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Background: Levofloxacin triple therapy has been used for the first-line and second-line treatment of Helicobacter pylori infection for more than 10 years., Aims: To systematically review the efficacy of levofloxacin triple therapy in the first- and second-line treatment, and to assess the time trend and factors that might affect its efficacy., Methods: Prospective trials reporting the efficacy of levofloxacin triple therapy in either the first-line or second-line treatment of H. pylori infection in adults were searched from the PubMed and Cochrane database from January 2000 to September 2015. Meta-analysis was performed to calculate the cumulative eradication rate and the efficacies in subgroups., Results: Of the 322 articles identified, a total of 4574 patients from 41 trials, including 16 trials in the first-line treatment and 25 trials in the second-line treatment were eligible for analysis. The cumulative eradication rate was 77.3% (95% confidence intervals, CI: 74.7-79.6) and was 80.7% (95% CI 77.1-83.7) in the first-line treatment and 74.5% (95% CI: 70.9-77.8) in the second-line treatment. The efficacies of levofloxacin triple therapy before 2008, between 2009 and 2011, and after 2012 were 77.4%, 79.6% and 74.8% respectively. The eradication rate was higher when levofloxacin was given once daily (80.6%, 95% CI: 77.1-83.7) than twice daily (73.6%, 95% CI: 69.7-77.2). The efficacy was significantly higher in levofloxacin-susceptible strains than resistant strains (81.1% vs. 36.3%, risk ratio 2.18, 95% CI: 1.6-3, P < 0.001)., Conclusion: The efficacy of levofloxacin triple therapy has been lower than 80% in many countries and it is not recommended when the levofloxacin resistance is higher than 5-10%., (© 2016 John Wiley & Sons Ltd.)

Background: Whether 10-day or 14-day sequential therapy is superior to 14-day triple therapy in the first-line treatment of Helicobacter pylori remains controversial., Aim: To compare the efficacy of 10-day or 14-day sequential therapy vs. 14-day triple therapy., Methods: Randomised controlled trials (RCTs) comparing 10-day or 14-day sequential therapy and 14-day triple therapy as first-line treatment in adults were searched from the PubMed and Cochrane databases from 2000 to October 2015. Abstracts from international annual conferences were also searched. The primary and secondary outcomes were the eradication rate according to the intention-to-treat analysis and adverse effects, respectively., Results: Of the 109 articles identified, 13 RCTs including 2749 patients in the sequential therapy group and 2424 patients in the 14-day triple therapy group were eligible. Overall, sequential therapy for 10 or 14 days was not significantly superior to 14-day triple therapy [Risk ratio (RR) 1.04, 95% confidence interval (CI) 0.99-1.08, P = 0.145]. However, there was significant heterogeneity (I(2) = 57.6%, P = 0.005). In the subgroup analysis of four trials, we found that 14-day sequential therapy was significantly more effective than 14-day triple therapy (RR: 1.09, 95% CI: 1.04-1.16, P = 0.002), and there was no significant heterogeneity (I(2) = 0%, P = 0.624) in this comparison. Sequential therapy given for 10 days was not superior to 14-day triple therapy (RR: 1.03, 95% CI: 0.98-1.09, P = 0.207). There was no significant difference in the risk of adverse effects., Conclusion: Sequential therapy given for 14 days, but not 10 days, was more effective than 14-day triple therapy as first-line treatment., (© 2015 John Wiley & Sons Ltd.)

