Helicobacter pylori infection, but not mucosal atrophy, significantly affects serum pepsinogen level after gastric cancer surgery

BACKGROUND/AIMS: Helicobacter pylori (Hp) infection is frequently observed in the remnant stomach after gastric cancer surgery, and is considered to play one of the important roles in chronic mucosal inflammation and cancer development. METHODOLOGY: Serum pepsinogen (PG) levels were measured in one hundred and eight patients after gastrectomy performed because of gastric cancer. The correlation between PG levels and the grade of mucosal inflammation in the remnant stomach was investigated together with the status of Hp infection. RESULTS: No statistical difference in serum PG level was found according to the severity of reflux gastritis, or grade of mucosal atrophy. Significantly higher serum PG II level and lower PG I/II ratio were found in cases with histologically severe mucosal inflammation than in those without inflammation. In Hp positive cases, PG I level stayed constant while PG II level scored a significantly higher value than those of negative cases. As a result, PG I/II ratio became significantly lower in cases with Hp infection than in those without infection. CONCLUSIONS: Hp infection and active mucosal inflammation, but not bile reflux or mucosal atrophy, significantly affect on the serum PG level in patients with remnant stomach after gastric cancer surgery. Serum PG level was suggested to indicate the grade of acute and chronic Hp-related inflammation in those patients.     

Influence of aging, gastric mucosal atrophy and dietary habits on gastric secretion

BACKGROUND/AIMS: Studies in Japan have reported on the association between gastric secretion and age with consideration given to gastric mucosal atrophy but not pepsin secretion. Though recent reports have shown enhanced gastric secretion in the Japanese, attributed to dietary westernization, the association between diet and gastric secretion is not clear. In this study, the association between gastric secretion and mucosal atrophy, age, and dietary habits was evaluated. METHODOLOGY: The subjects were 47 preoperative patients without upper gastrointestinal disorders. Acid secretion, pepsin secretion, serum pepsinogen level, and serum Helicobacter pylori antibody titer were measured. Dietary habits were investigated by questionnaire. RESULTS: Gastric secretion did not differ among the young, middle, and elderly age groups. Compared with the group without atrophy (pepsinogen I/II > 3.0, 32 subjects), the group with atrophy (I/II < or = 2.5, 11 subjects) showed significantly decreased gastric secretion and a significantly high Helicobacter pyloriseropositive rate. In the group without atrophy, acid and pepsin secretion was significantly correlated with energy intake, pepsin secretion was significantly correlated with glucose intake, and gastric secretion tended to increase with age. CONCLUSIONS: In the absence of gastric mucosal atrophy, gastric secretion does not decrease with age, and is related to dietary habits.     

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.     

Serological markers for gastric atrophy in asymptomatic patients infected with Helicobacter pylori

OBJECTIVE: Atrophic gastritis is a precancerous condition that is commonly caused by chronic Helicobacter pylori (H. pylori) infection. This blinded, controlled study was designed to determine if serum gastrin and pepsinogens were reliable markers of atrophy in asymptomatic patients. METHODS: One hundred and forty-seven asymptomatic patients underwent endoscopy with multiple gastric biopsies obtained for histology, culture, and rapid urease test. Fasting serum gastrin (total and G-17) and serum pepsinogens (I-II) were determined by standard immunoassays. Gastric atrophy was histologically assessed in accordance with internationally accepted criteria; three main patterns of gastritis were distinguished: (a) nonatrophic gastritis, (b) atrophic antrum-restricted and antrum-predominant gastritis, and (c) corpus-restricted gastritis. Receiving operating characteristic (ROC) analysis was used to determine the best cut-off for each serum test in nonatrophic gastritis versus antrum-restricted/antrum-predominant atrophic gastritis. RESULTS: No significant differences in serum gastrin and pepsinogens I-II were detected in nonatrophic gastritis versus patients with antrum-restricted/antrum-predominant atrophic gastritis. The positive likelihood ratios for an abnormal serum test to detect antrum-restricted/antrum-predominant atrophy in the gastric body were total serum gastrin 2.13 (95% CI 0.99, 4.6), gastrin-17: 1.55 (95% CI 0.75, 36.17), pepsinogen I: 2.74 (1.4, 5.4), pepsinogen II: 1.74 (1.27, 2.39), and the ratio of pepsinogen I and II: 1.8 (1.2-2.8). Negative likelihood ratios ranged from 0.20 to 0.65. CONCLUSION: In an asymptomatic population, serum gastrin (total and G-17) and pepsinogens I-II (and their ratio) do not discriminate nonatrophic versus antrum-restricted/predominant atrophic gastritis.     

