Role ofHelicobacter pylori in cirrhotic patients with peptic ulcer

Helicobacter pylori was found to be a promoter factor of peptic ulcer that has an incidence higher in patients with hepatic cirrhosis. To clarify the role betweenH. pylori and peptic ulcer in patients with hepatic cirrhosis, a serological test (ELISA test, HEL-p, AMRAD, Australia), was used to measure the presence ofH. pylori of patients with hepatic cirrhosis. Within two years, 108 cirrhotic patients who had received a panendoscopic examination were enrolled in this study. There were 79 males and 27 females with a mean age of 53.2 years. Sixty-four cases had positive serum HBsAg and 44 had negative serum. The results showed that the prevalence ofHelicobacter pylori in cirrhosis was 43.5% (47/108). There was no difference of HEL-p-positive rate between peptic ulcer and normal gastroduodenal mucosa (45.2% vs 46.1%,P>0.05). According to this study, there appears to be no relation between peptic ulcer andH. pylori in patients with hepatic cirrhosis. The etiology of peptic ulcer in cirrhotic patients need further study.     

胃部分切除术对血清幽门螺杆菌抗体水平影响的临床研究

本文选择３３例幽门螺杆菌（Ｈｐ）阳性的消化性质疡患者，观察胃部分切除术前后Ｈｐ感染状态变化及血清抗ＨｐＩｇＧ与ＩｇＡ的消长情况。结果表明，Ｈｐ阴转病例于术后２周即见到抗ＨｐＩｇＡ显著下降（Ｐ＜０．０５），比之抗ＨｐＩｇＧ更能敏感反映当前Ｈｐ感染状态。提示联合检测抗ＨｐＩｇＡ与ＩｇＧ，对于临床诊治Ｈｐ感染具有指导价值。     

High rate of Helicobacter pylori reinfection in Lithuanian peptic ulcer patients

AIM: To evaluate the frequency of Helicobacter pylori(H. pylori) reinfection in peptic ulcer patients during 9 years after H. pylori eradication.METHODS: We invited 117 peptic ulcer patients in whom eradication of H. pylori was confirmed 1 year after eradication treatment both by histology and by rapid urease test. In total, 57 patients were available for the study procedures: 34(59.6%) male, 23(40.4%) female; mean age 52.3 ± 13.0 years. There were 45(78.9%) patients with duodenal ulcer and 12(21.1%) with gastric ulcer. H. pylori was diagnosed by a rapid urease test and histology if endoscopy was performed. If endoscopy was refused, H. pylori was diagnosed by the C14-urea breath test and serology. H. pylori was established if at least one of the tests was positive.RESULTS: The mean follow-up was 8.9 ± 1.0 years(range, 6-12). H. pylori was established in 15 patients. In 2 H. pylori-negative patients, H. pylori was established during the follow-up period and eradicated. Therefore, we consider that reinfection occurred in 17 patients. In the per protocol analysis, reinfection was established in 17 of 57(29.8%; 95%CI: 19.2-42.2) patients during the follow-up period. The annual rate of infection was 3.36%. If all non-responders were considered H. pylori-negative, reinfection would be 14.5%(17/117), the annual ratebeing 1.63%. The mean age of patients with reinfection was 51.8 ± 14.0 years, and without reinfection was 52.5 ± 13.0 years, P 0.05; the mean body mass index of patients with reinfection was 27.2 ± 4.1 kg/m2, and without reinfection was 25.7 ± 4.2 kg/m2, P 0.05. There were no differences in the reinfection rates according the location of the peptic ulcer, the eradication regimen used, and smoking status.CONCLUSION: The reinfection rate of H. pylori is relatively high in Lithuania and probably related to the high prevalence of H. pylori, what may reflect differences in the socioeconomic status between Western and Eastern European countries.     