Chronic Helicobacter pylori-stimulated immune reactions determine the pathogenesis of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. We aimed to explore the genetic predisposition to this lymphoma and its clinical implication. A total of 68 patients and 140 unrelated controls were genotyped for 84 single-nucleotide polymorphisms in genes encoding cytokines, chemokines and related receptors that play important roles in T cell-mediated gastrointestinal immunity. Five genotypes in IL-22, namely CC at rs1179246, CC at rs2227485, AA at rs4913428, AA at rs1026788 and TT at rs7314777, were associated with disease susceptibility. The former four genotypes resided in the same linkage disequilibrium block (r(2)=0.99) that conferred an approximately threefold higher risk. In vitro experiments demonstrated that co-culturing peripheral mononuclear cells or CD4(+) T cells with H. pylori stimulated the secretion of interleukin-22 (IL-22), and that IL-22 induced the expression of antimicrobial proteins, RegIIIα and lipocalin-2, in gastric epithelial cells. Furthermore, patients with gastric tissue expressing IL-22 were more likely to respond to H. pylori eradication (14/22 vs 4/19, P<0.006). We conclude that susceptibility of gastric MALT lymphoma is influenced by genetic polymorphisms in IL-22, the product of which is involved in mucosal immunity against H. pylori and associated with tumor response to H. pylori eradication.

We recently showed that Helicobacter pylori (HP)-positive gastric 'pure' diffuse large B-cell lymphoma (DLBCL) may respond to HP eradication therapy. However, whether these HP-related 'pure' DLBCL of the stomach may differ fundamentally from those unrelated to HP remains unclear. In this study, we compared the clinicopathologic features of these two groups of patients who had been uniformly treated by conventional chemotherapy. Forty-six patients were designated HP-positive and 49 were HP-negative by conventional criteria. HP-positive patients had a lower International Prognostic Index score (0-1, 65% vs 43%, P=0.029), a lower clinical stage (I-IIE1, 70% vs 39%, P=0.003), a better tumor response to chemotherapy (complete pathologic response, 76% vs 47%, P=0.004) and significantly superior 5-year event-free survival (EFS) (71.7% vs 31.8%, P<0.001) and overall survival (OS) (76.1% vs 39.8%, P<0.001). To draw a closer biologic link with HP, HP-positive tumors were further examined for CagA expression in lymphoma cells. Compared with CagA-negative cases (n=16), CagA-positive cases (n=27) were associated with high phosphorylated SHP-2 expression (P=0.016), and even better 5-year EFS (85.2% vs 46.3%, P=0.002) and OS (88.9% vs 52.9%, P=0.003). HP-related gastric 'pure' DLBCL may be a distinct tumor entity, which is less aggressive, and responds better to conventional chemotherapy.

We recently reported that low-grade mucosa-associated lymphoid tissue lymphoma (MALToma) and diffuse large B-cell lymphoma (DLBCL) with MALToma (DLBCL[MALT]) of stomach are equally responsive to H. pylori eradication therapy (HPET) and that H. pylori-independent status is closely associated with nuclear translocation of BCL10. However, co-existing MALToma and DLBCL components of gastric DLBCL(MALT) may respond differentially to HPET and the underlying mechanism remains unclear. Tumour tissue samples from 18 patients with microdissectable co-existing MALToma and DLBCL cells were studied. The clonality of lymphoma cells was examined by polymerase chain reaction-based amplification of the CDR3 region of the IgH gene and confirmed by DNA sequence analysis. BCL10 expression was determined by immunohistochemistry. Differential response of co-existing MALToma and DLBCL to HPET was defined as complete eradication of one component while the other component remained. Five (27.8%) of the 18 patients showed different IgH gene rearrangements in the two components and three (60%) of these five patients had differential response of MALToma and DLBCL to HPET. By contrast, 13 patients showed identical IgH gene rearrangements and only one (8%) of them had differential response of the two components to HPET (p = 0.044). Further, all four patients with differential response of MALToma and DLBCL to HPET showed nuclear expression of BCL10 in the H. pylori-independent component and cytoplasmic expression of BCL10 in the H. pylori-dependent component while the expression patterns of BCL10 were identical in both of these components in the 14 patients who had similar tumour response to HPET. We conclude that different clonality is a common reason for the differential response of co-existing MALToma and DLBCL of gastric DLBCL(MALT) to HPET and that immunohistochemical examination of BCL10 expression may help to identify the co-existence of these components., (Copyright 2006 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.)

