Vaccine against Helicobacter pylori?

The burden of illness caused by Helicobacter pylori is considerable, and there is little doubt that a therapeutic vaccine would be very useful. However, the merits of using a prophylactic vaccine to eradicate H. pylori from the human population are debatable in light of arguments that it may act as a beneficial commensal organism for many of its human hosts. With regard to the practical side of designing vaccines against H. pylori, animal models have shown us that both therapeutic and prophylactic vaccines are feasible despite the fact that, as in human hosts, immune responses raised naturally to H. pylori cannot eradicate the infection. Many advances have been made in developing optimal vaccination protocols, and recently the first human trial of a therapeutic vaccine, which showed limited but nevertheless encouraging results, was published. However, a possibly quite serious problem is that prophylactic and perhaps also therapeutic vaccines may themselves cause disease.     

Helicobacter pylori: aggressor or innocent bystander?

Helicobacter pylori seeks gastric mucosa, whether found in the stomach, duodenum, or Barrett's esophagus. Definitive diagnosis can be secured by appropriate stains of mucosal biopsies and culture, but the rapid urease test, breath isotope studies, and serologic testing are also useful. The frequency of colonization increases with advancing age, but infection occurs earlier in underdeveloped countries. Although the reservoir is uncertain, water or food transmission seems likely. There is sufficient evidence to assign an etiologic role to the bacteria in the causation of type B antral gastritis. H. pylori is found in areas of gastric metaplasia within the duodenum and is associated with duodenitis. Although acute infection leads to hypochlorhydria, chronic colonization has little effect on acid secretion. Studies have thus far failed to establish a convincing relationship between H. pylori and nonulcer dyspepsia, although the bacteria may play a role in selected patients. H. pylori is found in association with most idiopathic gastric and duodenal ulcers, but it is unclear as to whether the bacteria plays a causative or permissive role. The organism has a predilection for intercellular spaces and the mucous layer, thus affording relative isolation from luminally active antibiotics. Monotherapy with bismuth preparations transiently eliminates the bacteria, but recolonization is rapid, probably due to regrowth of sequestered organisms. A combination of metronidazole, bismuth, and tetracycline (or amoxicillin) affords the best eradication rate, but the potential side effects of this program should be considered. The present therapy of duodenal ulcer disease is effective and without significant risk. Treatment of H. pylori should be reserved for those patients who relapse on adequate maintenance therapy. If a safe and effective antibiotic becomes available, more frequent testing and earlier treatment intervention may become more attractive. H. pylori is probably an "innocent bystander" for most patients, but the bacteria may sufficiently impair the defenses of the antral and duodenal mucosa to facilitate the development and relapse of ulcer disease in subsets of patients.     

Intrastrain Differences in Helicobacter pylori: A Key Question in Mucosal Damage?

Helicobacter pylori causes persistent infection and inflammation in the human stomach, yet only a small fraction of infected people develop Illness. An important question is why this diversity exists in infection outcome. In recent years, there has been evidence of substantial phenotypic as well as genotypic diversity of H. pylori. Three different phenotypes — production of vacuolating cytotoxin, presence of cagA, and ability for strong PMN activation — appear to be linked to one another and to the propensity for a H. pylori strain to cause peptic ulcer disease. Further investigation in this field may help to define which infected people bear the highest risk for serious clinical consequences, and ultimately to define optimal vaccine candidates and strategies.     

Helicobacter pylori Infection in Estonian Population: Is It a Health Problem?