Characteristics of gastric cancer in peptic ulcer patients with Helicobacter pylori infection

AIM:To evaluate the incidence and clinical characteristics of gastric cancer(GC) in peptic ulcer patients with Helicobacter pylori(H.pylori) infection.METHODS:Between January 2003 and December 2013, the medical records of patients diagnosed with GC were retrospectively reviewed.Those with previous gastric ulcer(GU) and H.pylori infection were assigned to the Hp GU-GC group(n = 86) and those with previous duodenal ulcer(DU) disease and H.pylori infection were assigned to the Hp DUGC group(n = 35).The incidence rates of GC in the Hp GU-GC and Hp DU-GC groups were analyzed.Data on demographics(age, gender, peptic ulcer complications and cancer treatment), GC clinical characteristics [location, pathological diagnosis, differentiation, T stage, Lauren's classification, atrophy of surrounding mucosa and intestinal metaplasia(IM)], outcome of eradication therapy for H.pylori infection, esophagogastroduodenoscopy number and the duration until GC onset were reviewed.Univariate and multivariate analyses were performed to identify factors influencing GC development.The relative risk of GC was evaluated using a Cox proportional hazards model.RESULTS:The incidence rates of GC were 3.60%(86/2387) in the Hp GU-GC group and 1.66%(35/2098) in the Hp DU-GC group.The annual incidence was 0.41% in the Hp GU-GC group and 0.11% in the Hp DUGC group.The rates of moderate-to-severe atrophy of the surrounding mucosa and IM were higher in the Hp GU-GC group than in the Hp DU-GC group(86% vs 34.3%, respectively, and 61.6% vs 14.3%, respectively, P 0.05).In the univariate analysis, atrophy of surrounding mucosa, IM and eradication therapy for H.pylori infection were significantly associated with the development of GC(P 0.05).There was no significant difference in the prognosis of GC patients between the Hp GU-GC and Hp DU-GC groups(P = 0.347).The relative risk of GC development in the Hp GUGC group compared to that of the Hp DU-GC group,after correction for age and gender,was 1.71(95%CI:1.09-2.70;P=0.02).CONCLUSION:GU patients with H.pylori infection had higher GC incidence rates and relative risks.Atrophy of surrounding mucosa,IM and eradication therapy were associated with GC.     

Helicobacter pylori in duodenal ulcer patients with idiopathic gastric acid hypersecretion

Thirty-three consecutive patients with idiopathic gastric acid hypersecretion (defined as a basal acid output >10.0 meq/hr with a normal fasting serum gastrin level and negative secretin stimulation test) who were being treated for duodenal ulcer disease and other acid-peptic disorders were evaluated for the presence ofHelicobacter pylori by means of a rapid urease test. Fourteen patients had duodenal ulcer and 19 had other acid-peptic disorders (gastroesophageal reflux in 14, including six with Barrett's esophagus; four with nonulcer dyspepsia; and one with erosive gastritis).Helicobacter pylori was present in 12 of the 14 ulcer patients (86%) compared to only two of the 19 nonulcer patients (11%) (P<0.0001). The distribution of basal acid output for patients with duodenal ulcer was similar to that for nonulcer patients, and no significant difference in the mean basal acid output was found amongHelicobacter pylori-positive compared toHelicobacter pylori-negative patients. Seven of the duodenal ulcer patients with a basal acid output greater than 15.0 meq/hr wereHelicobacter pylori-positive, suggesting that the organism can withstand even extreme levels of gastric acidity. In conclusion, this study demonstrates that the prevalence ofHelicobacter pylori infection in patients with duodenal ulcer disease associated with idiopathic gastric acid hypersecretion is not different from a majority of ulcer patients with normal acid secretory profiles and offers additional evidence that extreme levels of gastric acid are not bactericidal for the organism.     

Treatment of Helicobacter pylori Infection in Clinical Practice in the United States

Our objectives were to define treatment success, compliance, and side effects for treatment of Helicobacter pylori in clinical practice. In all, 224 consecutive patients received Helicobacter pylori treatment: 97 received two weeks of bismuth subsalicylate, metronidazole, tetracycline four times a day with a H₂-receptor antagonist twice a day (BMT); 89 received one week of metronidazole, lansoprazole, and clarithromycin twice a day (MLC); and 38 received one week of BMT with lansoprazole twice a day (BMT-PPI). Cure rates were: BMT 81% (95% CI 74–89%), MLC 90% (95% CI 84–96%) BMT-PPI 87% (95% CI 81–92%). More patients prescribed a bismuth-based regimen discontinued medications due to side effects compared to MLC (P = 0.049). Nausea was more common for BMT compared to MLC (P = 0.04). In conclusion, treatment of Helicobacter pylori infection with a one-week course of MLC achieves a high rate of cure in clinical practice. Significantly fewer patients prescribed PPI-based therapy discontinue medications due to side effects as compared to bismuth-based triple therapy.     

