Reflux esophagitis facilitates low Helicobacter pylori infection rate and gastric inflammation

BACKGROUND: Helicobacter pylori is regarded as an important pathogen in upper gastrointestinal diseases. However, little is known about the relationship between H. pylori infection and reflux esophagitis. Therefore, an investigation was undertaken in Korean subjects regarding the incidence of H. pylori infection, and a histopathological study of reflux esophagitis was also carried out. METHODS: Analysis of gastric biopsy specimens was conducted for 73 patients with reflux esophagitis and 132 control subjects without reflux esophagitis. The H. pylori infection was assessed by using rapid urease test and the immunohistochemical method, and gastric mucosal morphologic change was analyzed according to the updated Sydney system. RESULTS: The prevalence of H. pylori infection was significantly lower in patients with reflux esophagitis than in the non-reflux group. Grade of inflammation and glandular atrophy in the antrum and body were higher in patients in the non-reflux group compared with those in the reflux esophagitis group. CONCLUSIONS: It is suggested that H. pylori infection decreases the risk of reflux esophagitis by inducing atrophic gastritis.     

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.     

Helicobacter pylori infection prevents erosive reflux oesophagitis by decreasing gastric acid secretion

BACKGROUND: Helicobacter pylori infection is less prevalent and atrophic gastritis is less extensive in patients with reflux oesophagitis than those without it, but few studies have examined this relationship directly. AIMS: We investigated the relationship between H pylori infection, acid secretion, and reflux oesophagitis in Japanese subjects. SUBJECTS: A total of 105 patients with erosive reflux oesophagitis were compared with 105 sex and age matched patients without reflux oesophagitis. METHODS: The diagnosis of H pylori infection was made by histological examination of gastric mucosal biopsy specimens, rapid urease test, and detection of serum IgG antibodies. Acid secretion was assessed by the endoscopic gastrin test. RESULTS: H pylori infection was present in 36 patients with erosive reflux oesophagitis (34.3%) and in 80 control subjects (76.2%) (odds ratio 0.163, 95% confidence interval 0.09-0.29). Overall acid secretion was significantly greater in patients with reflux oesophagitis. Among H pylori positive patients, acid secretion was greater in patients with reflux oesophagitis than those without oesophagitis. CONCLUSION: In Japan, erosive reflux oesophagitis occurs most often in the absence of H pylori infection and gastric hyposecretion. Even in the presence of H pylori infection, reflux oesophagitis is more likely to develop in patients without gastric hyposecretion. H pylori infection may inhibit reflux oesophagitis by inducing hypoacidity.     

Influence of Helicobacter pylori infection on the prevalence of reflux esophagitis in Japanese patients

BACKGROUND AND AIM: Reflux esophagitis is caused by esophageal motor dysfunction in patients with sufficient gastric acid secretion. Helicobacter pylori causes atrophic gastritis and influences gastric acid secretion. Hiatus hernia (HH) of the esophagus causes motor dysfunction in the lower esophagus. Therefore, this study aimed to test whether H. pylori infection, gastric mucosal atrophy and HH are predictive factors for reflux esophagitis. METHODS: Helicobacter pylori infection was examined in 781 patients by the measurement of serum immunoglobulin (Ig)G antibody, bacteriological culture and histological examination of biopsy specimens. The prevalence of HH, endoscopically identified gastric mucosal atrophy (closed- or open-type) and reflux esophagitis were investigated by reviewing endoscopic films. Investigated patients were divided into three age groups, under 49, 50-69, and over 70 years. The prevalence of esophagitis, H. pylori infection, gastric mucosal atrophy, and HH were compared to identify the possible predictive factors for reflux esophagitis by using logistic regression analysis. RESULTS: Sixty-nine patients with reflux esophagitis were found among the 781 investigated cases. The odds ratios of negative H. pylori infection, endoscopically identified closed-type gastric mucosal atrophy, and HH for the prevalence of reflux esophagitis were 1.342, 1.751 and 5.527, respectively. These results indicated that the presence of H. pylori infection was only a weak negative risk factor, and that HH was the most reliable endoscopic predictive factor for reflux esophagitis. CONCLUSION: Helicobacter pylori infection is a weak negative risk factor for the prevalence of reflux esophagitis, while HH is the most reliable predictive factor.     