Gastric emptying of solids in long-term NSAID users: correlation with endoscopic findings and Helicobacter pylori status

OBJECTIVE: Prostaglandins regulate gastric motor function. Inhibition of prostaglandins by nonsteroidal antiinflammatory drugs (NSAIDs) may alter gastric emptying. To study gastric emptying of solids and its relation to endoscopic findings and Helicobacter pylori in patients receiving long-term NSAIDs, we undertook this study. METHODS: Ninety-five patients with arthritis, 65 taking long-term NSAIDs (Group I) and 30 not taking NSAIDs (Group II) were studied. Presence of dyspeptic symptoms was determined using a questionnaire. Mucosal damage was determined by endoscopy. H. pylori was detected by antral biopsies for rapid urease test and histology. Gastric emptying for solids was evaluated using a scintigraphic method. Thirty healthy volunteers were used as controls for gastric emptying (Group III). Patients with peptic ulcer were excluded from the analysis of gastric emptying. Logistic regression analysis was performed to identify predictive factors for gastric emptying. RESULTS: Nineteen patients from Group I with peptic ulcers were excluded. Dyspeptic symptoms were seen in 24 (52%) Group I and seven (23%) Group II patients. Gastroduodenal erosions were seen in 10 (21.7%) Group I patients and four (13.3%) Group II patients. H. pylori was detected in 17 patients in Group I (36.9%) and Group II (56.6%). Gastric emptying was delayed in 24 (52%) Group I patients, six (20%) Group II patients (p < 0.001), and in none of the Group III controls. The mean gastric emptying times were 99.5 (15.6) min and 89 (17.7) min for Groups I and II, respectively (p < 0.05). Endoscopic damage was found with similar frequency in Group I patients with delayed or normal gastric emptying. H. pylori infection was present in 37.5% Group I patients with delayed gastric emptying and in 36.3% with normal gastric emptying (p = ns). Logistic regression analysis identified NSAID therapy as the single factor most predictive of delayed gastric emptying. CONCLUSION: Delayed gastric emptying was seen in 52% of patients on long-term NSAID therapy.     

Noninvasive versus histologic detection of gastric atrophy in a Hispanic population in North America.

BACKGROUND & AIMS: Cancer risk is directly correlated with the severity and extent of mucosal atrophy, making identification of atrophy a goal in cancer prevention programs. The aim of this study was to compare targeted histology with noninvasive testing for the identification of antral and/or corpus atrophy in North America. METHODS: In a cross-sectional study of a random sample of households, 8 gastric biopsy specimens were obtained from defined locations in the antrum and corpus. Biopsies were scored for the presence of Helicobacter pylori and gastric atrophy (defined as loss of normal glandular components). Atrophy was scored by using the Sydney system and a system based on the number and location of corpus biopsies with atrophy. Patients' sera were examined for pepsinogen I, pepsinogen II, and gastrin-17 (fasting and stimulated). RESULTS: One hundred eighty volunteers, approximately 30 per age group and ranging in age from 18-82 years, participated. There were 76 men. The overall weighted prevalence of a corpus atrophy was 4.7% (95% confidence interval, 2.3-7.0). There was a significant inverse relationship between the grade of corpus atrophy and the pepsinogen I/pepsinogen II ratio (R = -0.31, P < .01). We failed to confirm the usefulness of the proposed algorithm by using gastrin-17, H. pylori serology, and serum pepsinogens to categorize the gastric histology. The Sydney system underestimated the prevalence of corpus atrophy by approximately 25%. CONCLUSION: Noninvasive testing is both possible and practical by using pepsinogen assays for the identification of the precancerous condition of moderate to severe corpus atrophy in North American Hispanic patients.     

