosed in biopsies from gastric antrum and corpus, and control cases without atrophy. A total of 208 pairs were matched for age, sex, GERD status (erosive vs non‐erosive), presence of Barrett's esophagus, and histological H. pylori status were retrieved. Serum pepsinogen‐I, gastrin‐17, and H. pylori antibodies were determined using specific enzyme immunoassays. Results: A significant negative correlation was found between the degree of corpus atrophy and the level of serum pepsinogen‐I. A previously‐reported negative correlation between the degree of antral atrophy and serum gastrin‐17 could not be confirmed. The low sensitivity (0.32) and specificity (0.70) of the GastroPanel algorithm were mainly due to over diagnosis and under diagnosis of advanced atrophy in the antrum. Conclusion: The diagnostic validity of the GastroPanel algorithm to diagnose gastric atrophy non‐invasively is not sufficient for general use in GERD patients.     

A 12-Year Follow-up Study of Chronic Gastritis and Helicobacter pylori in a Population-Based Random Sample

Background: The study is a 12-year endoscopic follow-up investigation on the course of chronic gastritis and Helicobacter pylori infection in a sample of 81 Estonian people. Methods: The series is a subset from a random sample of 227 subjects in whom a gastroduodenal endoscopy had been done. The grade of superficial gastritis (SG), atrophy, and colonization of the mucosa by H. pylori was evaluated in biopsy specimens from both antrum and corpus in accordance with the principles of the Sydney System. Resufrs: The healing rate of the H. pylori and gastritis was 0.3% (3 of 81); H. pylori colonization with gastritis developed in 5 of 81 during the follow-up. The mean prevalence of atrophic gastritis (AG) was three times more common in the corpus than in the antrum on the average. The formation of new cases of AG and the disappearance of AG were quite equal during the follow-up, and the overall changes in the grade of SG and atrophy were slow. The mean life span of corpus AG was nearly three times as long as that of antrum AG. In the antrum the grade of chronic inflammation correlated positively with the grade of H. pylori colonization. In cases of SG a low grade of colonization of H. pylori in the antral mucosa in connection with moderate inflammation predicted a reduction or even a healing of gastritis in the long term. Conclusions: New H. pylori infections with subsequent gastritis may occur in adulthood; a healing of gastritis occurs but is a quite rare event in the course of the 12-year follow-up. Further, in the present random sample of Estonian people atrophic corpus gastritis did not show an overall progression, in contrast to our earlier findings.     

Upper gastrointestinal bleeding in children with haemophilia: a clinical significance of Helicobacter pylori infection

Summary. For patients with haemophilia, gastrointestinal (GI) bleeding is a life‐threatening complication and can be caused by the Helicobacter pylori infection. Among children with haemophilia who had visited with GI bleeding, the prevalence of H. pylori infection and the recurrence rate after H. pylori eradication was investigated. Seven children with haemophilia A with hematemesis (age: 5.3–17.0 years) were evaluated for the causes of GI bleeding and the detection of H. pylori. Gastroendoscopy was done to find the bleeding focus and for further evaluation including rapid urease test and mucosal biopsy. Four patients had dyspepsia and abdominal pain for several weeks or months prior to hematemesis. Three patients did not show any symptoms of bleeding. From gastroendoscopy, four patients were diagnosed as duodenal ulcer, one as H. pylori associated chronic gastritis and one as haemorrhagic gastritis. One patient showing a normal finding was diagnosed with adenoid haemorrhage after nasopharyngoscopy. Helicobacter pylori infection was found in four of six patients with GI bleeding (3, duodenal ulcer; 1, H. pylori associated chronic gastritis). The patients with H. pylori infection had an eradication treatment of triple therapy and no recurrence happened. In children with haemophilia, H. pylori should also be considered as an important cause of GI bleeding. The recurrence of the infection and GI bleeding can be prevented with eradication of H. pylori. Screening test for H. pylori would be needed in children with haemophilia in endemic area.     

Effect of Helicobacter pylori Infection on Gastric Juice pH

Background: How Helicobacter pylori infection affects gastric acid secretion is still unclear. Methods: Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls. Results: Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed. Conclusions: These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.     

