Case of early gastric cancer with nodular gastritis

A case of depressed early gastric cancer with nodular gastritis is described. A 47‐year‐old Japanese man was referred to our hospital and admitted for surgical treatment of gastric cancer. Barium upper gastrointestinal study and endoscopy examination showed a 4.5 × 3.0 cm depressed lesion with a deep central ulceration in the anterior wall of the lower corpus. An unusual miliary pattern resembling ‘goose flesh’ was observed endoscopically in the antrum. Biopsy specimens from the tumor showed poorly differentiated adenocarcinoma, and specimens from the antrum showed many lymphoid follicles with a germinal center. Immunoglobulin G antibody and histological tests (Giemsa stain) for Helicobacter pylori were both positive. Early gastric cancer with nodular gastritis was diagnosed and a subtotal gastrectomy was performed. Histological examination of the resected specimen showed a stage I tumor infiltrating a poorly differentiated adenocarcinoma with a depressed lesion in the corpus (type 0 IIc + III) and nodular gastritis in the antrum. The patient is doing well 1 year after surgery.     

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.     

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.     

Helicobacter pylori‐eradication therapy decreases the level of neutrophil‐derived oxidants in the ulcerous mucosa of the human stomach: Relationship between ulcer stage and mucosal oxidant level

Background: The purpose of the present study was to determine the effect of Helicobacter pylori eradication on the intensity of inflammation in the ulcerous mucosa by measuring the level of neutrophil‐associated oxidants and to understand the role of mucosal inflammation in ulcer relapse from the viewpoints of the scarring stage and the H. pylori‐infection status. The level of inflammation in the gastric mucosa after the eradication of H. pylori was examined using biopsy samples obtained from patients with gastric ulcers. Methods: Gastric mucosal specimens were endoscopically obtained before and after H. pylori‐eradication therapy from 39 patients with gastric ulcers and a positive H. pylori‐infection status. The level of neutrophil‐derived oxidants was then measured in each sample using a luminol‐dependent chemiluminescence (ChL) assay. Results: Chemiluminescence activity in the ulcer portion and the background gastric mucosa (antrum and corpus) was significantly reduced 3 months after successful therapy (n = 32). The ChL activity was further decreased 9 months after successful therapy, but the activity in the ulcer portion remained unchanged. In patients who did not respond to the H. pylori‐eradication therapy (n = 7), the ChL activities were not altered in any mucosal portion after the therapy. Before the H. pylori‐eradication therapy, a higher ChL activity was observed in open ulcer tissue than in scarred tissue. The ChL activity in the scarred tissue was reduced 3 months after the successful eradication of H. pylori; however, the ChL activity in the red scars was significantly higher than that in the white scars. The ChL level in the white scars was almost equivalent to that in the background mucosa 9 months after the completion of the H. pylori‐eradication therapy. Conclusion: The eradication of H. pylori may reduce the level of oxidant production in gastric ulcers, promoting the prevention of ulcer recurrence. Furthermore, the presence of a red scar may indicate unstable healing, even after the successful eradication of H. pylori.     

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.     

Helicobacter pylori infection accelerates human gastric mucosal cell proliferation

Helicobacter pylori causes chronic atrophic gastritis and intestinal type gastric cancer arises against a background of atrophic gastritis. Increased proliferation of epithelial cells is an important indicator of increased risk for gastric adenocarcinoma. We investigated gastric mucosal cell proliferation inH. pylori-associated gastritis and the effect of eradication therapy on this proliferation in 45 patients endoscopically diagnosed (31 with persistent eradication and 14 in whomH. pylori) recurred.H. pylori status was determined by culture and histology in biopsied specimens from the gastric antrum and corpus. Eradication of the infection was defined as reversal to negative on both tests. In vitro Ki-67 immunostaining of endoscopic biopsy specimens was used to measure mucosal cell proliferation inH. pylori-associated gastritis before and after therapy. The proliferative zone was defined as the distance of Ki-67-positive gastric epithelial cells between the highest and the lowest cells. In patients in whomH. pylori was eradicated, cell proliferation in both the antral and corpus mucosa had decreased 4 weeks after completion of the eradication therapy (P<0.01,P<0.001), and 6 months later, it had markedly decreased (P<0.05,P<0.05) and returned to normal. In patients in whomH. pylori recurred, only antral epithelial cell proliferation was reduced 4 weeks after eradication therapy, but whenH. pylori recurred, determined by culture and histology, cell proliferation level was the same as that before eradication. These results suggest thatH. pylori infection accelerates cell proliferation in gastric mucosa and may play a causal role in the chain of events leading to gastric carcinoma.     