How closely is Helicobacter pylori infection related to gastroduodenal lesions?

BACKGROUND/AIMS: Various studies have indicated a relationship between Helicobacter pylori infection and upper gastrointestinal lesions, but this relationship needs to be assessed in individuals not seeking medical treatment for complaints. METHODOLOGY: We screened community residents for H. pylori infection and upper gastrointestinal lesions during an annual mass health examination aiming to determine relationships between infection and lesions. In 932 examinees we performed a 13C-urea breath test for H. pylori infection, and assessed degree of gastric atrophy by measuring pepsinogen I and II in serum. In 738 subjects we also performed upper gastrointestinal radiography with or without endoscopy. RESULTS: Prevalence of H. pylori infection increased with age, and the ratio of serum pepsinogen I to II decreased with age. Prevalence of H. pylori infection did not differ significantly between subjects with and without radiographically or endoscopically evident lesions. Of H. pylori-positive subjects with peptic ulcer, 73.2% had no recurrence of ulcer despite absence of medical treatment. CONCLUSIONS: Prolonged H. pylori infection was associated with atrophy of the gastric mucosa, but little relationship was evident between H. pylori infection and development or recurrence of peptic ulcer.     

Relationship of Helicobacter pylori to serum pepsinogens in an asymptomatic Japanese population.

A seroepidemiologic study of the prevalence of Helicobacter pylori infection in Japan was performed, and the relationship between serum pepsinogen I and II levels (markers of gastritis and gastric atrophy) and H. pylori infection was investigated. Four hundred and eighteen asymptomatic children and adults were studied. The prevalence of anti-H. pylori immunoglobulin G antibody increased with age. For persons born after 1950, the frequency of H. pylori infection increased at approximately 1% per year; for those born before 1950 the prevalence was high (70%-80%) and relatively constant. Serum pepsinogen I and II levels were significantly higher in H. pylori-infected volunteers than in H. pylori-uninfected volunteers [51.6 +/- 3 vs. 42.9 +/- 2 ng/mL (P less than 0.05) for pepsinogen I; 16.0 +/- 1 vs. 7.5 +/- 0.8 ng/mL (P less than 0.001) for pepsinogen II]. The ratio of pepsinogen I to pepsinogen II was significantly lower in H. pylori-infected volunteers (3.5 +/- 0.2) than in uninfected volunteers (6.3 +/- 0.3; P less than 0.001). The apparent decrease in prevalence of H. pylori accompanying the Westernization of Japan may eventually be accompanied by a reduction in the frequency of atrophic gastritis, the precursor lesion of the epidemic form of gastric carcinoma, and ultimately result in a decrease in the incidence of gastric carcinoma in Japan.     

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...     

Role of anti-parietal cell antibody in Helicobacter pylori-associated atrophic gastritis: evaluation in a country of high prevalence of atrophic gastritis

BACKGROUND: Helicobacter pylori plays an important part in the progression of atrophic gastritis; however, markers for predicting the progression of atrophic gastritis remain unidentified. We investigated the relation between the degree of atrophic gastritis and the amount of anti-parietal cell antibodies (APCAs) present. METHODS: In 219 Japanese patients, APCA was investigated by enzyme-linked immunosorbent assay (ELISA) and by Western blotting. The grade of corpus atrophy was estimated by histology and serum pepsinogen levels. Serum levels of pepsinogen were evaluated by radioimmunoassay. RESULTS: Helicobacter pylori infection did not affect the APCA levels determined by ELISA. Long-term administration of proton-pump inhibitors and H. pylori eradication did not influence the levels of APCAs. However, in H. pylori-positive patients, the levels of APCA determined by ELISA were statistically higher in patients with severe atrophy than in those with mild atrophy as determined histologically (0.67+/-0.48 versus 0.45+/-0.40; A492, mean+/-s, P=0.01) and serologically by pepsinogen levels (0.66+/-0.51 versus 0.44+/-0.40. P=0.002). The levels of pepsinogen I/II ratio were correlated with APCA levels only in the H. pylori-positive group. Western blotting showed that major antigen was identical with the beta-subunit of H+,K+-ATPase. CONCLUSION: APCA plays an important part in the progression of corpus atrophy after H. pylori infection.     

