“Cervia Working Group Report”: Guidelines on the diagnosis and treatment of Helicobacter pylori infection

Different national attitudes exist between countries in Europe concerning eradication of Helicobacter pylori infection due to the wide differences in Helicobacter pylori prevalence, gastric cancer risk, bacterial resistance to antibiotics, health care systems and financial resources. The Cervia Working Group Report has been established in order to fill the gap in the absence of National Guidelines in Italy concerning the diagnosis and treatment of Helicobacter pylori infection. The recommendations made are, by and large, similar to the European Guidelines but differ slightly with regard to the "test-and-treat" approach to young dyspeptics without sinister symptoms. In the absence of a national validation of this strategy a case-by-case assessment of dyspepsia has been promoted, both at primary care and specialist level. Another area of partial disagreement concerns the eradication of Helicobacter pylori in patients undergoing long-term proton pump inhibitor treatment which has not been generally recommended as scientific evidence in support of this policy is at present rather weak.     

Empirical Helicobacter pylori “rescue” therapy after failure of two eradication treatments

AIM: Even with the current most effective Helicobacter pylori treatment regimens, approximately 20% of patients do not eradicate the infection. Several "rescue" therapies have been recommended, but they still fail to eradicate H. pylori in approximately 20-30% of the cases. Our aim was to evaluate the efficacy of different rescue therapies prescribed to patients in whom two consecutive H. pylori eradication regimens had failed. METHODS: Design. Prospective single-centre study. Patients. Consecutive patients in whom two eradication regimens had failed to eradicate H. pylori. Intervention. Third eradication regimens included: (1) omeprazole-amoxicillin-clarithromycin for 7 days; (2) quadruple therapy with omeprazole-bismuth-tetracycline-metronidazole for 7 days; (3) omeprazole-amoxicillin-clarithromycin-bismuth for 14 days; and (4) omeprazole-amoxicillin-rifabutin for 14 days. H. pylori antibiotic susceptibility was unknown and, therefore, rescue regimens were chosen empirically. In no case, was the same regimen repeated. Outcome. H. pylori eradication was defined as a negative in 13C-urea breath test 8 weeks after completing the therapy. RESULTS: Forty-eight patients were included (mean age 45 years, 44% males, 82% with peptic ulcer and 18% with functional dyspepsia). No patient was lost from follow-up. Adverse effects were described in 21% of the patients. One patient receiving omeprazole, amoxicillin and rifabutin was removed from medication due to adverse effects (vomiting). Overall, mean H. pylori eradication with third therapy after failure of two eradication treatments was 34/48 (71%; 95% confidence interval 57-82%) by intention-to-treat and 34/47 (72%; 95% confidence interval 58-83%) by per-protocol. CONCLUSION: It seems that performing culture even after a second eradication failure may not be necessary, as it is possible to construct an overall strategy to maximise H. pylori eradication, based on the different possibilities of empirical treatment.     

Helicobacter pylori “test-and-scope” strategy for dyspeptic patients. Is it useful and safe?

AIM: To evaluate outcome of test-and-scope strategy using 13C-urea breath test, Helicobacter pylori IgG serology, and CagA serology. PATIENTS AND METHODS: A series of 100 dyspeptic patients were studied. Biopsies were obtained for histology and rapid urease test (gold standard). Serum samples were obtained for Helicobacter pylori IgG and CagA serology, and 13C-urea breath test was carried out. RESULTS: If endoscopy had not been performed in Helicobacter pylori patients based on 13C-urea breath test, <45 years, without alarm symptoms, and without non-steroidal anti-inflammatory drug use, 15% of endoscopies would have been saved, and one gastric ulcer and two oesophagitis would have been missed. Based on Helicobacter pylori IgG serology, 21% of endoscopies would have been saved. Finally, if endoscopy had been performed only in CagA+ patients, 31% of endoscopies would have been saved, missing one gastric ulcer and two cases of oesophagitis. CONCLUSIONS: In our geographical area, the test-and-scope strategy based on 13C-urea breath test or Helicobacter pylori IgG serology would have saved only 15-20% of endoscopies. Although some relevant pathology would have been missed, it is not of a malignant type. 13C-urea breath test is the preferred non-invasive method to be used in this strategy, while Helicobacter pylori IgG serology is of limited value due to its low accuracy. With the use of CagA serology a larger number of unnecessary endoscopic examinations can be avoided.     