Dysfunction of E-cadherin and catenin has been linked to invasiveness and differentiation of tumors. This study aimed to characterize the expression of cadherins and catenins in early gastric carcinoma and their relationship to clinicopathologic characteristics and Helicobacter pylori infection. E-cadherin and alpha-, beta- and gamma-catenins were strongly expressed in normal epithelium but abnormal immunoreactivity of at least one of these four proteins was noted in 48 (90.6%) of 53 early gastric carcinomas. Only 5 cases with intestinal-type tumors had intact expression of E-cadherin and alpha-, beta-, and gamma-catenins. Abnormal immunoreactivity in the tumor tissue was observed in 18 patients (34.0%) for E-cadherin, in 35 (66.0%) for alpha-catenin, in 20 (37.7%) for beta-catenin, and in 37 (69.8%) for gamma-catenin. In diffuse-type tumors, abnormal expression of E-cadherin (60.9 vs. 13.3%, p < 0.0005), alpha-catenin (82.6 vs. 53.3%, p < 0.05) and gamma-catenin (91.3 vs. 53.3%, p < 0.005) was more frequent than in the intestinal type. Ten tumors with lymph node metastasis showed a relatively higher frequency of abnormal expression of E-cadherin (70 vs. 25.6%, p < 0.05) but a lower frequency of abnormal expression of beta-catenin (10 vs. 44.1%, p = 0.07) than those without metastasis. No significant association was found between cadherin/catenin expression and the depth of invasion or the H. pylori status. It was concluded that abnormal expression of E-cadherin and the catenin-mediated cell-cell adhesion system occurs frequently in early gastric carcinogenesis and may play an important role in the genesis of histologic differentiation and in the mode of metastasis of early gastric carcinomas., (Copyright 2001 S. Karger AG, Basel.)

Background & Aims: The association of Epstein-Barr virus (EBV) and gastric carcinomas (GCs) has been shown to vary among different populations and certain histological subtypes. Few studies have addressed the status of Helicobacter pylori infection and genetic alterations in these EBV-positive or -negative GCs., Methods: Eleven gastric lymphoepithelioma-like carcinomas (LELCs) and 139 cases of common non-LELCs were evaluated for the presence of EBV DNA using polymerase chain reaction (PCR) and RNA in situ hybridization. H. pylori infection was determined by anti-H. pylori immunoglobulin G in preoperative sera. Immunostaining for p53, c-erbB-2, and E-cadherin was performed. Microsatellite instability was analyzed by PCR using 10 primers., Results: EBV was detected in 11 (100%) LELCs and in 19 (13.7%) of 139 common GCs. Compared with EBV-negative GCs, gastric LELCs tended to have a relatively higher frequency of proximal location, diffuse histological subtype, p53 overexpression, and reduced E-cadherin expression but a lower frequency of lymph node metastasis, previous H. pylori infection, and c-erbB-2 overexpression. In contrast, no significant difference of clinicopathologic and genetic profiles was observed between EBV-positive non-LELC GCs and EBV-negative GCs. No correlation of microsatellite instability was found among these 3 subsets of GCs., Conclusions: Dissecting clinicopathologic characteristics and infection status of EBV and H. pylori provide additional evidence of etiological and genetic heterogeneity for GC. Distinct clinicopathologic and genetic pathways exist in gastric LELCs, in which EBV may play a more important role than H. pylori infection.

Background/aims: To access the reliability of a newly developed test, the Helicobacter pylori (H. pylori) stool antigen (HpSA) test was used for detection of H. pylori infection., Methodology: Stool specimens were collected from 33 consecutive patients (19 males and 14 females, age range: 16-73 years, mean: 49 years) who received upper gastrointestinal endoscopic examination for gastrointestinal symptoms. The H. pylori status was evaluated based on six different tests: culture, histology, biopsy urease test, 13C-urea breath test (13C-UBT), serology, and HpSA test. A commercial kit using an enzyme-linked immunosorbent assay examined HpSA in the stool. H. pylori status was defined as positive when the culture was positive or concordance of three of the other four tests (histology, biopsy urease test, 13C-UBT, and serology) was positive., Results: Twenty patients were diagnosed as H. pylori-positive. The HpSA test was positive in 19 patients and negative in 14 patients. The sensitivity and specificity were 95.0% and 100%, respectively. The overall accuracy rate was 96.3%., Conclusions: The HpSA test is a new, simple, non-invasive method for accurate diagnosis of H. pylori infection.