Seroepidemiology of gastritis in Japanese and Dutch working populations: evidence for the development of atrophic gastritis that is not related to Helicobacter pylori.

Serological markers of gastritis, like pepsinogen A, pepsinogen C, gastrin, and Helicobacter pylori antibodies, can be used to explore the state of the gastric mucosa in populations with contrasting cancer risks. A decreasing pepsinogen A:C ratio and an increasing serum gastrin are known to reflect an increasing severity of atrophic corpus gastritis, which is a precursor of gastric cancer. In 723 subjects (without gastroduodenal surgery) from Japanese (n = 225) and Dutch (n = 498) working populations, which had a similar composition of age (mean 48 years), sex (male to female ratio 6:1), and type of occupation, fasting serum samples were analysed for IgG antibodies to H pylori, pepsinogen A, pepsinogen C, and gastrin in the same laboratory. H pylori infection was significantly more prevalent in the Japanese than in the Dutch (74.7% and 31.3%); as was a very low pepsinogen A, indicative of severe mucosal atrophy (4.4% and 1.6%). Among subjects with and without severe mucosal atrophy the H pylori seropositivity rate was similar. Between the Japanese and the Dutch there were significant differences in mean gastrin (31.8 and 13.4 pmol/l) and pepsinogen A:C ratio (1.7 and 2.9). These intercountry differences were as great for H pylori negative subjects (gastrin: 23.7 and 10.3 pmol/l, pepsinogen A:C ratio: 2.4 and 3.2) as for H pylori positive subjects (gastrin: 34.6 and 20.1 pmol/l, pepsinogen A:C ratio: 1.5 and 2.5). The intercountry difference in gastrin nearly disappeared after stratification into categories of pepsinogen A:C ratio. In conclusion, the intercountry differences in pepsinogen A:C ratio and gastrin reflect a higher prevalence of mild and severe mucosal atrophy of the corpus in the Japanese than in the Dutch, both among H pylori positive and negative subjects. Thus, these findings suggest that in the Japanese the development of atrophic gastritis is in part unrelated to H pylori.     

Predicting the development of gastric cancer from combining Helicobacter pylori antibodies and serum pepsinogen status: a prospective endoscopic cohort study

BACKGROUND AND AIMS: Helicobacter pylori infection and gastric atrophy are both risk factors for gastric cancer. We aimed to elucidate the natural history of gastric cancer development according to H pylori infection and gastric atrophy status.Subjects and METHODS: A total of 9293 participants in a mass health appraisal programme were candidates for inclusion in the present prospective cohort study: 6983 subjects revisited the follow up programme. Subjects were classified into four groups according to serological status at initial endoscopy. Group A (n = 3324) had "normal" pepsinogen and were negative for H pylori antibody; group B (n = 2134) had "normal" pepsinogen and were positive for H pylori antibody; group C (n = 1082) had "atrophic" pepsinogen and were positive for H pylori antibody; and group D (n = 443) had "atrophic" pepsinogen and were negative for H pylori antibody. Incidence of gastric cancer was determined by annual endoscopic examination. RESULTS: Mean duration of follow up was 4.7 years and the average number of endoscopic examinations was 5.1. The annual incidence of gastric cancer was 0.04% (95% confidence interval (CI) 0.02-0.09), 0.06% (0.03-0.13), 0.35% (0.23-0.57), and 0.60% (0.34-1.05) in groups A, B, C, and D, respectively. Hazard ratios compared with group A were 1.1 (95% CI 0.4-3.4), 6.0 (2.4-14.5), and 8.2 (3.2-21.5) in groups B, C, and D, respectively. Age, sex, and "group" significantly served as independent valuables by multivariate analysis. CONCLUSIONS: The combination of serum pepsinogen and anti-H pylori antibody provides a good predictive marker for the development of gastric cancer.     

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.     