Discrepancy between Helicobacter pylori stool antigen assay and urea breath test in the detection of Helicobacter pylori infection

Background. The reference diagnostic methods available for detection of Helicobacter pylori infection are either invasive (histology) or expensive and highly sophisticated (Urea Breath Test). A new enzyme immunoassay, which can be easily performed in any laboratory, has been developed to detect Helicobacter pylori in stool specimens (HpSA - Meridian Diagnostics, Cincinnati, USA). Aim of the study was to compare HpSA to Urea Breath Test.Patients and methods. A total of 125 patients (52 never treated for Helicobacter pylori infection and 73 after Helicobacter pylori eradication therapy) referring to our Department, underwent both tests within two weeks.Results. Contrasting results between the two tests were found in 30% of cases: in 19% of the untreated patients and in 37% of the treated patients (p<0.001). The main discrepancy consisted in positive HpSA associated with negative Urea Breath Test. Mean HpSA value in such conditions was 0.273 optical density, while in patients with both positive tests, it was 1.192 optical density. In untreated, but not in treated patients, raising the HpSA cut off value significantly decreased the percentage of conflicting results.Conclusions. Some disagreement was detected between HpSA and Urea Breath Test results, especially in treated patients. Possible explanations for our findings are a low HpSA cut off value together with the identification of Helicobacter pylori coccoid forms by the immunoassay but not by the urease based Urea Breath Test. The higher percentage of discrepancy detected in treated patients might support this hypothesis.     

Helicobacter pylori infection in subjects with acute ischaemic stroke

AIMS: To determine whether infection with Helicobacter pylori is a significant risk factor for stroke. SUBJECTS: A total 467 in-patients with clinical evidence of acute ischaemic stroke and 388 healthy controls with no evidence of cerebrovascular disease. METHODS: This was a case control study. The prevalence of Helicobacter pylori was measured by enzyme-linked immunosorbent assay in stroke patients and controls. A positive titre was defined as >15 U/ml and relationship with circulating plasma fibrinogen and social depravation was expressed using the Townsend Index. RESULTS: There were significantly more Helicobacter pylori positive individuals (274/398 (69%)) in the cases compared to the controls (206/352 (58.5%)). Fibrinogen levels were also significantly higher in Helicobacter pylori positive (mean 4.14, standard deviation 1.33) than negative individuals (mean 3.78, standard deviation 1.28). The association between Helicobacter pylori and stroke was lost in a logistic model controlling for socio-economic status. Furthermore, fibrinogen levels were not associated with Helicobacter pylori status in a linear regression model controlling for socio-economic status. CONCLUSIONS: Infection with Helicobacter pylori is associated with an increased risk of stroke and increased fibrinogen levels but these findings can be attributed to a confounding effect of socio-economic status.     

Severe acute gastritis associated with Helicobacter pylori infection

We describe the case of a young female referred to our unit because of acute upper abdominal symptoms. Upper gastrointestinal endoscopy showed a gastric picture resembling lymphoma or acute non-steroidal anti-inflammatory drug gastropathy (deep, large and irregular ulcers), but the clinical history and the histological examination of gastric biopsies were consistent only with acute gastritis Helicobacter pylori-correlated. The patient was treated with omeprazole and antibiotics with complete recovery. As the patient's cat had suffered from an acute gastrointestinal distress two weeks earlier, a case of zoonosis was hypothesized and an upper gastrointestinal endoscopy was performed also on the cat. Unfortunately, we were not able to detect Helicobacter pylori in the cat gastric mucosa, but only urease-producing spiral microorganisms. Possible sources of infection and pathogenetic mechanisms of the severe gastritis are discussed.     