Pathogenetic role ofHelicobacter pylori in duodenal ulcer disease

The pathogenesis of duodenal ulcer disease is multifactorial and the contribution ofHelicobacter pylori in relation to the other factors to the release of duodenal ulcer is unknown. To investigate this, we studied 147 patients with endoscopically proven healed ulcers. These patients were randomized to receive either placebo, misoprostol 200 g or misoprostol 300 g four times daily, and clinical, personal, physiological and endoscopic characteristics were obtained prospectively. Endoscopy was performed at the active phase of the ulcer and when the ulcer healed. Biopsies were taken from the antrum to assess histologically for: (1) the activity of gastritis as assessed by the degree of polymorph infiltration, (2) the degree of chronic inflammation by the degree of chronic inflammatory cells infiltration and degree of mucosal degeneration, and (3) bacteriologically for the presence ofH. pylori. The severity of the gastritis and the bacterial density were graded independently by two pathologists. The patients were assessed at two-month intervals for 12 months or until the ulcer relapsed. The results demonstrated that the relapse rates of duodenal ulcer were similar in the three treatment groups. The relapse rate was higher in the group with higher density of the bacteria (P<0.05). The degree of gastritis did not affect the relapse rate of duodenal ulcer in either the placebo or misoprostol group or in all patients combined. Stepwise logistic regression analysis identified that increased duodenal inflammation, male sex, early-onset disease, andH. pylori adversely affected relapse of the ulcer. We conclude that multiple factors affect the relapse of duodenal ulcer andH. pylori is one of them.     

High prevalence of reflux symptoms in duodenal ulcer patients who develop gastro-oesophageal reflux disease after curing Helicobacter pylori infection

BACKGROUND: Gastro-oesophageal reflux disease may develop following eradication of Helicobacter pylori. However gastro-oesophageal reflux disease could be preexistent and misdiagnosed since patients often misinterpret gastro-oesophageal reflux disease symptoms or focus their attention on abdominal symptoms. A questionnaire for analysis of gastro-oesophageal reflux disease symptoms has not been used until now. METHODS: A total of 70 patients with duodenal ulcer and Helicobacter pylori gastritis, without oesophagitis and/or typical gastro-oesophageal reflux disease symptoms were studied. All patients received a questionnaire with 5 items focused on abdominal symptoms and 5 on gastro-oesophageal reflux disease symptoms. The two symptom scores were calculated separately. After Helicobacter pylori treatment, follow-up consisted of clinical controls every 3 months for 1 year. Patients were asked to describe their complaints and to answer the questionnaire. If gastro-oesophageal reflux disease symptoms recurred endoscopy was performed. RESULTS: At interview, all patients reported a significant improvement in their abdominal symptoms after eradication; however 23 patients (32.8%: group A) reported the occurrence of gastro-oesophageal reflux disease symptoms, and 5 of them developed oesophagitis; gastrooesophageal reflux disease symptoms did not appear in the remaining 47 patients (group B). Basal gastro-oesophageal reflux disease score was significantly higher in group A than in group B (1.9+/-1.5 vs 0.9+/-0.9, p<0.005), while the abdominal symptoms score was not different. Following eradication, the score for abdominal symptoms decreased significantly (4.2+/-1.5 vs 1+/-0.8, p<0.0001) in the two groups; conversely, the total gastro-oesophageal reflux disease score remained unchanged, improving in 2 patients in group A and 11 in B, and worsening in 5 in group A and in 1 in B. Presence of hiatus hernia and male sex significantly correlated with the development of reflux symptoms. CONCLUSIONS: Patients who present with gastro-oesophageal reflux disease after Helicobacter pylori eradication are likely to already be affected by gastro-oesophageal reflux disease.     

Role of Helicobacter pylori infection and nonsteroidal anti-inflammatory drug use in bleeding peptic ulcers in Japan