Two distinct aetiologies of cardia cancer; evidence from premorbid serological markers of gastric atrophy and Helicobacter pylori status

BACKGROUND: Non-cardia gastric adenocarcinoma is positively associated with Helicobacter pylori infection and atrophic gastritis. The role of H pylori infection and atrophic gastritis in cardia cancer is unclear. AIM: To compare cardia versus non-cardia cancer with respect to the premorbid state of the stomach. METHODS: Nested case-control study. To each of 129 non-cardia and 44 cardia cancers, three controls were matched. Serum collected a median of 11.9 years before the diagnosis of cancer was tested for anti-H pylori antibodies, pepsinogen I:II and gastrin. RESULTS: Non-cardia cancer was positively associated with H pylori (OR 4.75, 95% CI 2.56 to 8.81) and gastric atrophy (pepsinogen I:II <2.5; OR 4.47, 95% CI 2.71 to 7.37). The diffuse and intestinal histological subtypes of non-cardia cancer were of similar proportions and both showed a positive association with H pylori and atrophy. Cardia cancer was negatively associated with H pylori (OR 0.27, 95% CI 0.12 to 0.59), but H pylori-positive cardia cancer showed an association with gastric atrophy (OR 3.33, 95% CI 1.06 to 10.5). The predominant histological subtype of cardia cancer was intestinal and was not associated with gastric atrophy compared with the diffuse subtype ((OR 0.72, 95% CI 0.19 to 2.79) vs (OR 3.46, 95% CI 0.32 to 37.5)). Cardia cancer in patients with atrophy had an intestinal: diffuse ratio (1:1) similar to non-cardia cancer (1.9:1), whereas cardia cancers in patients without atrophy were predominantly intestinal (7:1). CONCLUSION: These findings indicate two aetiologies of cardia cancer, one associated with H pylori atrophic gastritis, resembling non-cardia cancer, and the other associated with non-atrophic gastric mucosa, resembling oesophageal adenocarcinoma. Serological markers of gastric atrophy may provide the key to determining gastric versus oesophageal origin of cardia cancer.     

Plasma ghrelin concentration correlates with the levels of serum pepsinogen I and pepsinogen I/II ratio--a possible novel and non-invasive marker for gastric atrophy

BACKGROUND/AIMS: Ghrelin, a novel growth-hormone-releasing peptide, has been reported to be localized mainly in the A-like cells in the gastric fundic mucosa. With the extension of gastric inflammation caused by H. pylori infection, gastric mucosal atrophy extends from the antrum to the corpus, which is the predominant site of localization of the ghrelin-producing A-like cells. The present study was designed to investigate the correlation between the plasma ghrelin levels and the extent of gastric mucosal atrophy in patients with chronic gastritis caused by H. pylori infection. METHODOLOGY: Sixty-nine patients with dyspeptic symptoms were enrolled for the study. Of these, 41 patients were confirmed to become negative for H. pylori after therapy to eradicate the infection. The other 28 patients were diagnosed as positive for H. pylori infection. Blood samples were collected from all the patients after 12 hours of fasting, before upper gastrointestinal endoscopy was performed. The plasma levels of total and active ghrelin, as well as the serum levels of pepsinogen I (PGI) and pepsinogen II (PGII) were measured by radioimmunoassay. Based on endoscopic assessment, the atrophic changes in the gastric mucosa were classified as open-type atrophy or closed-type atrophy. RESULTS: There were no significant differences in the plasma total and active ghrelin levels between H. pylori-positive and H. pylori-eradicated (negative) patients. The serum levels of PGI correlated well with the plasma levels of total ghrelin (p<0.01, r=0.38) and active ghrelin (p<0.05, r=0.29). The ratio of serum PGI to PGII level (PG I/II ratio) also correlated well with the plasma level of total ghrelin (p<0.05. r=0.31) and active ghrelin (p<0.05, r=0.27). The plasma levels of total as well as active ghrelin were significantly decreased in patients with low PG levels as compared with those in patients with high PG levels (PGI > 70 ng/mL or PGI/II >3.0). The plasma levels of total as well as active ghrelin were also significantly decreased in patients with endoscopically diagnosed open-type atrophy as compared with those in patients with endoscopically diagnosed closed-type atrophy (p < 0.01), especially in the H. pylori-eradicated cohorts. CONCLUSIONS: The plasma levels of ghrelin, which correlated well with the serum levels of PGI as well as the PGI/II ratio, decreased with increasing extent of gastric mucosal atrophy, suggesting that it could be a potentially useful non-invasive marker for chronic atrophic gastritis.     