Treatment of Helicobacter pylori infection. indications and regimens: an update

The management of Helicobacter pylori infection is still surrounded by controversy and uncertainties. Indications and correct application of current regimens for Helicobacter pylori infection are still considered a matter of debate. Regarding indications, only peptic ulcer and mucosa associated lymphoid tissue lymphoma are considered clear indications for treatment. In other conditions, such as atrophic gastritis, post gastric cancer resection, first-degree relatives of gastric cancer patients, dyspeptic patients, patients with gastro-oesophageal reflux disease and non-steroidal anti-inflammatory drug users, the value of Helicobacter pylori eradication is still controversial. The regimens for first-line and second-line treatment of Helicobacter pylori infection have been recommended by the Maastricht 2 Consensus Report. Although all the treatments are considered to be effective, physicians still do not agree on what first-line regimen should be used. Furthermore, a consensus on the duration of the antibiotic treatment is still lacking, although Maastricht guidelines for treatment of Helicobacter pylori infection recommend a one-week therapy. Also regimens, as a third-line treatment, and methods to improve compliance and clinical outcome are still a matter of debate. All these points will be considered in the present review.     

Helicobacter pylori diagnosis in patients with liver cirrhosis

BACKGROUND: In cirrhotics, Helicobacter pylori infection is the major cause of peptic lesions, which are an important cause of upper intestinal haemorrhage in these patients. However, some diagnostic methods are not accurate for H. pylori detection in cirrhotics. AIMS: The study assessed the accuracy of different diagnostic methods for H. pylori detection in cirrhotics with and without gastroduodenal lesions. METHODS: The study population comprised of 53 cirrhotics. All patients underwent upper endoscopy: three biopsies were taken in the antrum and three in the gastric body. Four biopsies were used for Giemsa staining, while two were used for a rapid urease test. A blood sample was obtained for serology using Western blotting, and a [13C]urea breath test was performed in all patients. Histological assessment was regarded as the gold standard for diagnosis of H. pylori infection. RESULTS: H. pylori infection was detected at histological assessment in 28 (52.8%) patients. The [13C]urea breath test, rapid urease test, and serology were positive in 27 (51%) patients, 23 (43.4%) patients, and 34 (64.1%) patients, respectively. Sensitivity and specificity were 92.9 and 96% for the [13C]urea breath test, 78.6 and 96% for the rapid urease test, and 78.6 and 52% for serology. CONCLUSIONS: The [13C]urea breath test is very accurate in cirrhotics, whilst both serology and the rapid urease test give disappointing results.     

Role of Helicobacter pylori infection in pernicious anaemia

Background. Pernicious anaemia is associated with atrophic body gastritis and considered an autoimmune disease. Whether Helicobacter pylori is involved in the induction of pernicious anaemia is uncertain.Aims. To investigate the prevalence of Helicobacter pylori infection in pernicious anaemia patients and to ascertain whether the Helicobacter pylori positive patients had distinctive clinical and gastric morphofunctional characteristics.Patients and Methods. A series of 81 consecutive pernicious anaemia patients underwent serological, functional and endoscopic/histological investigations.Results. A total of 49 (60.5%) patients were Helicobacter pylori-positive (males 61.2% vs females 38.8%). No difference was observed in clinical and morphofunctional characteristics between Helicobacter pylori-positive and negative patients, whereas distinctive functional/histological features between histologically Helicobacter pylori-positive (n=8) and serologically Helicobacter pylori-positive (n=41) cases were detected. In the histologically Helicobacter pylori-positive group, Pepsinogen I was higher [13 [0–58] vs 5 [0–26] ng/ml; P=0.0025]) and positivity for anti-parietal cell antibodies was lower [42.9% vs 76.9, P=0.0867). Antral histological variables of the gastritis score were significantly higher in the histologically Helicobacter pylori-positive than in the serologically Helicobacter pylori-positive patients, but this latter group had a higher score of body atrophy (2.63± 0.12 vs 1.71 ± 0.29; P=0.0051). Body inflammation was also significantly higher in the histologically Helicobacter pylori-positive group (chronic inflammation: 1.43±0.2 vs 1.05±0.06; P=0.0271; inflammation acitivity:: 0.57±0.3 vs 0.15±0.06, P=0.0220). Antral mucosa was normal in 24/41 (58.5%) of the serologically Helicobacter pylori-positive patients, but only in 1/8 (12.5%) of the histologically Helicobacter pylori-positive patients (p=0.232).Conclusions. Almost two thirds of pernicious anaemia patients have evidence of Helicobacter pylori, but only those with an active Helicobacter pylori infection have distinctive functional and histological features. These findings support the hypothesis that Helicobacter pylori infection could play a triggering role in a subgroup of pernicious anaemia patients.     