Background/aims: Both intestinal metaplasia (IM) and Helicobacter pylori (H. pylori) infection have been linked to gastric carcinogenesis in an age-dependent manner. However, their relationship remains ill defined, especially with respect to age., Methodology: Three hundred and two asymptomatic subjects (167 males and 135 females; mean age 44.3+/-11.1 years) underwent complete endoscopic examination and biopsy at the antrum and the corpus. H. pylori infection was diagnosed according to histopathology and serology, while IM was determined by histopathology., Results: Eighty-four patients (27.8%) had IM, while 185 patients (61.3%) were seropositive to H. pylori. The frequency of IM was higher in patients with gastric ulcer (9/14, 64.3%) than in those with minimal change (68/229, 29.7%) or duodenal ulcer (7/59, 11.9%), both p<0.01. Patients with IM had a higher mean age (49.5+/-14.1 vs. 42.3+/-9.0, p<0.01) and a higher H. pylori prevalence than those without IM (61/84, 72.6% vs. 124/218, 56.9%, p<0.01). The concordance rate of H. pylori infection between histopathologic and serologic diagnosis was lower in patients with IM (67/84, 79.8%) than those without (196/218, 89.9%, p<0.05). Using logistic regression analyses, the development of IM was noted to be independently related to both H. pylori infection (odds ratio=1.97, 95% confidence interval: 1.1(3.53)) and age (odds ratio = 1.93, 95% confidence interval: 1.51(2.47))., Conclusions: These data suggest that age and H. pylori infection are independent risk factors for the development of IM. Furthermore, H. pylori infection may have been underestimated in patients with IM because of the use of a single method of detection.

Background/aims: The frequent association of gastric atrophy and intestinal metaplasia in gastric cancer (GC) might preclude serologic detection of Helicobacter pylori (H. pylori) infection in GC. By using polymerase chain reaction (PCR) for detection, we would like to determine whether there exists a subset of genuinely H. pylori-negative GC patients, and whether they have distinct clinicopathologic features or not., Methodology: IgG antibodies against H. pylori were determined by ELISA in sera, and H. pylori DNA was detected by PCR in resected gastric specimens from 160 GC patients. Clinicopathologic characteristics were then compared among group A: seropositive, group B: seronegative but PCR-positive, and group C: seronegative and PCR-negative., Results: Among 160 patients, 105 (65.6%) were classified as group A, 25 (15.6%) as group B, and 30 (18.8%) as group C. Group B patients were older and had more infiltrative tumor growth than group A. Group C had a significantly higher frequency of female predominance, and their cancers were of a more cardiac location and of the diffuse histologic subtype than those of groups A and B., Conclusions: A significant portion (15.6%) was negative to ELISA but positive to PCR, suggesting that older ages and infiltrative tumor growth might preclude serologic detection of H. pylori infection by impairing humoral responses. Although the majority (81.2%) has a strong association with H. pylori infection, an H. pylori-negative subset indeed exists and has distinct clinicopathologic features, supporting that causes other than H. pylori infection are involved in GC carcinogenesis.

Helicobacter pylori (H. pylori) infection and intestinal metaplasia (IM) are each associated with an increased risk of gastric cancer (GC). To explore further the influences of H. pylori and IM on GC, H. pylori and subtypes of IM were evaluated in 135 sex and age-matched case and control pairs. Odds ratios (ORs) with 95% confidence intervals of developing GC were calculated for each risk factor using multiple logistic regression analysis. ORs for H. pylori infection and IM were 2.43 (1.29-4.65) and 4.59 (2.58-8.16), respectively, and those for different IM subtypes gave values of 0.82 (0.28-2.36) for type I, 2.03 (0.95-4.34) for type II and 39.75 (14.34-110.2) for type III. Stratification analysis by histological subtype and stage of GC showed a particularly high OR for IM in intestinal type (12.8, 4.73-34.83) and early GC (6.40, 2.25-18.18). Our data indicate that both H. pylori and IM are related to GC risk. Type III IM is a more specific marker of premalignancy, with relevance, in particular, to the early and intestinal type of GC.