Background Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) are well-known major causes of peptic ulcers. This study aimed to characterize the features of bleeding peptic ulcers in Japan. Methods This prospective study evaluated 116 patients revealed to have bleeding peptic ulcers from January 2000 to December 2002. Results Eighty-eight of the 116 patients (75.9%) had H. pylori infection. Seventy (60.3%) patients were positive for H. pylori with no history of NSAID use (group A), and 18 (15.5%) were positive for H. pylori with a history of NSAID use (group B). Among the H. pylori-negative patients, 15 (12.9%) were associated with NSAID use (group C). Thirteen (11.2%) patients had no H. pylori infection or history of NSAID use (group D). Among the 33 patients with a history of NSAID use, 11 were on-demand NSAID users and 14 took daily low-dose aspirin. The patients in groups B and C were significantly older that those in groups A and D, and they more frequently had coexisting diseases compared with group A. In group D, 11 patients had atrophic changes revealed by endoscopic examination, suggesting a past H. pylori infection, and these atrophic changes remained at the time of bleeding. Many of the patients in group D had serious comorbidity. Compared with healthy control subjects, the concentrations of both phosphatidylcholine and phosphatidylethanolamine were significantly decreased in the antral gastric mucosa in all patient groups. Conclusions NSAID use contributed to bleeding ulcers in 28.4% of patients; thus, low-dose aspirin or on-demand NSAID use may cause bleeding ulcers. There were only two (1.7%) confirmed cases of H. pylori-negative, non-NSAID ulcers.     

Optimal initiation of Helicobacter pylori eradication in patients with peptic ulcer bleeding

AIM:To evaluate when Helicobacter pylori(H.pylori)eradication therapy(ET)should be started in patients with peptic ulcer bleeding(PUB).METHODS:Clinical data concerning adults hospitalizedwith PUB were retrospectively collected and analyzed.Age,sex,type and stage of peptic ulcer,whether endoscopic therapy was performed or not,methods of H.pylori detection,duration of hospitalization,and specialty of the attending physician were investigated.Factors influencing the confirmation of H.pylori infection prior to discharge were determined using multiple logistic regression analysis.The H.pylori eradication rates of patients who received ET during hospitalization and those who commenced ET as outpatients were compared.RESULTS:A total of 232 patients with PUB were evaluated for H.pylori infection by histology and/or rapid urease testing.Of these patients,53.7%(127/232)had confirmed results of H.pylori infection prior to discharge.In multivariate analysis,duration of hospitalization and ulcer stage were factors independently influencing whether H.pylori infection was confirmed before or after discharge.Among the patients discharged before confirmation of H.pylori infection,13.3%(14/105)were lost to follow-up.Among the patients found to be H.pylori-positive after discharge,41.4%(12/29)did not receive ET.There was no significant difference in the H.pylori eradication rate between patients who received ET during hospitalization a n d t h o s e w h o c o m m e n c e d E T a s o u t p a t i e n t s[intention-to-treat:68.8%(53/77)vs 60%(12/20),P=0.594;per-protocol:82.8%(53/64)vs 80%(12/15),P=0.723].CONCLUSION:Because many patients with PUB who were discharged before H.pylori infection status was confirmed lost an opportunity to receive ET,we should confirm H.pylori infection and start ET prior to discharge.     

雷贝拉唑在消化性溃疡治疗中的作用及其安全性的大规模临床研究

目的观察雷贝拉唑片剂(波利特)单独应用或联合抗幽门螺杆菌(Hp)治疗对消化性溃疡患者主要症状的治疗作用及其安全性。方法在全国24个省市进行多中心、开放试验。经胃镜诊断为消化性溃疡活动期或愈合期的患者由医师根据其具体情况安排单独应用雷贝拉唑(10mg,每天1次,7d)或联合抗Hp治疗(其中雷贝拉唑为10mg,每天2次,每个疗程5d或7d)。观察治疗前(d0)、用药后第1(d1)、2(d2)、5(d5)和7天(d7)的症状,并记录不良反应。结果试验共入选患者25609例,其中包括胃溃疡、十二指肠溃疡、复合性溃疡、食管溃疡、应激性溃疡、吻合口溃疡。Hp总体阳性率为71.0%。单独用雷贝拉唑者11386例,联合用药14223例。在d1、d2、d5和d7,上腹痛的缓解率分别为63.0%、91.2%、99.2%和99.7%;消失率为16.0%、47.8%、80.3%及94.8%。总体症状缓解率分别为66.5%、94.6%、99.7%和99.9%。上述指标在两组之间比较差异均无统计学意义。共发生不良反应476例(1.9%)。单独用药组147例(1.3%),联合用药组329例(2.3%),两组间比较差异有非常显著意义(P<0.01)。多数不良反应轻微。结论雷贝拉唑在单独用药及与抗Hp药物合用时,对消化性溃疡患者的主要症状都具有明显的治疗作用,并具有良好的安全性。     