Dyspepsia and Helicobacter pylori infection: a prospective multicentre observational study

OBJECTIVES: Dyspepsia still represents an unsolved clinical enigma. AIM: The aims of this study were to determine whether symptoms and Helicobacter pylori infection are predictors of organic disease in uninvestigated dyspepsia, and if H. pylori eradication improves symptoms in functional dyspepsia. METHODS: An observational study was performed on outpatients with uninvestigated dyspepsia. Symptoms were scored and H. pylori status determined. Patients with functional dyspepsia and H. pylori infection were randomly given either a standard eradicating treatment or a 1-month course of empirical treatment. The latter was also given to functional dyspeptic patients without infection. Symptoms were re-assessed in functional dyspeptic patients at 2- and 6-month follow-up visits. Patients receiving eradicating treatment were re-tested for H. pylori at the 2 month visit. RESULTS: A total of 860 patients were studied and 605 (70.3%) were affected by functional dyspepsia. H. pylori infection was diagnosed in 71.8% of patients with organic dyspepsia and in 65.0% with functional dyspepsia (p=0.053). Male sex, anaemia, smoking habit, age over 45 years, and severe epigastric pain, but not H. pylori infection, were independent predictors of organic disease. Symptoms significantly improved in most functional dyspeptic patients regardless of their H. pylori status and type of treatment. CONCLUSION: H. pylori infection is not a strong predictor of organic disease in uninvestigated dyspepsia. H. pylori eradication is not essential to improve symptoms in functional dyspepsia.     

Hypersecretory duodenal ulcer and Helicobacter pylori infection: for-year follow-up study

Background. About 10% of duodenal ulcer patients are characterized by gastric acid hypersecretion with normal gastrin values. Relapsing duodenal ulcer after Helicobacter pylori cure has been related to high acid output and maintenance antisecretory therapy has been suggested in hypersecretory duodenal ulcer patients. The role of Helicobacter pylori infection and the effects of Helicobacter pylori cure in hypersecretory duodenal ulcer patients still remain to be fully studied.Aim. To study: a) whether gastric acid hypersecretion “per se” is a risk factor for duodenal ulcer recurrence; b) whether maintenance antisecretory therapy is necessary after eradication in hypersecretory duodenal ulcer patients.Patients. The study population comprised 8 hypersecretory duodenal ulcer patients, selected from a population of 79 Helicobacter pylori-positive duodenal ulcer patients.Methods. Hypersecretory duodenal ulcer patients were followed-up for at least 4 years after eradication. Gastric acid secretion was measured again 12 months after Helicobacter pylori eradication. Gastroscopy with histology was performed 3, 6, 12 and 36 months after treatment, ¹³C-urea breath test after 42 months; clinical questionnaires were completed every 6 months.Results. After eradication, despite a not significantly reduced high acid output (median value of basal acid output and pentagastrin-stimulated acid output, respectively, 23.1 mEg/h and 64. 1 mEg/h before treatment vs 16 mEg/h and 49.7 mEq/h 12 months after treatment), all patients were free from symptoms, none of them had duodenal ulcer relapse or complications (7/8 before treatment), or needed antisecretory maintenance therapy, except for one patient taking non-steroidal anti-inflammatory drugs.Conclusions. These findings, obtained in a selected population of hypersecretory duodenal ulcer patients with long-term follow-up, suggest that after successful Helicobacter pylori eradication gastric acid hypersecretion “per se” is not able to determine the recurrence of duodenal ulcer.     