The relationship of gastrin, pepsinogen, and Helicobacter pylori in erosive reflux esophagitis]

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection is known as a major cause of atrophic gastritis and is associated with serum gastrin, pepsinogen, and gastric acid secretion. There is still a controversial association between gastroesophageal reflux disease and H. pylori infection. This study was designed to investigate the relationship among serum gastrin, pepsinogen, and H. pylori infection in the erosive reflux esophagitis (ERD) patients. METHODS: Patients who were diagnosed as ERD by one gastroenterologist at the Kangnam St. Mary's hospital were prospectively enrolled. The persons without ERD in the control group were matched for age and sex. We examined the gastrin, pepsinogen I (PG I), PG II, PG I/II ratio, and H. pylori infection. RESULTS: Forty five patients were enrolled in ERD group and 66 persons in control group. The H. pylori infection rate in ERD group was lower than that in the control group (11.1% vs. 43.9%, p<0.001). PG I/II ratio in ERD group was higher than that in the control group (7.0+/-3.1 vs. 5.3+/-2.6, p=0.003). The PG II (p=0.016) and gastrin (p=0.029) in ERD group were lower than those in the control group. BMI in ERD group was higher than that in the control group (24.5 vs. 23.1 kg/m2, p=0.013). CONCLUSIONS: The H. pylori infection rate in ERD group was lower and PG I/II ratio was higher than that in the control group. Reflux esophagitis is thought to be reversely associated with the atrophy of gastric mucosa.     

The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with Barrett's esophagus in Japan

OBJECTIVES: The acidity of the refluxate into the esophagus is a key factor for the pathogenesis of gastroesophageal reflux disease. Helicobacter pylori (H. pylori) infection can influence gastric acid secretion. We have reported that H. pylori infection prevents reflux esophagitis by decreasing gastric acid secretion in Japanese patients, but the role of this organism in Barrett's esophagus is unclear. The aim of this study was to investigate the prevalence of H. pylori infection and gastric acid secretion in Japanese patients with reflux esophagitis with or without Barrett's esophagus. METHODS: We enrolled 112 reflux esophagitis patients who were examined for the status of H. pylori and acid secretion in this study. They were divided into three groups, according to the presence or absence of Barrett's esophagus as follows: reflux esophagitis group without Barrett's esophagus (reflux esophagitis alone) (80 patients); short-segment Barrett's esophagus group (16 patients); and long-segment Barrett's esophagus group (LSBE) (16 patients). Age- and sex-matched control subjects were also assigned to the 80 patients with reflux esophagitis alone. The prevalence of H. pylori infection was determined by histology, rapid urease tests, and serum IgG antibodies. Gastric acid secretion was evaluated by the endoscopic gastrin test (EGT). RESULTS: The overall prevalence of H. pylori infection in the reflux esophagitis patient group (24.1%) was significantly lower than the control group (71.2%) (odds ratio 0.13, 95% confidence interval 0.07-0.24; p < 0.0001). The prevalence of H. pylori infection in the patients with Barrett's esophagus tended to be lower than that in the patients with reflux esophagitis alone (reflux esophagitis alone; 30.0%, SSBE; 18.7%, LSBE; 0%), especially in the patients with LSBE compared with the reflux esophagitis alone group (p < 0.01). The EGT value of the respective reflux esophagitis patient group was significantly higher than the control group. The EGT value in the patients with Barrett's esophagus tended to be higher than that in the patients with reflux esophagitis alone, but the difference was not statistically significant. When examined in H. pylori-negative subjects, no difference was found in the EGT value between the control subjects and the patients with reflux esophagitis alone, but it was significantly higher in patients with Barrett's esophagus than the control subjects (p < 0.05). On the other hand, when examined in the H. pylori-positive subjects, the EGT value was significantly higher in the patients with reflux esophagitis alone than in the control subjects (p < 0.01). CONCLUSIONS: H. pylori infection may play a protective role in the development of Barrett's esophagus, especially in the development of LSBE in Japan. Gastric acid hypersecretion may be concerned with the development of Barrett's esophagus in addition to the absence of H. pylori infection.     