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.     

Five‐year follow‐up study on histological and endoscopic alterations in the gastric mucosa after Helicobacter pylori eradication

Background: To investigate long‐term changes in the gastric mucosa after Helicobacter pylori eradication, we examined histological and endoscopic ?ndings of the gastric mucosa before and 5 years after eradication. Methods: The subjects comprised 59 H. pylori‐positive patients with peptic ulcer who had been periodically followed for 5 years after H. pylori eradication. Acid‐suppressive drugs were not given after eradication, and endoscopic examination and tests for H. pylori infection (urea breath test (UBT), culture and histology) were performed before and 1 to 2 months, 1 year, and 5 years after eradication. Biopsy samples were taken from the greater curvature of the gastric antrum and upper corpus, and were scored histologically according to the Updated Sydney System. The atrophic border was evaluated endoscopically based on Kimura and Takemoto's classi?cation. Antral erosion and spotty redness in the corpus were also scored. Results: (1) Neutrophil in?ltration was signi?cantly reduced 1 to 2 months after eradication and remained around the reduced level over the next 5 years. Mononuclear cell in?ltration began to decrease 1 to 2 months after eradication and continued to subside 1 year and 5 years later. (2) Histological atrophy of the gastric glands was signi?cantly improved 1 year and 5 years after eradication. However, endoscopy revealed no consistent alteration in the atrophic border. (3) There was no signi?cant change in the degree of intestinal metaplasia for 5 years. (4) In some cases, antral erosion became more conspicuous after 5 years. Spotty redness in the corpus was observed in 15% of cases (9/59) before and 10% (6/59) 1 year after eradication, but had disappeared in all cases 5 years later. Conclusions: Neutrophil in?ltration improved rapidly after H. pylori eradication in contrast with mononuclear cell in?ltration, which decreased gradually over 5 years. Glandular atrophy improved in the long term, whereas intestinal metaplasia had not altered 5 years after eradication. Spotty redness in the gastric corpus disappeared in all cases after eradication, suggesting that it is an endoscopic ?nding related to H. pylori infection.     

SMALL EARLY GASTRIC CANCER OCCURRING IN A YOUNG WOMAN WITH NODULAR GASTRITIS

We found a small gastric cancer in a 25‐year‐old woman with nodular gastritis. Endoscopically, the cancer was identified as a whitish area in the gastric antrum. There was also a miliary pattern in the gastric antrum and corpus. In addition, serology and histology revealed the patient to have been infected by Helicobacter pylori. Histological examination of the resected stomach showed that the cancer was poorly differentiated adenocarcinoma with signet‐ring cell restricted to the mucosal layer. In the surrounding mucosa, there were chronic inflammatory cell infiltrates and enlarged lymphoid follicles with germinal centers. Our case suggests that nodular gastritis may be at a high risk for the development of gastric cancer of poorly differentiated type.     