Previous data on the association of Helicobacter pylori infection with gastric cancer by demographic or histological features are inconsistent due to a univariate analysis of limited case numbers. The aim of the present study was to determine such an association by the use of a large series of patients and multiple variables analysis. The serum IgG antibodies against H. pylori were measured in 397 patients with histologically verified gastric cancer. A multiple logistic regression analysis was used to define the association between seropositivity and demographic or tumour characteristics of gastric cancer. The overall seropositivity of H. pylori was 63%. In univariate analysis, the prevalence was significantly lower among patients with cardia (50%) or diffuse-type (56.6%) cancers than those with non-cardia (64.8%) or intestinal-type (70.3%) cancer (P < 0.05 and P < 0.01, respectively). There was no statistical difference between H. pylori infection rate and gender, age or tumour stage. A multiple logistic regression analysis showed tumour location and histology remained significant factors associated with seropositivity of H. pylori with an odds ratio of approximately 2.0. Analysis of combined histology and location revealed that patients with intestinal-type cancer at non-cardia locations had the highest odds ratio of 3.93 (95% confidence interval (CI): 1.55-10.0) compared with the lowest odds ratio of 0.69 (95% CI: 0.30-1.62) in diffuse cardia cancer (P < 0.005). Our data indicate H. pylori infection in gastric cancer is independently affected by the histological subtype and by tumour location.

Background & Aims: A different spectrum of genetic changes including p53, c-erbB-2, c-met, adenomatous polyposis coli (APC), and deleted in colorectal cancer (DCC) is involved in gastric cancer (GC). The aim of this study was to correlate these alterations with histological subtypes, tumor stages, and Helicobacter pylori infection., Methods: Specimens of 163 patients with GC were immunostained for p53, c-erbB-2, and c-met, and polymerase chain reaction was performed in them to determine loss of heterozygosity (LOH) of APC and DCC., Results: Overexpression of p53 was more frequent in early intestinal than early diffuse GC and was noted in the stage progression of diffuse but not intestinal GC. Overexpression of c-erbB-2 occurred more commonly in intestinal GC and advanced GC of both types. Overexpression of c-met was greater in diffuse GC, particularly at advanced stage. LOH of APC was more common in intestinal GC irrespective of the stage but rarely in diffuse GC. LOH of DCC occurred primarily in advanced intestinal GC and infrequently in early GC or advanced diffuse GC. Alterations of these five genes were not correlated with H. pylori infection., Conclusions: A distinct genetic pathway exists in gastric carcinogenesis of different histological subtypes and their tumor progression, in which H. pylori infection may play an equal role or no role.

Background: Helicobacter pylori is known as a major cofactor in ulcerogenesis. However, the role of H pylori in surgical patients with peptic ulcer and its possible influence on surgical treatment is unclear., Objectives: To determine the prevalence of H pylori infection in surgical patients with complicated peptic ulcer diseases and analyze its clinical significance., Design: A prospective, controlled study., Setting: University-affiliated hospital and tertiary care center., Subjects: Two study groups: surgical group (n = 66), i.e., patients who received surgical treatment for their peptic ulcer disease), and control group (n = 377) comprising 3 subgroups: normal volunteers (NV subgroup, n = 136) and patients who required only medical treatment for duodenal ulcer (DU subgroup, n = 119) or gastric ulcer (GU subgroup, n = 122) from January 1, 1994 to June 30, 1995., Methods: Preoperative or overnight fasting serum samples were collected, and H pylori state was assessed by serum anti-H pylori IgG., Results: Seropositivity was similar between the surgical group (60.6%) and NV control subgroup (58.8%), but it was highest in the DU control subgroup (87.4%) (P < .001 compared with NV control subgroup), followed by GU control subgroup (76.2%) (P < .01 compared NV). The patients with surgical peptic ulcer who had both seropositive and seronegative results for H pylori were similar for sex, age, social status, ulcer history, associated major medical problems, use of nonsteroid anti-inflammatory drugs, ulcer location, type of surgery, and ulceration recurrence rate. Although patients who underwent elective surgery had a higher seroprevalence rate (88.9%) than those requiring emergency surgery (56.4%) and patients who were seronegative for H pylori seemed to be associated with a higher major morbidity, these results were not statistically significant., Conclusion: No significant association of H pylori infection and peptic ulcer was noted between patients who required surgical treatment compared with those who required only medical treatment; H pylori played only a limited role in the cause of disease in surgical patients, perhaps only in the cases complicated with stenosis or intractable ulcers. This suggests that presently adequate acid reduction procedure will still be the main objective of surgical treatment and prevention of the ulcer recurrence.