Increased prevalence of Helicobacter pylori infection in gastric cardia of patients with reflux esophagitis: a study from Jordan

BACKGROUND: The role of H. pylori infection in GERD is highly controversial. Our aim was to investigate the relationship between reflux esophagitis and H. pylori infection in Jordanian subjects and to examine the gastric site for H. pylori that is most strongly associated with reflux esophagitis. METHODS: During endoscopy two biopsies from the cardia and another two biopsies from the antrum were taken from 100 consecutive patients with reflux esophagitis (RE group) and from a sex- and age-matched group of 50 patients, who were referred to the endoscopy unit for evaluation of upper gastrointestinal symptoms and whose endoscopic findings were normal (control group). The biopsies were examined histologically for the presence of gastritis and H. pylori. RESULTS: Antral histological gastritis, Barrett's esophagus and hiatus hernia were significantly more common in the RE group than in the control group. Out of the 100 patients, 68 (68%) in the RE group and 26 of 50 (52%) in the control group were found to have H. pylori infection. The presence of H. pylori in both antral and cardiac biopsies was significantly more frequent in patients of the RE group. Forty-four patients in the RE group had positive H. pylori in both antral and cardiac biopsies (44%), while only 12 out of 50 patients of the control group (24%) had positive H. pylori in both biopsies. In the control group the prevalence of H. pylori in the antrum was similar to that of patients of the RE group (52% vs. 59%), but colonization of H. pylori in the cardia was significantly much lower than that of the RE group (24% vs. 53%; P = 0.0007). CONCLUSIONS: The increased prevalence of H. pylori colonization in the cardia is associated with reflux esophagitis and further controlled clinical study is required to show the impact of H. pylori eradication in patients with reflux esophagitis.     

Corpus gastritis and erosive esophagitis: a report from the Middle East.

OBJECTIVE: To assess whether corpus gastritis due to Helicobacter pylori protects against erosive esophagitis in an area with high prevalence of H. pylori infection. METHODS: Biopsies obtained from gastric corpus and antrum in 151 patients with symptoms of gastroesophageal reflux disease were studied for presence of H. pylori and endoscopic evidence of gastritis. Presence and grade of esophagitis at endoscopy was recorded. RESULTS: Fifty-four (36%) patients had endoscopic esophagitis. Patients with severe esophagitis (>or= grade II) less often had active gastritis (15/45 vs. 55/98; p=0.02) and had a lower density of H. pylori (p=0.0003) than those without esophagitis. CONCLUSION: Active corpus gastritis due to H. pylori infection may protect against erosive esophagitis in patients with gastroesophageal reflux disease in the Middle East.     

A close relationship between Helicobacter pylori infection and gastric xanthoma.

BACKGROUND: Although the pathogenesis of gastric xanthoma (GX) remains unclear, an association of GX with atrophic gastritis has been reported. Helicobacter pylori is closely related to atrophic gastritis. The aim of this study was to investigate the relationship among GX, H. pylori, and atrophic gastritis. METHODS: Sixty-seven patients with GX were assessed for H. pylori infection by serum anti-H. pylori IgG antibody, in addition to the rapid urease test, culture, and histologic examination using biopsy specimens of the antrum and corpus. The findings were compared with 67 age- and sex-matched control subjects without GX. The distribution of atrophic gastritis was assessed endoscopically. The severity of atrophic gastritis was determined endoscopically and histologically. Serum pepsinogen (PG) levels were also measured. Immunohistochemical staining of GX samples for H. pylori antigen was performed. H. pylori clinical isolates from patients with GX and controls were assessed for cagA by means of polymerase chain reaction. RESULTS: The prevalence of H. pylori was significantly higher in patients with GX than in controls (94% and 72%, respectively). A significantly more extensive atrophic gastritis was present in patients with GX, as determined endoscopically and histologically, than in controls. Serum PG-I levels and the PG-I/PG-II ratio were significantly lower in the GX group than in the control group. H. pylori antigens were frequently identified in the cytoplasm of xanthoma cells in H. pylori-positive specimens of GX (54 of 63 specimens, 86%), whereas no immunoreactivity for H. pylori antigens was detected in H. pylori-negative specimens of GX. There was no significant difference in the positive rate of cagA between the two groups. CONCLUSIONS: Our results identified a close relationship among H. pylori infection, GX, and atrophic gastritis. A proportion of GXs may be provoked by H. pylori infection.     