Comparison of two new rapid serology tests for diagnois of Helicobacter pylori infection in Chinese patients

Background. Rapid serology test is a simple and convenient way for diagnosing Helicobacter pylori infection. However, performances of these tests are usually less satisfactory than expected, particularly in developing countries.Aim. To evaluate the performances of two newly developed rapid serology tests for Helicobacter pylori infection.Patients. Consecutive Chinese dyspeptic patients undergoing upper gastrointestinal endoscopy.Methods. Gastric biopsies were obtained from antrum and corpus for rapid urease test and histological examination. Diagnosis of Helicobacter pylori infection was based on two or more positive results in rapid urease test, histology and [¹³C] urea breath test. Patients' sera were tested against two rapid serology tests: ASSURE Hp Rapid Test (Genelabs Diagnostics, Singapore) and SureStep (Applied Biotech, San Diego, CA, USA).Results. A total of 148 patients were evaluated and Helicobacter pylori infection was diagnosed in 78 (53%) patients by gold standard. The sensitivities of ASSURE Hp and SureStep were, respectively, 94% and 71 % (p=0.0003). Specificities of the two test kits were both 90%. The overall accuracy of ASSURE Hp was significantly higher than SureStep (92% versus 80%, P=0.004).Conclusion: Both rapid serology tests appear to be specific in diagnosing Helicobacter pylori infection in the Chinese populations. However, the ASSURE Hp test is more sensitive and accurate than the SureStep test.     

Effect of Helicobacter pylori infection on gastric cell proliferation and genomic instablity in a paediatric population of Southern Italy

Background. The incidence of gastric cancer is high in areas with a high prevalence of Helicobacter pylori infection. Cell transformation and tumour progression occur over a long period of time and markers of genomic instability usually precede morphological changes.Aim. To evaluate the effect of Helicobacter pylori infection on cell proliferation, DNA status and oncogene expression in children.Patients and Methods. Morphometric and immunohistochemical techniques were used to analyse DNA content, p53 and c-myc oncogene expression and cell proliferation on gastric biopsies of 53 children (27 Helicobacter pylori-negative and 26 Helicobacter pylori-positive).Results. Gastric mucosa was normal in 11 % of Helicobacter pylori-positive and in 33% of Helicobacter pylori-negative subjects. Most children had chronic non-atrophic gastritis regardless of Helicobacter pylori infection, and only a minority of children affected by Helicobacter pylori had mild atrophic gastritis. Cell proliferation was significantly higher in children with Helicobacter pylori-positive gastritis than in those with Helicobacter pylori-negative gastritis. No metaplasia, dysplasia, p53 overexpression or altered DNA content was found in any child. Interestingly, 46% of children with and 29% without Helicobacter pylori infection had c-myc overexpression closely related to the cell proliferation rate.Conclusion. Helicobacter pylori infection in children may coexist with a normal gastric mucosa, and it is not associated with genomic instability markers in cases of chronic gastritis.     

Probiotic intervention decreases serum gastrin-17 in Helicobacter pylori infection

BACKGROUND: Previously we showed that a probiotic combination with L. rhamnosus GG was beneficial as an adjuvant therapy during H. pylori eradication. AIM: To evaluate whether probiotic combination with LGG adheres to the upper gastrointestinal mucosa and modifies H. pylori colonisation and H. pylori induced inflammation. METHODS: Thirteen patients referred for gastroduodenoscopy received a drink consisting of equal doses (2.5x10(9)CFU) of LGG, L. rhamnosus LC705, Propionibacterium freudenreichii JS and Bifidobacterium lactis Bb12 daily. Recovery of probiotics in biopsies (antrum, corpus, duodenum) and faecal samples was evaluated by strain-specific quantitative polymerase chain reaction. H. pylori colonization and gastric inflammation was investigated by urease activity ((13)C-urea breath test), histology and serum pepsinogen I, II and gastrin-17 measurements. RESULTS: Twelve patients were fully investigated; of these three of the patients had LGG adhering to the biopsies at end of the intervention. Other probiotic strains were not detected, even though the recovery of all individual probiotic strains from the faeces was significantly increased (p<0.01). After the treatment, the level of (13)C-urea breath test (p=0.063) and gastrin-17 (p=0.046) decreased. CONCLUSIONS: The decreases in (13)C-urea breath test and gastrin-17 indicate that the probiotic combination exerts a beneficial effect on gastric mucosa in H. pylori infected patients. LGG showed marginal ability to adhere to the upper gastrointestinal tract mucosa.     