Concentrations of α- and β-defensins in gastric juice of patients with various gastroduodenal diseases

AIM: To determine the concentration of α- and β-defensins in gastric juice of patients with various gastroduodenal diseases. METHODS: Concentrations of human neutrophil peptides (HNPs) 1-3, the major forms of α-defensins, and human β-defensin (HBD)-I and HBD-2 were measured by radioimmunoassay in plasma and gastric juice of 84 subjects, consisting of 54 Helicobacter pylori-infected and 30 uninfected subjects. They included 33 patients with chronic gastritis (CG), 12 with gastric ulcer (GU), 11 with duodenal ulcer (DU), 11 with benign gastric polyp (BGP) and 16 with normal mucosa (N group) on upper endoscopy. Plasma pepsinogen Ⅰ and Ⅱ levels, biomarkers for gastric mucosal inflammation and atrophy, were also measured. RESULTS: Gastric juice HNPs 1-3 levels in patients with CG, GU and BGP were significantly higher than those in patients with DU and N. Gastric juice HBD-2 concentrations in patients with CG and GU were significantly higher than those in the N group, but were significantly lower in DU patients than in GU patients. Gastric juice HBD-1 levels and plasma levels of these peptides were similar in the patient groups. Concentrations of gastric juice HNPs 1-3 and HBD-2 of in H pylori-infected patients were significantly different from those in uninfected subjects. HNPs 1-3 concentrations in gastric juice correlated negatively with plasma pepsinogen Ⅰ levels and Ⅰ/Ⅱ ratios. HBD-2 levels in gastric juice correlated positively and negatively with plasma pepsinogen Ⅱ concentrations and Ⅰ/Ⅱ ratios, respectively. CONCLUSION: HNPs 1-3 and HBD-2 levels in gastric juice are diverse among various gastrointestinal diseases, reflecting the inflammatory and atrophic events of the background gastric mucosa affected by H pylori。     

Anti-parietal cell antibody and serum pepsinogen assessment in screening for gastric carcinoma

BACKGROUND: Anti-parietal cell antibody is found in patients with Helicobacter pylori-positive gastritis and is related to atrophic gastritis and gastric carcinoma. AIM: To identify the characteristics of patients at high-risk for gastric carcinoma in terms of anti-parietal cell antibody and serum pepsinogen. PATIENTS AND METHODS: Subjects were 92 H. pylori-positive patients (54 men, 38 women; mean age, 57.9 years; range, 15-88 years). The serum concentrations of pepsinogen I and II were determined by radioimmunoassay, and the presence of anti-parietal cell antibody was assessed by enzyme-linked immunosorbent assay. Degrees of inflammation and atrophy in the corpus of the stomach were evaluated histologically. RESULTS: Patients were classified into four groups according to anti-parietal cell antibody status and pepsinogen I/II ratio. Anti-parietal cell antibody-negative/pepsinogen I/II-low patients had the highest risk for gastric carcinoma (prevalence of gastric carcinoma: 7/13=53.8%, odds ratio=7.6, 95% confidence interval, 1.2-48.0). Anti-parietal cell antibody titre was high when inflammation in the corpus was severe (p=0.06) and significantly low when atrophy in the corpus was severe (p=0.01). CONCLUSION: Our results showed that patients with a negative anti-parietal cell antibody titre and low pepsinogen I/II ratio are at high-risk for gastric carcinoma.     

Serum pepsinogen I and II levels in various gastric disorders with special reference to their use as a screening test for carcinoma stomach.