Long-term monitoring of gastric atrophy and intestinal metaplasia after Helicobacter pylori eradication

Improvements of atrophy and intestinal metaplasia which is seen after H. pylori eradication may be regarded as an important factor of gastric cancer prevention. Although many studies reported the alteration of gastric mucosa after H. pylori eradication, most of the results do not agree. Recently, two meta-analyses showed significant improvement of atrophy (one study showed improvement in both corpus and antrum, and the other showed improvement in corpus but not in antrum), whereas improvement of intestinal metaplasia was not shown in either corpus or antrum. However, one reason why conclusions are different is considered to be that the observation period after eradication was short, and another reason is considered to be that almost studies examined only two points in gastric mucosa for histological analysis. Further examination with a greater number of subjects and with longer follow up period should be required to clarify the mechanism of gastric injury and improvement of gastric mucosa, especially atrophy and intestinal metaplasia after H. pylori eradication.     

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.     

NODULAR GASTRITIS WITH HELICOBACTER PYLORI INFECTION IS STRONGLY ASSOCIATED WITH DIFFUSE‐TYPE GASTRIC CANCER IN YOUNG PATIENTS

Background: Nodular gastritis (NG), a particular type of gastritis, is now defined as antral nodularity. Recent studies have shown that NG is strongly associated with Helicobacter pylori infection, and we recently showed that it may be associated with diffuse‐type gastric cancer of the corpus. We retrospectively investigated the relation between NG and gastric cancer in patients aged 29 years or less. Patients and Methods: The study group comprised 150 patients (48 males, 102 females; mean age, 27.7 years) who were endoscopically diagnosed with NG and were less than 29 years of age; 3939 sex‐ and age‐matched patients without NG who were H. pylori‐positive served as the control group (1184 males, 2755 females; mean age, 27.5 years). We estimated the risk of gastric cancer development in patients with NG relative to that of patients without NG. Results: The prevalence of gastric cancer was significantly higher in patients with NG than in the control patients (7/150; 4.7% vs 3/3939; 0.08%, P < 0.001). The odds ratio for the risk of gastric cancer in patients with NG was found to be 64.2 (95% confidence interval; 16.4–250.9). The seven cases of gastric cancer with NG showed the same characteristics: all were diagnosed histologically as the diffuse type and were located in the corpus with H. pylori infection. Conclusion: NG with H. pylori infection is strongly associated with diffuse‐type gastric cancer of the corpus in young patients.     

Clinical prevention of gastric cancer by Helicobacter pylori eradication therapy: a systematic review

Helicobacter pylori (H. pylori) infection plays an important role in gastric carcinogenesis. We conducted a systematic review concerning gastric cancer development after H. pylori eradication therapy. In total 15 papers matched our criteria, the results were reviewed. The H. pylori eradication therapy statistically diminished the prevalence of clinical gastric cancer by approximately one-third. The studies from Japan supported this conclusion; however, studies from overseas reported conflicting results. The differences in these conclusions lie in the diagnostic ability of endoscopic examination, since the clinical stage was quite different between these studies. Gastric cancer that developed after eradication revealed a mainly intestinal type histology and depressed-type appearance. The following are possible reasons for reduced gastric cancer: (1) eradication therapy inhibits the new occurrence of gastric cancer, (2) eradication regresses or inhibits the growth of gastric cancer, and (3) eradication interferes with the discovery of gastric cancer. Considering the biological nature of cancer cell proliferation, a sufficiently long-term follow-up may clarify the effect of eradication therapy on inhibition of the development (not discovery) of gastric cancer and reduction of gastric cancer-related mortality.     

Gastric epithelial cell turnover and mucosal protection in Japanese children with Helicobacter pylori infection