Epidemiology of Helicobacter pylori and peptic ulcer in India

BACKGROUND: There is a wide variation in the prevalence of peptic ulcer in India both before and since the use of endoscopy. We studied the prevalence of peptic ulcer disease in a community in northern India and its relationship with Helicobacter pylori infection. METHODS: A house-to-house survey of residents aged 15 years or above in a sub-sector of Chandigarh was performed as part of a pilot survey. Subsequently, the study randomly covered all sectors of Chandigarh and we screened 2649 persons. A questionnaire was administered to each subject by trained staff. All individuals with history of peptic ulcer/dyspepsia and an equal number of asymptomatic individuals were asked to attend the outpatient department of the Institute. Diagnosis of peptic ulcer was based on endoscopy or history of previous ulcer surgery. RESULTS: Two hundred and fifty-four individuals attended the outpatient department at the Institute and 147 underwent endoscopy, biopsy for histology and rapid urease test, and blood was collected for H. pylori serology. There were 80 symptomatic and 67 asymptomatic individuals. Helicobacter pylori was positive in 38 (56.7%) asymptomatic and 49 (61.3%) symptomatic individuals (P > 0.05). The point prevalence of active peptic ulcer was 3.4% and the lifetime prevalence was 8.8%. The duodenal-to-gastric ulcer ratio was 12:1. Helicobacter pylori was present in 11/13 (84.6%) subjects with peptic ulcer. Peptic ulcer was more common in elderly and dyspeptic individuals and there was no effect of sex or socioeconomic status. Helicobacter pylori was associated with age only and did not depend on sex, socioeconomic status or dyspepsia. Of the 38 asymptomatic persons having H. pylori infection, none had active peptic ulcer. CONCLUSIONS: This study demonstrates frequent occurrence of peptic ulcer and H. pylori in this part of the country. Peptic ulcer was more prevalent in the elderly and dyspeptic subjects. Helicobacter pylori was not associated with dyspepsia, and was more prevalent in elderly subjects. There was a low prevalence of peptic ulcer in asymptomatic H. pylori-infected persons in this community.     

Persistence of Helicobacter pylori infection in patients with peptic ulcer perforation

Objective. In patients with perforated peptic ulcer (PPU) the convergence between the high eradication rate of Helicobacter pylori infection and low rates of ulcer relapse after treatment has been associated with reinfection by non-virulent strains. The objective of this study was to evaluate the persistence of infection by virulent H. pylori strains and ulcer recurrence in 33 patients with PPU one year after surgery and antimicrobial treatment. Material and methods. The histological evaluation and molecular detection of H. pylori cagA and ureA genes, vacA allelic types and the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analyses of the glmM gene products from antral mucosa specimens were performed initially, 2–5 months and 1 year after therapy. Results. The density of H. pylori colonization was temporarily decreased (p<0.05) 2–5 months after therapy. After one year, complete eradication was achieved in only 7 patients (23%) at histological examination and recurrent ulcers were found in 3/33 (9%) patients. The vacA s1a allelic type of cagA-positive strains persisted in 19/33 (58%) PPU patients with identical PCR-RFLP fingerprints in 8/9 (89%) of the patients. Conclusions. In PPU patients with a low eradication rate of H. pylori infection after surgical and antimicrobial treatment, the frequent recrudescence of the infection is mostly caused by the persisting virulent strains of the cagA and vacA s1a subtypes. In the 1-year follow-up period the recurrent ulceration can be postponed just by the lowered colonization density of H. pylori after eradicative therapy.     

Helicobacter pylori status,endoscopic findings,and serology in HIV-1-positive patients

We have carried out a large prospective study of the frequency ofH. pylori infection and HIV-1 status in a community of ex-drug abusers including subjects with (N=210) and without (N=259) upper gastrointestinal symptoms, endoscopy and serology. Control groups were patients with upper gastrointestinal symptoms not at high risk of HIV-1 infection (N=219) and asymptomatic blood donors (n=322).H. pylori was present in 52% of symptomatic community resident having endoscopy and 55% of the control patients with symptoms but not at high risk of HIV-1 infection.H. pylori was less common in HIV-1-positive patients (40%) than those who were negative (66%;P<0.001). In patients with AIDS (33%), the frequency ofH. pylori infection was reduced compared to HIV-1-positive patients without AIDS (53%;P=0.05). All the residents with AIDS had upper gastrointestinal symptoms. In community residents, peptic ulcer was always associated withH. pylori infection. ByH. pylori serology, there was no difference in the frequency of infection in asymptomatic residents (56%) whether HIV-1 positive (55%) or HIV-1 negative (58%) compared with those residents with symptoms. Overall,H. pylori was less common in HIV-1-positive residents (49%) than those who were HIV-1 negative (61%;P<0.05). This difference was due mainly to the low frequency of infection in residents with AIDS (33%).H. pylori infection is common in HIV-1 positive patients, and only slightly reduced when compared with at-risk HIV-1-negative subjects. Peptic ulcer is associated withH. pylori in HIV-1 infection. Serology is a reliable marker ofH. pylori infection in HIV-1-positive patients, including those with advanced disease.     