INTRODUCTION: The role of serum pepsinogen in the diagnosis of gastric carcinoma is well established. Its role in other common upper alimentary disorders has not been widely studied. The aim of this study was to describe the effect of various gastric disorders on the levels of pepsinogen I, pepsinogen II and pepsinogen I/II ratio, with an emphasis on the diagnosis of carcinoma stomach in the South Indian population. METHODS: A total of 210 patients in seven groups, including one control group, were studied. The groups included patients with carcinoma stomach, Helicobacter pylori gastritis, peptic ulcer, portal hypertensive gastropathy, non-ulcer dyspepsia and erosive gastritis. Serum pepsinogen I, pepsinogen II and pepsinogen I/II ratio were estimated using an enzyme-linked immunosorbent assay technique. RESULTS: Patients with carcinoma of the stomach, when compared with controls, had a significantly lower pepsinogen I level (87.2 microg/L vs. 158.1 microg/L, p=0.0002) and pepsinogen I/II ratio (4.3 vs. 7.2, p = 0.0001). No significant change in pepsinogen levels occurred in the other groups. The cut-off levels of pepsinogen I (115.3 microg/L) and pepsinogen I/II ratio (6.2), determined by THE ROC curve, when applied in parallel provided a sensitivity of 97% and a negative predictive value of 91.4% for the diagnosis of carcinoma stomach. When the tests were applied in parallel, the likelihood ratio of a negative test was 0.06, indicating that individuals without carcinoma stomach were 16 times more likely to have a negative test than those with carcinoma. This fulfilled the essential prerequisites of an ideal screening test. CONCLUSION: Serum pepsinogen estimation is a useful diagnostic tool in the diagnosis of carcinoma stomach. The significance of serum pepsinogen level in portal hypertensive gastropathy, non-ulcer dyspepsia, peptic ulcer, Helicobacter pylori gastritis and erosive gastritis was not established.     

Relationship between Helicobacter pylori status and serum pepsinogens as serologic markers in atrophic gastritis.

BACKGROUND/AIMS: Serum pepsinogen levels are considered as a non-endoscopic blood test in the diagnosis of atrophic gastritis. The objective of the present study was to investigate whether there is any difference between pepsinogen levels in Helicobacter pylori-positive and -negative patients with atrophic gastritis, and to analyze the relationship between histopathology and pepsinogen levels after treatment in H. pylori-positive patients with atrophic gastritis. METHODS: The study enrolled a total of 30 cases with atrophic gastritis (18 H. pylori-positive and 12 H. pylori-negative). The H. pylori-positive cases received a one-week eradication treatment. Initially for all and after the treatment for H. pylori-positive cases, serum pepsinogen I and II levels, anti-H. pylori IgG titration and histopathologic analysis were carried out. RESULTS: In the H. pylori-positive patients with atrophic gastritis, the levels of pepsinogen I and pepsinogen I/II ratio were lower while the levels of pepsinogen II were higher compared to the H. pylori-negative patients (p<0.05 for all). The post-treatment serum pepsinogen I levels and pepsinogen I/II ratios did not change in the H. pylori-positive group, while the levels of pepsinogen II, H. pylori antibody titration and gastric atrophy degree remarkably decreased (p<0.05 for all). CONCLUSIONS: In atrophic gastritis, the levels of serum pepsinogen and pepsinogen I/II ratio show a difference in H. pylori-negative versus -positive cases. Additionally, the usage of pepsinogen II as a serum marker in predicting the eradication of H. pylori with atrophic gastritis could be more reliable than pepsinogen I or the I/II ratio.     

胃癌与十二指肠溃疡患者血清胃蛋白酶原比较

目的 比较胃癌患者与十二指肠溃疡患者血清胃蛋白酶原水平的差异及探讨其与H．pylori感染的关系。方法 采用时间分辨荧光免疫分析方法检测108例胃癌和96例十二指肠溃疡患者血清胃蛋白酶原Ⅰ、Ⅱ（PGⅠ，PGⅡ），ELISA方法检测血清H．pylori抗体。结果 胃癌和十二指肠溃疡患者之间PGⅠ水平有显著性差异，胃癌组和十二指肠溃疡组中H．pylori阳性和阴性间PGⅠ、PGⅡ、PGⅠ，PGⅡ水平等无显著性差异。结论 胃癌患者血清PGⅠ水平显著低于十二指肠溃疡患者，H．pylori感染对胃癌和十二指肠溃疡患者血清胃蛋白酶原水平和PGⅠ，PGⅡ比值均无影响。