Helicobacter pylori infection in patients with liver cirrhosis: facts and fictions

Helicobacter pylori infection could play a role in different clinical alterations observed in cirrhosis, from gastroduodenal lesions to hepatic encephalopathy. Although its prevalence in cirrhotics is similar to that in controls, H. pylori infection is responsible for the increased prevalence of peptic ulcer observed in these patients. The ammonia production by H. pylori urease does not seem to increase blood ammonia levels during cirrhosis, indicating that its role in hepatic encephalopathy could be marginalized in clinical practice. Dual and triple therapies have been shown to be equally effective for H. pylori eradication in these patients.     

Primary and secondary antibiotic resistance of Helicobacter pylori strains isolated in central Italy during the years 1998–2002

BACKGROUND: Antibiotic resistance of Helicobacter pylori is the most common reason for failure in its eradication. AIM: To determine the incidence of primary and secondary resistance to tinidazole, clarithromycin and amoxycillin in Helicobacter pylori isolates from dyspeptic patients in central Italy and to evaluate the modifications of resistance over the period from 1998 to 2002. METHODS: H. pylori strains were isolated from antral biopsies taken during upper endoscopy in 406 dyspeptic patients with no previous therapy against H. pylori, and in 96 patients who had already undergone one or more triple therapies. Antibiotic susceptibility test was performed using the screening agar method and agar dilution method. RESULTS: Overall primary resistance to tinidazole, clarithromycin and amoxycillin was 36.7, 23.4 and 0.2%, respectively. Secondary resistance rates were: tinidazole 69.8%, clarithromycin 82.3% and amoxycillin 1%. Resistance to clarithromycin was often associated with tinidazole resistance and was significantly higher in female patients (p<0.05). Primary and secondary antibiotic resistance did not change during the 4 years of observation. CONCLUSIONS: The dyspeptic population with H. pylori infection in central Italy shows high levels of antibiotic resistance. Primary resistance to clarithromycin is most frequent in female patients. In patients with secondary resistance, dual resistance to clarithromycin and tinidazole is found in the majority of cases.     

Breath test is very reliable for diagnosis of Helicobacter pylori infection in real clinical practice

AIMS: To determine the accuracy of the most common available tests for the diagnosis of Helicobacter pylori infection in an unselected and untreated population of patients. PATIENTS AND METHODS: Prospective study including 314 unselected patients from a population of 814 patients referred for upper endoscopy at one hospital. H. pylori infection was diagnosed by rapid urease test (RUT), histology, culture and 13C-urea-breath test (UBT) and serum IgG (EIA). H. pylori infection was defined as positive if culture or at least two of the other tests were positive. RESULTS: The prevalence of H. pylori infection in this population was 72%. The diagnostic test with the greatest combination of sensitivity (97%) and specificity (100%) was the UBT. EIA had a good sensitivity (96%), but it was the test with the least specificity (71%). RUT, histology and culture showed a high specificity (>98%) but a sensitivity lower than 90%. In elderly patients (>65 years old, n=120), UBT was also the test with the greatest combination of sensitivity (94%) and specificity (100%). CONCLUSIONS: In conditions of real clinical practice the 13C-urea-breath test is a reliable test for H. pylori diagnosis, both in young and elderly patients.     