Helicobacter pylori and perforated peptic ulcer. Prevalence of the infection and role of non-steroidal anti-inflammatory drugs

AIMS: To study the prevalence of Helicobacter pylori infection in patients with perforated peptic ulcer, to compare it with the prevalence in patients with uncomplicated ulcer, and to assess the role of non-steroidal anti-inflammatory drugs in this prevalence. METHODS: Consecutive patients with perforated peptic ulcer were included in this retrospective study. As a control group, patients undergoing elective outpatient evaluation for the investigation of dyspepsia during the same time period and found to have a peptic ulcer at endoscopy were included. A 13C-urea breath test was carried out in all patients to diagnose H. pylori infection. RESULTS: Sixteen patients with perforated peptic ulcer and 160 with non-complicated peptic ulcer were included. Sixty-two percent of the patients with perforated peptic ulcer were infected by H. pylori, while the microorganism was detected in 87% of the patients without this complication (P = 0.01). Non-steroidal anti-inflammatory drugs intake was more frequent (P = 0.012) in patients with perforated peptic ulcers (56%) than in those without perforation (26%). H. pylori prevalence in perforated peptic ulcers was of 44% in patients with non-steroidal anti-inflammatory drugs intake, but this figure increased up to 86% when only patients not taking non-steroidal anti-inflammatory drugs were considered (P = 0.09). In the multivariate analysis, non-steroidal anti-inflammatory drugs intake was the only variable that correlated with peptic ulcer perforation [odds ratio, 3.6 (95% confidence interval, 1.3-10); P = 0.016]. CONCLUSION: The mean prevalence of H. pylori infection in patients with perforated peptic ulcer is, overall, of only about 60%, which contrasts with the 90-100% figure usually reported in non-complicated ulcer disease. However, the most important factor associated with H. pylori-negative perforated peptic ulcer is non-steroidal anti-inflammatory drugs use, and if this factor is excluded, prevalence of infection is almost 90%, similar to that found in patients with non-perforating ulcer disease.     

Helicobacter pylori Seroprevalence in Patients with Autoimmune Hepatitis

Autoimmune hepatitis is characterized by a continuing hepatocyte necrosis that usually progresses to liver cirrhosis. Autoimmunity is also a feature of chronic infection by Helicobacter pylori, a gram-negative bacterium involved in the pathogenesis of peptic ulcer and upper gastrointestinal bleeding, with both events frequently occurring in patients with chronic liver disease. A newly described pathogenetic mechanism for chronic hepatitis and hepatocellular carcinoma in the mouse is linked to Helicobacter spp. infection. A high prevalence of H. pylori infection was demonstrated in patients with viral-related cirrhosis but never studied in cases of autoimmune hepatitis. In a case-control study, we examined 31 consecutive patients (25 women and 6 men, age range 20–66, mean age 46 ± 4.3 years) suffering from autoimmune hepatitis and 62 sex- and age-matched blood donors (50 women, 12 men, age range 20–65, mean age 46 ± 5.4 years) resident in the same area. Antibodies to H. pylori were present in 20 of 31 (64.5%) autoimmune patients compared to 33 of 62 (53.2%) controls (P = 0.3, odds ratio 1.60, 95% CI 0.60–4.28). The difference was not statistically significant either in female or male patients. In conclusion, the prevalence of H. pylori infection in patients and controls was similar in our study of patients with chronic autoimmune hepatitis.     