Background/aims: Conflicting results concerning the relationships between abnormal expression of p53 and c-erbB-2 and biologic behavior of gastric cancer are noted. Therefore, overexpression of p53 and c-erbB-2 in relation to the following aspects of gastric cancer: tumor histopathology, Helicobacter pylori infection, and prognosis are explored., Materials and Methods: Expression of p53 and c-erbB-2 by immunohistochemistry was correlated with histopathology, H. pylori infection and prognosis of gastric cancer in 112 patients., Results: Positive p53 staining was found in 61 (54.5%) of 112 tumors examined. There was no association of p53 expression with sex, age, lymph node metastasis, H. pylori infection or prognosis. A significantly higher frequency of p53-positive staining was observed in advanced (60.7%), intestinal (69.8%) and cardia (76.5%) than in early (30.4%, p < 0.01), diffuse (34.7%, p < 0.01) and noncardia (50.5%, p < 0.05) carcinoma, respectively. Expression of c-erbB-2 was found in 34 cases (30.3%), and was not related to sex, age, H. pylori infection and tumor location. Tumors with positive c-erbB-2 staining appeared to behave more aggressively in view of higher rates of nodal metastasis (38.0% vs 17.1%, p < 0.05), advanced stage (37.1% vs 4.3%, p < 0.01) and poor mean survival (p < 0.01). Patients with intestinal type tumors also had a significantly higher rate of c-erbB-2 expression than those with diffuse tumors (39.7% vs 18.4%, p < 0.01)., Conclusions: Our results indicate that immunohistochemical expressions of p53 and c-erbB-2 are significantly associated with some histopathological phenotypes. Genetic alterations of c-erbB-2 or p53 may not be affected by H. pylori infection. C-erbB-2 expression may be used as a marker for identifying more aggressive gastric cancer for designing further therapy.

Background/aims: To investigate the frequency of endoscopic transmission of Helicobacter pylori and the efficiency of disinfection in different washing methods of endoscopes., Materials and Methods: IgG antibodies to H. pylori in patients prospectively followed who underwent first endoscopic examination at the National Taiwan University Hospital from 1982 to 1993 were measured. A total of 132 subjects who were negative for H. pylori IgG antibody test before examination and who were with negative endoscopic findings were enrolled. Among the 132 seronegative patients, 60 were examined before June 1989 when manual washing was adopted for endoscope cleaning and 72 received examination after mechanical washing were routinely used in our endoscopy unit., Results: During a follow-up period of 6 months or more, 5 patients in the manual washing group sero-converted while none in the mechanical washing group seroconverted (5/60 vs 0/72. p = 0.02)., Conclusion: The results suggested that the risk of endoscopic transmission of H. pylori is substantial and mechanical washing is efficient in preventing this iatrogenic spread.