Two new treatment regimens for Helicobacter pylori eradication: a randomised study

BACKGROUND: Several studies have found a fairly low Helicobacter pylori eradication rate using a standard 7-day triple therapy in Italy. Recently, two new therapeutic schedules have been proposed with an eradication rate higher than 90%. This study compared the efficacy of these two treatment regimens. PATIENTS AND METHODS: A total of 131 patients with Helicobacter pylori infection and either non-ulcer dyspepsia (73 patients] or peptic ulcer (58 patients) were enrolled. Helicobacter pylori infection was assessed by rapid urease test and histology on gastric biopsies. Patients were randomised to receive either a 5-day course of ranitidine bismuth citrate 400 mg bid, clarithromycin 500 bid, and tinidazole 500 bid, or a 10-day course of omeprazole 20 mg bid plus amoxycillin 1 g bid for the first 5 days, and omeprazole 20 mg bid, clarithromycin 500 mg bid and tinidazole 500 mg bid for the remaining 5 days. Eradication was assessed by endoscopy 4-6 weeks after therapy. RESULTS: Overall, 4 patients (2 for each treatment group) were lost to follow-up. Helicobacter pylori eradication rates were 67.2% (95% confidence interval: 55.7-78.7) and 65.2% (95% confidence interval: 53.7-76.6) at per protocol and intention-to-treat analyses, respectively, after the 5-day regimen, and 96.8% (95% confidence interval: 92.5-100) and 93.8% (95% confidence interval: 88-99.7) after the 10-day regimen (p<0.05). Both treatments were well tolerated, and no major side-effects were reported. CONCLUSIONS: The 5-day regimen gave disappointing results, while the eradication rate after the 10-day regimen was very high.     

Seroprevalence and epidemiology of Helicobacter pylori infection in patients with cirrhosis

Background: Helicobacter pylori infection is the major pathogenic factor for peptic ulcer disease. Its epidemiology is not fully known; few data are available in patients with chronic liver disease.Aims: To investigate the seroprevalence and factors associated with Helicobacter pylori infection in a series of liver cirrhosis patients.Methods: Two hundred and twenty consecutive patients were prospectively included in a study aimed to evaluate the effect of dietary intervention on cirrhosis complications and survival. At inclusion, an epidemiological and clinical questionnaire was completed. Sera were obtained and stored at −70°C until analyzed. They were tested for Helicobacter pylori antibodies using a commercial ELISA kit.Results: Eleven out of 220 patients had borderline anti-Helicobacter pylori IgG titers. Of the remaining 209 patients, 105 (50.2%) showed positive titers of Helicobacter pylori IgG. Univariate analysis showed that Helicobacter pylori infection was more frequent in older patients, those born outside Catalonia, and in patients with a low educational level. Past ethanol consumption and current smoking correlated negatively with Helicobacter pylori infection. Multivariate analysis selected age (OR 3.1, 95% CI 1.46–6.45), educational level (OR 2.2. 95% CI 1.18–4.2) and alcohol consumption (OR 0.7 95% CI 0.45–0.99) as the variables independently related to Helicobacter pylori infection.Conclusions: Helicobacter pylori infection in cirrhosis has the same epidemiological pattern as in the general population. Suggestions that the etiology or the severity of the liver disease could be related to Helicobacter pylori infection were not confirmed by our study.     

Natural history of Helicobacter pylori infection

This report describes the modalities of chronic gastritis induced by Helicobacter pylori infection in different populations. The full gamut of lesions representing the precancerous cascade is very prevalent in populations of low socioeconomic background experiencing very high gastric cancer risk, as seen in the Latin American Andes Mountains. In populations of high socioeconomic standards and high cancer risk, such as Japan and Korea, the precancerous cascade predominates and “early” cancers are also diagnosed frequently. Some reports describe frequent corpus atrophy, not prominent in the former group. The so-called African enigma is seen in populations of low socioeconomic standards, usually living at low altitudes, with high prevalence of infection but low frequency of cancer and precancerous lesions. In populations in transition from high to low cancer risk, duodenal ulcer and antral non-atrophic gastritis are frequently seen. In affluent societies at low risk of cancer, such as Western Europe, Australia and North America, mild non-atrophic gastritis associated with low virulence Helicobacter pylori genotypes predominate. The varied phenotypes of gastritis may reflect secular changes in the ecology of our species.