Background In adults, epithelial cell proliferation and apoptosis of the gastric mucosa are induced by Helicobacter pylori infection and are associated with gastric atrophy or gastric carcinoma. In children, there are few studies about such epithelial changes. To elucidate the role of H. pylori infection in gastric mucosal inflammation, we immunohistochemically examined gastric mucosa of Japanese children.Methods Biopsy specimens obtained from the gastric antrum and corpus of H. pylori-infected (n = 13) and noninfected children (n = 15) were studied for immunolocalization of Ki-67, single-strand DNA, manganese superoxide dismutase (Mn-SOD), and CD68, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling. In 10 patients with successful eradication, pre- and posttreatment results were compared.Results In both gastric antrum and corpus, neutrophil and mononuclear cell infiltration, epithelial cell proliferation, and apoptosis significantly increased in H. pylori-infected patients, predominantly in the antrum. In the antrum of H. pylori-infected patients, there was positive correlation between the degrees of neutrophil infiltration and cell proliferation (P < 0.05) or apoptosis (P < 0.05). H. pylori eradication improved mucosal inflammation, cell proliferation (P < 0.001), and apoptosis (P < 0.01) in the antrum. Mn-SOD immunoreactivity and CD68-positive macrophages in the antrum, which significantly increased in H. pylori-infected patients, decreased after the eradication.Conclusions H. pylori infection induced gastric mucosal inflammation and epithelial cell turnover in children. Moreover, gastric mucosal defense mechanism against H. pylori infection was activated. H. pylori eradication in childhood might prevent the accumulation of gastric epithelial cell damage.     

PRIMARY GASTRIC PLASMACYTOMA REFRACTORY TO HELICOBACTER PYLORI ERADICATION THERAPY

A 49‐year‐old woman underwent upper gastrointestinal endoscopic examination for epigastric discomfort, revealing giant folds on the greater curvature of the stomach. Histological examinations of biopsy specimens taken from the giant folds showed signs of chronic inflammation, and Helicobacter pylori was also identified. She underwent first‐step H. pylori eradication. On follow‐up endoscopy, H. pylori was not identified. However, endoscopic findings were unchanged and repeated biopsies showed dense infiltration of atypical plasma cells. No proliferation of centrocyte‐like cells was seen. Immunohistochemically, plasma cells were positive for λ‐chain. Primary gastric plasmacytoma was diagnosed. Total gastrectomy was carried out with splenectomy and regional lymph node dissection. The patient remains disease free as of 6 years postoperatively.     

Sequential therapy in clarithromycin-sensitive and -resistant Helicobacter pylori based on polymerase chain reaction molecular test

Background and Aim: The present study was designed to determine the eradication rate of 10 day sequential therapy in genotypic clarithromycin‐resistant Helicobacter pylori group identified by molecular polymerase chain reaction (PCR) detection in Thai patients. Methods: Between May 2007 and June 2010, patients who had undergone gastroscopic examination at the King Chulalongkorn Memorial Hospital, for dyspeptic symptoms were recruited. Two biopsy samples from gastric antrum were obtained, one for rapid urease test and another for PCR. PCR‐sequencing was performed to determine point mutations in 23S rRNA gene. Patients received 10 day sequential therapy consisting of lanzoprazole 30 mg and amoxicillin 1 g twice daily for 5 days followed by lanzoprazole 30 mg, clarithromycin 500 mg and nitroimidazole 500 mg twice daily for the remaining 5 days. Urea breath test (UBT) was performed to assess eradication therapy. Results: A total of 151 patients (mean age 52.7 years, 75 males and 76 females) were recruited in this study. All patients completed sequential therapy without significant side effects. Point mutations at A2143G and A2142G were detected in 17 patients (11.3%). Overall eradication rate was 94%. The eradication rate in the group with point mutation was significantly lower than the eradication rate in the group without point mutation (64.7% vs 97.8%; odds ratio = 19.6 and 95% confidence interval = 4.3–88.8; P < 0.0001). Conclusion: Genotypic clarithromycin resistance was detected in only 11.3% of H. pylori infections in Thailand. Sequential therapy is highly effective in clarithromycin‐sensitive but is less effective in clarithromycin‐resistant H. pylori. PCR‐molecular test could be a useful tool to identify antimicrobial resistance for optimizing an eradication regimen.     