This study was carried out to develop a scoring system for the diagnosis of gastric adenocarcinoma (GAC). A total of 686 subjects, 150 patients with GAC, 182 with gastric ulcer, 127 with duodenal ulcer, and 227 subjects with negative findings, were enrolled. Analysis of the likelihood ratio (LR) showed that patients with advanced age, ulcer in the stomach, low serum levels of pepsinogen I (PGI), low PGI x gastrin values, and low PGI/gastrin ratio were likely to have GAC. Of these indicators, the serum PGI level had the greatest weight, with a LR of 7.59 for the group with a level < 30 ng/ml. A scoring system combining serum PGI level, Helicobacter pylori seropositivity, and gastric ulcer status was derived, using a logistic regression model. This scoring system was found to be better than any one-parameter criterion for diagnosing GAC after evaluation by the area under the receiver operating characteristic curve (0.84; 95% confidence interval, 0.81-0.88) or by specificity-fixed sensitivity (sensitivity 0.82 at specificity 0.72, sensitivity 0.87 at specificity 0.66, sensitivity 0.96 at specificity 0.44). This scoring system may be potentially useful as a new model for the noninvasive diagnosis of GAC in the future.

The efficacy of H2-blocker and triple therapy in curing duodenal ulcer was compared and the contribution of the eradication of Helicobacter pylori on ulcer remission was assessed. Forty-two duodenal ulcer patients infected with H. pylori were randomized to receive either H2-blocker therapy with famotidine (n = 21) or triple therapy with bismuth, amoxicillin, and metronidazole (n = 21). All patients received treatment for four weeks. Endoscopic evaluation of ulcer status and bacteriologic identification of H. pylori were performed at two, six and 12 months after therapy. Triple therapy had a similarly high healing rate to H2-blocker therapy (100% vs 90.5%) at two months of follow-up. However, at 12 months of follow-up, the ulcer remission rate in the triple therapy group (94.4%) was significantly higher than that of the H2-blocker therapy group (38.9%) (p < 0.05), resulting in the former therapy having a significantly lower rate of H. pylori infection compared to the latter (5.6% vs 100%, p < 0.005). Patients with persistent H. pylori infection at two months of follow-up had a significantly higher ulcer recurrence rate (64.7%) at 12 months than those without infection (5.3%) (p < 0.05). The success of triple therapy in ulcer remission may be attributed to the high eradication rate of H. pylori.

To investigate Helicobacter pylori (H. pylori) infection in subjects with and without gastroduodenal diseases in Taiwan, IgG antibodies to H. pylori were examined in 136 healthy volunteers, 101 patients with non-ulcer dyspepsia, 122 gastric ulcers, 119 duodenal ulcers, and 161 gastric adenocarcinomas. The seropositivity was highest in duodenal ulcers (87.4%) (p < 0.001, as compared to healthy volunteers), followed by gastric ulcers (76.2%) (p < 0.01, as compared to healthy volunteers), but similar among gastric adenocarcinomas (60.3%), healthy volunteers (58.8%), and patients with non-ulcer dyspepsia (55.5%). Higher acquisition of H. pylori in younger patients with duodenal and gastric ulcers suggests a strong association with H. pylori. No ulcer characteristics, including number, location, and activity, were significantly statistically associated with the seropositivity of H. pylori in gastric and duodenal ulcers. Similarly, the location, extent of invasion, and histology of gastric adenocarcinoma was not significantly statistically associated with the seropositivity of H. pylori.

The association between Helicobacter pylori (H. pylori) and gastric adenocarcinoma remains controversial. However, the prevalence of H. pylori infection in gastric adenocarcinoma varies with the method of detection used, eg, serology, histology, culture, and polymerase chain reaction. However, studies on gastric adenocarcinoma by these methods remain inconclusive. We compared the results of serology, histology, and polymerase chain reaction for detection of H. pylori infection in 12 patients with gastric adenocarcinoma to investigate the actual status of H. pylori infection in gastric adenocarcinoma. IgG antibodies to H. pylori were examined in the sera, and histology and polymerase chain reaction were used for identification of H. pylori on the resected gastric tissues of 12 patients with gastric adenocarcinoma. Among them. H. pylori infection was verified by serology in eight, polymerase chain reaction in seven, and histology in five. In all positive cases, H. pylori was identified only in the non-tumorous part of the gastric tissue. In all four seronegative patients, H. pylori was not present in any of the tissues examined by histology and polymerase chain reaction. We conclude that: 1) polymerase chain reaction is more sensitive than histology; 2) a good correlation between serology and polymerase chain reaction is found; and 3) H. pylori infection is absent in a proportion of patients with gastric adenocarcinoma identified by these methods.