Dyslipidemia and H pylori in gastric xanthomatosis

AIM: To investigate the relationship among gastric xanthomatosis (GX), H pylori, dyslipidemia, and gastritis in Korea, a well-known H pylori endemic area. METHODS: A total of 771 patients who had undergone gastroduodenoscopy by one endoscopist were included in this study. Among them, 54 patients with GX were assessed for H pylori infection and their endoscopic characteristics and serum lipid profiles. The findings were compared with 54 age-and sex-matched control subjects without GX. RESULTS: The prevalence of GX was 7% (54/771) with no sex difference. GX was mainly single (64.8%) and located in the antrum (53.7%). The mean diameter was 7 ± 3 mm. Mean body mass index (BMI) of patients with GX was 23.1 ± 2.8 and no one was above 30. Compared with the controls, lipid profiles of GX group showed significantly lower HDL-cholesterol (48.8 ± 12.3 vs 62.9 ± 40.5, P = 0.028) and higher LDL-cholesterol (112.9 ± 29.9 vs 95.9 ± 22.4, P = 0.032). The level of total serum cholesterol, triglyceride and the existence of dyslipoproteinemia were not related to the presence of GX. However, GX showed a close relationship with endoscopically determined atrophic gastritis and histologic severity (24/53, 44.4% vs 8/54, 14.8%, P = 0.0082). H pylori infection and bile reflux gastritis were not significantly related with GX. CONCLUSION: The prevalence of GX is 7% and it may be an increasing entity in Korea. Moreover, dyslipidemia and atrophic gastritis are found to be related to GX, but H pylori infection is not.     

Differences in clinical characteristics between patients with endoscopy-negative reflux disease and erosive esophagitis in Japan

OBJECTIVE: Helicobacter pylori infection and atrophic gastritis are inversely related to erosive esophagitis. Whether these factors affect the pathogenesis of endoscopy-negative reflux disease is not clear. We aimed to elucidate the differences in clinical characteristics between endoscopy-negative erosive disease and erosive esophagitis. METHODS: 253 subjects (89 with endoscopy-negative reflux disease and 164 with erosive esophagitis) were studied. Gastric atrophy was assessed by measurement of serum pepsinogen. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence intervals (CI) of endoscopy-negative reflux disease compared with erosive esophagitis. RESULTS: Among GERD patients, female gender (OR = 2.27, 95% CI, 1.25-4.10), smoking (OR = 0.45, 95% CI, 0.22-0.91), and the presence of hiatal hernia (OR = 0.30, 95% CI, 0.17-0.56) were significantly associated with endoscopy-negative reflux disease compared with male gender, not smoking, and absence of hiatal hernia, respectively. Body mass index (BMI) was also significantly associated with a decreased OR for endoscopy-negative reflux disease. Although H. pylori infection and gastric atrophy were significantly more common in patients with endoscopy-negative reflux disease, these associations did not persist in a multiple-adjustment model. After adjustment for gender, BMI, smoking, and hiatal hernia, a decrease in serum pepsinogen I/II ratio was significantly associated with an increased OR for endoscopy-negative reflux disease (p for trend = 0.018). CONCLUSIONS: Female gender, low BMI, not smoking, absence of hiatal hernia, and severity of gastric atrophy were positively associated with endoscopy-negative reflux disease compared with erosive esophagitis among Japanese patients.     

胃食管反流病与幽门螺杆菌感染的关系探讨

目的探讨胃食管反流病与幽门螺杆菌感染之间的相关性。方法将经过电子胃镜确诊的GERD患者120例及对照组轻度慢性浅表性胃炎患者120例予血清幽门螺杆菌抗体检测和14C呼气试验法进行H.pylori检测,对比两组H.pylori感染情况;将90例反流性食管炎患者分为LA-A、B组及LA-C、D组,对比两组H.pylori感染情况;将120例GERD患者分为轻度症状组、中度症状组、重度症状组及极重度症状组,比较组间H.pylori感染情况。结果 GERD组H.pylori感染的阳性率(39.17%)低于对照组H.pylori感染的阳性率(62.50%),差异有统计学意义(P<0.05)。LA-A、B组H.pylori感染的阳性率(60.87%)高于LA-C、D组H.pylori感染的阳性率(29.55%),差异有统计学意义(P<0.05)。轻度症状组、中度症状组、重度症状组及极重度症状组H.pylori感染的阳性率分别是40.00%、41.67%、40.63%、31.82%。结论幽门螺杆菌感染是反流性食管炎的保护因素,幽门螺杆菌感染与GERD症状的发生无相关性。     

Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy

BACKGROUND: Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection. AIMS: To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients. PATIENTS/METHODS: A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. RESULTS: Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection. CONCLUSIONS: Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.     