CLINICAL EVALUATION OF NODULAR GASTRITIS IN ADULTS

Background: Nodular gastritis (NG) was considered a physiological change with little pathological significance, mostly in young women. In recent years, however, it has been often reported in patients with Helicobacter pylori (H. pylori) infection, or in patients with gastroduodenal ulcer/gastric cancer, suggesting possible clinical significance. Methods: From July 2003 to July 2006, 59 patients were diagnosed with NG among 32 404 patients examined endoscopically. The incidence of NG was evaluated in relation to age, sex, H. pylori infection status, symptoms leading to endoscopy, associated lesions in the upper digestive tract at the time of NG diagnosis, and existence of other systemic conditions. Results: The NG patients consisted of 13 out of 18 152 (0.07%) male patients and 46 out of 14 252 (0.32%) female patients, with a mean age of 45.3 ± 17.7 years. All 28 patients who were examined for H. pylori infection were positive. Endoscopic examination was performed for precordial pain and upper abdominal pain in 24 (40.7%) patients, symptoms of gastroesophageal reflux disease in eight (13.6%) patients, and symptoms of functional dyspepsia in six (10.2%) patients. NG was associated with duodenal ulcer in eight (13.6%) patients, hyperplastic gastric polyps in five (8.5%), gastric ulcer in one (1.7%), and gastric cancer in one (1.7%) patient. Conclusion: NG is a specific gastritis resulting from H. pylori infection that may be strongly associated with H. pylori‐related lesions.     

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.     

Safety of first-line triple therapy with a potassium-competitive acid blocker for Helicobacter pylori eradication in children

Background

Helicobacter pylori infection is a risk factor for gastric cancer, and it has been reported that eradication of H. pylori is effective for preventing such cancer. Recently, H. pylori eradication has been performed in children as first-line therapy against gastric cancer. Here, we report use of triple therapy with a potassium-competitive acid blocker (P-CAB) for H. pylori eradication in children.

Methods

H. pylori infection testing and eradication therapy began in fiscal year 2015 in junior high school students located in Yurihonjo city and Nikaho city, Akita prefecture, Japan. Urine-based immunochromatography, stool antigen enzyme-linked immunosorbent assay tests, and serum antibody tests were performed as the initial screening examination. Those who tested positive on one of the three examinations then underwent a urea breath test (¹³C-UBT). Those who tested positive on ¹³C-UBT and expressed the desire to undergo H. pylori eradication then received eradication therapy comprising 20 mg P-CAB, 750 mg amoxicillin, and 200 mg clarithromycin twice a day for 7 days. At least 8 weeks after treatment, eradication success was evaluated using ¹³C-UBT.

Results

A total of 118 students received eradication therapy. Eradication rates were 81.3% (95% confidence interval: 74.3–88.4, 96/118) in ITT analysis and 85.7% (95% confidence interval: 79.1–92.9 96/112) in PP analysis. Adverse effects associated with eradication therapy were observed in 25 of 118 subjects (21.1%), seven of whom required hospital treatment (rash in five, vomiting in two). All seven subjects either discontinued therapy or were administered anti-allergy drugs, which resulted in swift alleviation of symptoms.

Conclusions

First-line triple therapy with a P-CAB for H. pylori eradication in children was found to be safe.

     

DEVELOPMENT OF SPORADIC GASTRIC FUNDIC GLAND POLYP AFTER ERADICATION OF HELICOBACTER PYLORI

The pathogenesis of sporadic gastric fundic gland polyps (FGP) without familial adenomatous polyposis remains unclear. However, development of FGP is associated with normal gastric mucosa without Helicobacter pylori infection. We report two cases of FGP newly developed after successful eradication therapy of H. pylori infection. H. pylori‐associated gastric ulcers occurred in the two patients; H. pylori eradication was performed in the patients and was successful. The patients have not received medication of long‐term proton pump inhibitors. Follow‐up gastrointestinal endoscopy demonstrated a FGP in the fundus of the stomach of each patient after eradication therapy. Regression of sporadic FGP can be observed to coincide with the acquisition of H. pylori infection. Conversely, the present cases demonstrated that the curing of H. pylori infection could lead to the development of FGP.