The influence of Helicobacter pylori infection on serum levels of pepsinogen I and gastrin in gastric carcinoma was investigated by simultaneous determination of serum pepsinogen I, gastrin, and IgG antibodies against Helicobacter pylori in 100 patients with gastric carcinoma, and in another 100 age- and sex-matched healthy controls. Serum pepsinogen I level was significantly lower in gastric carcinoma than in controls (55.5 +/- 28.1 vs. 76.9 +/- 25.1 ng/ml, p < 0.005), but there was no difference in serum gastrin between them (63.2 +/- 30.2 vs. 57.4 +/- 28.5 pg/ml, p = 0.16). Helicobacter pylori infection caused a significant increase in serum PGI level in advanced, intestinal type, and non-cardia gastric carcinoma. The serum gastrin level was affected by neither Helicobacter pylori infection nor any of the tumor characteristics. It is concluded that pepsinogen I, rather than gastrin, in the serum is greatly influenced by Helicobacter pylori infection and tumor characteristics in gastric carcinoma.

The association between gastric adenocarcinoma and Helicobacter pylori infection remains controversial. A seroprevalence study of Helicobacter pylori infection in 143 patients with gastric adenocarcinoma and a control group of 823 subjects randomly selected from four areas in Taiwan, was carried out to elucidate the association. The overall seropositivity of Helicobacter pylori in gastric adenocarcinoma patients (62.9%) was higher than in controls (54.4%), but the difference was not statistically significant (p > 0.05). The seropositivity of early gastric adenocarcinoma (61.5%) was not significantly different from that of advanced gastric adenocarcinoma (63.2%). Various demographic factors such as sex, blood type, cigarette smoking, tumor histology and location were not associated with the seroprevalence of Helicobacter pylori. The age-specific seroprevalence of Helicobacter pylori tended to be higher in younger patients and decreased after the age of 60 years in gastric adenocarcinoma, in contrast to a stepwise increase of seropositivity in controls. This suggests that Helicobacter pylori infection in early life may be a contributory factor in gastric carcinogenesis.

Sera from 14 patients with duodenal ulcer and their families were tested for IgG antibodies to Helicobacter pylori. Fourteen serologically negative patients and their families served as controls. Index patients and their family members who were serologically positive were advised to undergo endoscopic biopsy. Gastric biopsy tissues were subjected to HaeIII restriction analysis of nested polymerase chain reaction products of the urease gene. By serology, 28 (49.0%) of 57 in index families and 11 (27.5%) of 40 in control families tested positive. A higher prevalence rate was found in children of index patients (11/31, 35.5%) than in those of control patients (1/18, 5.6%; P < .05). On DNA analysis, 11 patterns were found in 13 patients, and 6 families underwent endoscopy. Children in 5 families exhibited identical patterns to those of their siblings and, in 3 of the 5 families, identical to the pattern of 1 of the parents. These results suggest that parent-to-child transmission and common infection source are probable causes of intrafamilial clustering of H. pylori.

To investigate the association of Helicobacter pylori and gastric ulcer and adenocarcinoma, IgG antibodies against H. pylori were examined in 823 randomly selected subjects, 92 healthy volunteers, 117 patients with gastric ulcer, and 148 with gastric adenocarcinomas in Taiwan, where the prevalence of gastric adenocarcinoma is high. The seropositivity of this population in Taiwan was 54.4%. Gastric ulcer patients had a higher seropositivity (83.8%) than healthy volunteers (62.0%) and gastric adenocarcinoma patients (62.2%) (P < 0.001). Gender difference, blood type, and habit of smoking were not associated with the seroprevalence in any study groups. Gastric ulcer coexistent with duodenal ulcer had a higher seropositivity (94.7%) (P < 0.05). The seropositivity of H. pylori in gastric adenocarcinoma patients was higher than in healthy volunteers only in younger age and was not associated with histologic type, invasion, and location of major tumors. The results reemphasize the association of H. pylori infection with gastric ulcer but not with gastric adenocarcinoma in Taiwan.