Prevalence of Non-Organ-Specific Autoantibodies in Patients Suffering from Duodenal Ulcer With and Without Helicobacter pylori Infection

Autoimmunity, a feature of chronic infection by Helicobacter pylori, is first directed against gastric cells but is also associated with extragastric diseases. The aim of the present work was to look for the influence of the infection on induction of non-organ-specific autoantibodies (NOSAs). We compared 49 patients (28 males and 21 females; age range, 36-72 years; mean, 61 +/- 4.6 years) suffering from duodenal ulcer and H. pylori infection (Group A) to 38 subjects (20 male, 18 female; age range, 40-78 years; mean, 63 +/- 3.8 years) affected by duodenal ulcer related to the assumption of nonsteroidal antiinflammatory drugs (Group B). H. pylori infection was diagnosed by histology, 13C-urea breath test, and serum IgG antibodies. Autoimmunitary pattern was demonstrated by the presence of NOSAs in serum. Antinuclear (ANA), anti-smooth muscle (SMA), and anti-liver/kidney microsomal-1 (LKM-1) antibodies were present in 5 of 49 (10.2%), 2 of 49 (4%), and 0 Group A patients, respectively. In Group B, ANA was present in 3 of 38 (7.9%), SMA in 3 of 38 (7.9%), and anti-LKM-1 in 0 patients. The difference was not statistically significant. In this population, H. pylori infection is not associated with an increased prevalence of NOSAs.     

DNA-DNA hybridization demonstrates apparent genetic differences betweenHelicobacter pylori from patients with duodenal ulcer and asymptomatic gastritis

We asked whether different clinical outcomes ofHelicobacter pylori infection might be a reflection of genetic differences in infecting organisms. Using DNA-DNA hybridization we examined whether hybridization levels groupedH. pylori isolates corresponding to the type of disease (gastric ulcer, duodenal ulcer, asymptomatic gastritis) from which they were recovered. Target DNAs were prepared fromH. pylori strains cultured from gastric biopsy specimens of 25 patients; 5 with gastric ulcers, 9 with duodenal ulcers, and 11 from asymptomatic volunteers endoscopically proven not to have peptic ulcer disease. DNA-DNA hybridization was performed with whole genomic probes made from an isolate from each of the three disease categories. Using a DNA probe from an isolate from a duodenal ulcer patient, we found that isolates from patients with duodenal ulcer and nonulcer gastritis yielded significant differences in levels of hybridization. The levels of hybridization of DNA fromH. pylori isolates from duodenal ulcer patients, gastric ulcer patients and nonulcer gastritis controls were 85.5%±7%, 83%±3%, and 78.3%±5%, respectively (mean±sd), and the difference between the hybridization levels obtained with duodenal ulcer and nonulcer control target DNAs was statistically significant (P=0.025). These data suggest that the outcome of infection (eg, ulcer or no ulcer) may be due to virulence factors encoded by genomic DNA. If such differences exist, it should be possible to produce probes that would identify the ulcer virulence gene(s) and clearly distinguish between ulcerogenic and nonulcerogenic strains ofH. pylori.This work was supported by Veterans Affairs; by grant DK 39919 from the National Institute of Diabetes and Digestive and Kidney Diseases and by the generous support of Hilda Schwartz.     

Unique features ofHelicobacter pylori disease in children

In a six-year period, 41 children had endoscopically documented duodenal ulcer disease or primaryH. pylori antral gastritis without duodenal ulcer. Of 37 children withH. pylori gastritis, group 1 comprised 23 patients with duodenal ulcer disease and group 2 had 14 patients without ulcers (primaryH. pylori gastritis). Group 3 comprised four children with duodenal ulcer disease andH. pylori-negative antral biopsies. During the study period, all primary chronic ulcer disease was duodenal; no primary chronic gastric ulcer was present. Two distinct types of duodenal ulcer disease were identified; the majority (85%) was always associated with significant activeH. pylori antral gastritis (group 1). The minority (15%) had virtually absent gastritis and noH. pylori (group 3). Native Indian children were represented in group 1 quite out of proportion to the referral population and had the most severe disease. While it is established that a higher prevalence of asymptomaticH. pylori infection exists in non-Caucasians, this appears to be the first demonstration of a higher prevalence of symptomatic ulcer disease in non-Caucasian children or adults. Caucasian children tended to have primaryH. pylori gastritis (group 2) or duodenal ulcer withoutH. pylori (group 3). Antral nodularity was found to be an important specific endoscopic sign, unique to those children withH. pylori disease. It has not been described in adultH. pylori disease. Non-Caucasian children, especially Native Indians, in British Columbia have more prevalent and more severeH. pylori disease than Caucasians. Endoscopy with gastric antral biopsies is necessary to distinguish different types of duodenal ulcer disease and to diagnose primaryH. pylori gastritis.