Long-Term Follow-up Study of Gastric Emptying and Helicobacter pylori Eradication Among Patients with Functional Dyspepsia

Studies on the influence of Helicobacter pylori gastritis on gastric motility have produced inconclusive results. We investigated the effect of Helicobacter pylori eradication therapy on gastric emptying in patients with functional dyspepsia in a placebo-controlled double-blind study with one year follow-up. A standardized scintigraphic double-tracer examination was used. Of the 40 subjects, 29 were H. pylori-positive patients with functional dyspepsia and 11 were asymptomatic control subjects. Gastric emptying parameters were: postlag 50% retention time for solids (T50), gastric emptying half-time for liquids (T1/2), solid lag duration, and intragastric distribution of solids. At baseline, the scintigraphic examination was performed for all study subjects to detect any major alterations between dyspeptic patients and asymptomatic control subjects. Thereafter every patient was randomized to receive either H. pylori eradication therapy or placebo; in addition they also received omeprazole 20 mg once a day for three months to stabilize the acid suppression therapy. After one year scintigraphy was repeated for the patients. The solid lagtime was prolonged among dyspeptic patients compared with asymptomatic controls (P = 0.02). After one year there was no significant difference between H. pylori-eradicated and placebo-treated patients in any gastric emptying parameter. However, good reproducibility of the scintigraphic examination showing the gastric emptying rate of solids (r = 0.43, 95% CI: 0.07–0.69; P = 0.02) and liquids (r = 0.44, 95% CI: 0.09–0.69; P = 0.02) continued even after one year of follow-up. In conclusion, eradication of H. pylori has no impact on gastric emptying in patients with functional dyspepsia, but the long-term trend in individual gastric emptying rate is stable.     

Helicobacter pylori eradication therapy for functional dyspepsia: Systematic review and meta-analysis

AIM: To evaluate whether Helicobacter pylori(H. pylori) eradication therapy benefits patients with functional dyspepsia(FD).METHODS: Randomized controlled trials(RCTs) investigating the efficacy and safety of H. pylori eradication therapy for patients with functional dyspepsia published in English(up to May 2015) were identified by searching Pub Med, EMBASE, and The Cochrane Library. Pooled estimates were measured using the fixed or random effect model. Overall effect was expressed as a pooled risk ratio(RR) or a standard mean difference(SMD). All data were analyzed with Review Manager 5.3 and Stata 12.0.RESULTS: This systematic review included 25 RCTs with a total of 5555 patients with FD. Twenty-three of these studies were used to evaluate the benefits of H. pylori eradication therapy for symptom improvement; the pooled RR was 1.23(95%CI: 1.12-1.36, P 0.0001). H. pylori eradication therapy demonstrated symptom improvement during long-term follow-up at ≥ 1 year(RR = 1.24; 95%CI: 1.12-1.37, P 0.0001) but not during short-term follow-up at 1 year(RR = 1.26; 95%CI: 0.83-1.92, P = 0.27). Seven studies showed no benefit of H. pylori eradication therapy on quality of life with an SMD of-0.01(95%CI:-0.11 to 0.08, P = 0.80). Six studies demonstrated that H. pylori eradication therapy reduced the development of peptic ulcer disease compared to no eradication therapy(RR = 0.35; 95%CI: 0.18-0.68, P = 0.002). Eight studies showed that H. pylori eradication therapy increased the likelihood of treatment-related side effects compared to no eradication therapy(RR = 2.02; 95%CI: 1.12-3.65, P = 0.02). Ten studies demonstrated that patients who received H. pylori eradication therapy were more likely to obtain histologic resolution of chronic gastritis compared to those who did not receive eradication therapy(RR = 7.13; 95%CI: 3.68-13.81, P 0.00001).CONCLUSION: The decision to eradicate H. pylori in patients with functional dyspepsia requires individual assessment.     

Preferential location of idiopathic peptic ulcers

Objective: Helicobacter pylori infection-negative, nonsteroidal antiinflammatory drugs (NSAIDs)-negative peptic ulcers, which are termed idiopathic peptic ulcers (IPUs), have been increasing worldwide. In this study, we investigated the preferential locations of gastric ulcers according to their cause (e.g., H. pylori and NSAIDs), with special attention to IPUs.

Material and methods: A total of 361 patients consecutively diagnosed with a peptic ulcer over a period of one year were classified into four groups according to H. pylori-infection status and NSAIDs usage. The ulcer location was divided into the antrum, angularis, and body, and was compared among the four ulcer groups.

Results: The ulcers of 43 patients were classified as IPUs. Compared with simple H. pylori ulcers, IPUs more preferentially located in the antrum (14% vs. 52%, p?H. pylori eradication or those with severe atrophic gastritis were excluded, and 79% of these IPUs were located in the antrum. With duodenal ulcers taken together, the vast majority of (86%) these IPUs occurred in the duodenal bulb or the antrum. The proportion of antral ulcers in NSAISs users also differed depending on the presence of concomitant H. pylori infection (positive: 22% vs. negative: 62%, p?Conclusion: There was a striking difference in the ulcer location within the stomach depending on the cause of the ulcer, and IPUs predominantly occurred in the antrum. This information on the preferential locations of ulceration should provide endoscopists with some hints concerning the etiology of ulcers.