Characteristics of gastritis in patients with Helicobacter pylori-positive reflux esophagitis

BACKGROUND AND AIM: The influence of Helicobacter pylori on gastric acid secretion differs with the status of gastritis. The histological characteristics of gastritis in H. pylori-positive patients with reflux esophagitis have not been fully investigated. We therefore studied the pattern of endoscopic gastric mucosal atrophy and degree of histological gastritis in such patients. METHODS: Subjects comprised 41 H. pylori-positive patients with reflux esophagitis, 41 age- and sex-matched patients with duodenal ulcer, and 41 patients with early gastric cancer. The endoscopic pattern of gastric mucosal atrophy was reviewed, and the degree of histological gastritis in biopsy specimens from the antrum and corpus was assessed in accordance with the updated Sydney system. RESULTS: The grade of endoscopic and histological gastric mucosal atrophy in patients with reflux esophagitis was significantly lower than that in patients with gastric cancer, and the histological scores for antral atrophy and metaplasia in patients with reflux esophagitis tended to be lower than those in patients with duodenal ulcer. In patients with reflux esophagitis and duodenal ulcer, the scores for antral inflammation and activity tended to be higher than those for the corpus. Conversely, the inflammation and activity score in patients with early gastric cancer showed a corpus-predominant gastritis pattern. CONCLUSION: In H. pylori-positive patients with reflux esophagitis, the degree of endoscopic gastric mucosal atrophy is low and histologically there is an antral-predominant gastritis pattern. Therefore, gastric acid secretion in H. pylori-positive patients with reflux esophagitis may be augmented by H. pylori infection.     

Effects of very long (up to 10 years) proton pump blockade on human gastric mucosa

BACKGROUND: Long-term use of proton pump inhibitors (PPI) has been reported to worsen oxyntic mucosa gastritis and the resulting gland atrophy has been considered a potential risk factor for neoplastic changes in the gastric mucosa. AIMS: The present study examines the effect of extended continuous PPI treatment for up to 10 years on the exocrine and endocrine stomach of patients with acid-related diseases of the upper GI tract. METHODS: Biopsies from the antral and oxyntic mucosa taken at regular time intervals were examined for gastritis, atrophy, intestinal metaplasia, Helicobacter pylori and argyrophil cells and correlated to serum gastrin levels. RESULTS: A general amelioration of antral gastritis without relevant changes of atrophy or intestinal metaplasia, contrasted with the worsening of gastritis and gland atrophy seen in the oxyntic mucosa of reflux esophagitis (but not gastric or duodenal ulcer) patients in the presence of H. pylori infection. In association with PPI- induced hypergastrinemia, argyrophil cell hyperplasia (but not dysplasia or neoplasia) developed in the oxyntic mucosa. CONCLUSION: The present results outline the milder pretreatment pattern and higher proneness to PPI-related, H. pylori-restricted worsening of oxyntic mucosa gastritis in reflux esophagitis compared to gastric ulcer or duodenal ulcer patients. In addition, they confirm a substantial safety of long-term PPI therapy as concerns neoplastic changes in the exocrine and endocrine human stomach.     

Diagnosis of Helicobacter pylori infection in patients with atrophic gastritis: comparison of histology, 13C-urea breath test, and serology

BACKGROUND: Atrophic gastritis, a risk factor for gastric cancer, is a late consequence of Helicobacter pylori infection in approximately one-third of the infected patients. It has been suggested that gastric cancer would develop less frequently if H. pylori were eradicated. However, the prevalence of H. pylori infection may be underestimated in patients with atrophic gastritis and intestinal metaplasia if only biopsy-based diagnostic methods are used. METHODS: We compared histology, 13C-urea breath test (13C-UBT), and serology in H. pylori diagnostics in 50 male patients with atrophic corpus gastritis. RESULTS: H. pylori was detected in 15 (30%) patients by histology and in 14 (28%) by 13C-UBT, whereas increased serum antibody levels indicating H. pylori infection were found in 41 (82%) patients (P < 0.0001 between serology and both histology and 13C-UBT). H. pylori infection was associated with atrophic corpus gastritis in 84% of the present patients (in one patient with normal antibody titres H. pylori was defined histologically). CONCLUSIONS: H. pylori infection would have been missed in most patients with atrophic gastritis without the analysis of H. pylori antibodies. Therefore, in patients with atrophic gastritis, the use of serology is encouraged in diagnosing H. pylori infection.     

Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings

The role of Helicobacter pylori infection in the development and exacerbation of reflux esophagitis was investigated. The prevalence of Helicobacter pylori infection, the severity of atrophic gastritis, and esophageal motility (determined by esophageal manometry by an infusion catheter method) were assessed in patients with mild (n = 46) and severe (n = 27) reflux esophagitis and subjects without reflux (n = 28). Compared with the prevalence of Helicobacter pylori infection in the non-reflux group, the prevalence in the mild and severe reflux groups (60.7%, 47.8%, and 14.8%, respectively) was significantly (P < 0.05) lower. Atrophic gastritis was milder in both reflux groups than in the non-reflux group. The degree of gastritis was also milder in the severe reflux group than in the mild reflux group. The esophageal sphincter pressure was significantly (P < 0.05) lower in the reflux groups than in the non-reflux group, and the amplitude of primary peristalsis was significantly (P < 0.05) lower in the severe reflux group than in the non-reflux group. There were no significant differences between reflux patients with and without Helicobacter pylori infection in the parameters of esophageal manometry. These data imply that a low prevalence of Helicobacter pylori infection may result in a milder grade of atrophic gastritis, and consequently, exacerbate reflux esophagitis. Received: July 21, 1998 / Accepted: April 28, 1999     

Short-segment Barrett��s esophagus and cardia intestinal metaplasia: A comparative analysis

AIM:To investigate the endoscopy and histology of short-segment Barrett’s esophagus (SSBE) and cardia intestinal metaplasia (CIM),and their correlation with Helicobacter pylori (H. pylori) gastritis and gastroesophageal reflux disease (GERD). METHODS:Biopsy specimens were taken from 32 SSBE patients and 41 CIM patients with normal appearance of the esophagogastric junction. Eight biopsy specimens from the lower esophagus,cardia,and gastric antrum were stained with hematoxylin/eosin,Alcian blue/periodic acid-Schiff,Alcian blue/high iron diamine and Gimenez dye. Results were graded independently by one pathologist. RESULTS:The SSBE patients were younger than the CIM patients (P < 0.01). The incidence of dysplasia and incomplete intestinal metaplasia subtype was higher in SSBE patients than in CIM patients (P < 0.01). H. pylori infection was correlated with antral intestinal metaplasia (P < 0.05),but not with reflux symptomatic,endoscopic,or histological markers of GERD in CIM patients. SSBE was correlated with reflux symptomatic and endoscopic esophagitis (P < 0.01),but not with H. pylori infection and antral intestinal metaplasia. CONCLUSION:Dysplasia risk is significantly greater in SSBE patients than in CIM patients. CIM is a manifestation of H. pylori-associated and multifocal atrophic gastritis,whereas SSBE may result from GERD.     

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determi...     

Correlation between duodenogastric reflux and remnant gastritis after distal gastrectomy

BACKGROUND/AIMS: Many patients who undergo distal gastrectomy develop remnant gastritis. This report describes the correlation between remnant gastritis and the amount of duodenogastric reflux and looks at the relationship between Helicobacter pylori infection and duodenogastric reflux in remnant gastritis. METHODOLOGY: Sixty-two patients who underwent curative distal gastrectomy for gastric cancer with radical lymphadenectomy were studied. The period of bile reflux (percent time) into the gastric remnant was measured with the Bilitec 2000 under standardized conditions. Remnant gastritis was semi-quantified using the neutrophil infiltration score based on the updated Sydney System, and the presence of H. pylori infection was determined 12 weeks after the surgery. RESULTS: Overall, the correlation was not significant between the neutrophil infiltration score and the percent time (p=0.08). Similarly, the correlation was not significant in patients with H. pylori infection (p=0.30), but it was significant in patients without H. pylori infection (p=0.03). CONCLUSIONS: Duodenogastric reflux after distal gastrectomy can cause remnant gastritis in patients without H. pylori infection. Reconstruction with biliary diversion is protective against the development of remnant gastritis.