The role of Helicobacter pylori infection In traditionally noncommunicable diseases as chronic gastritis, peptic ulcer and gastric carcinoma became more evident during the first decade of H. pylori studies. To analyse and evaluate the prevalence of H. pylori infection in Estonia as a population health problem, the data of three randomly selected samples of Estonian population aged over 15 years were used. The infection rate assessments in two representative samples of the population (Kambja 157 persons and Kuressaare 224 persons) were based on H. pylori colonization in the gastric mucosa, and in one sample (Karksi-Nula 1467 persons) on seroconversion of H. pylori IgG antibodies. The persons studied were divided into groups according to birth cohorts. The population studies in Estonia showed a high prevalence of H. pylori infection among Estonians: 73% in the Kuressaare sample, 78% in the Kambja sample, and 87% in the Karksi-Nuia sample. From the Kuressaare population sample 38 families with 290 persons were included in a family H. pylori infection study and 92.5% of the persons in these families were found to be H. pylori positive. H. pylori infection was frequent in persons who were born at the beginning of this century as well as in those born after World War II up to 30 years ago. It was concluded that H. pylori infection is common in Estonia, both in random persons and their families. It is probable that the infection rate of H. pylori depends to a great extent on the socioeconomic conditions of this country and that acquisition of H. pylori in Estonia starts at an early age.     

Helicobacter pylori: what schemes of eradication are essential today?

Current approaches to treatment of Helicobacter pylori infection, basic international recommendations, problems of growing H. pylori resistance to antibiotics are reviewed. Much attention is given to prospects of new eradication schemes, for example combinations based on bismuth tripotassium dicitrate and successive treatment schedules.     

What Are the Specific Features of Helicobacter pylori Gastritis in Children?

Children with recurrent abdominal pain and dyspeptic symptoms often present histological gastritis and Helicobacter pylori infection. No specific symptomatology has been found, however, to discriminate H. pylori positive from negative subjects. Certain differences exist in gastritis in paediatric age groups, in comparison with adults. In terms of treatment, children also form a special entity because of the long exposure time of H. pylori infection. This article describes the typical findings of H. pylori gastritis in children and discusses their significance from a clinical point of view.     

Detection of Helicobacter pylori infection: when to perform which test?

This paper reviews current diagnostic techniques for Helicobacter pylori infection and critically questions their value under different diagnostic circumstances. As long as we do not have general treatment recommendations for H. pylori infection, endoscopy is still the basis for primary diagnosis because it assesses therapy indications. In addition, histology characterizes the gastroduodenal lesions observed and may reveal malignant diseases. New rapid urease tests from the biopsies are inexpensive, simple, and quick giving results reliably within 1 h. Culturing H. pylori from gastric samples after therapy failure and testing the strains for antimicrobial susceptibility is becoming increasingly important with higher prevalence of drug resistances. Nonendoscopic tests are more convenient to the patient. Serological tests inexpensively detect circulating IgG or IgA antibodies. However, inspite of the cost attractiveness, serology might be problematic in indicating present H. pylori infection. The tests of choice for noninvasive monitoring therapy success or failure are the 13C-urea breath test and the faecal antigen immunoassay. Both tests are also of value for first diagnosis in children when endoscopy is not indicated. In the future, serological detection of virulence factors and polymerase chain reaction with molecular fingerprinting might help to identify H. pylori strains with high pathogenicity or antibiotic resistance.     

Serum pepsinogen C: A useful marker of Helicobacter pylori eradication?

Medical treatment for Helicobacter pylori (Hp) infection is now recommended in several types of gastroduodenal disease, and its success is usually monitored by hystology. The end-points of our work were to identify the most suitable serum index of Hp eradication among pepsinogen A (PGA), pepsinogen C (PGC), PGA/PGC ratio, gastrin, and IgG anti-Hp (IGG). We studied a total of 289 Hp positive (Giemsa staining) patients, who were treated with 40 mg/day omeprazole (140 cases) or with 480 mg/day bismuth subsalicylate (149 cases) for 4 weeks. All the patients also received 1 g/day metronidazole + 2 g/day amoxycillin for the first 2 weeks of treatment. Two months after the end of therapy, the patients underwent a second endoscopy and Hp histological assessment: the infection was eradicated in 192 and still present in the remaining 97 subjects. Gastrin, PGA, PGC, and IGG were measured before and after therapy. All indices significantly decreased after therapy in eradicated patients, while PGA and gastrin significantly decreased after therapy in both eradicated and noneradicated patients, although in the latter group the variations were less pronounced. We calculated the per cent decrease of the studied indices. PGC, with a decrease of more than 25%, was found to be the most accurate biochemical index. Variation in PGC levels before and after treatment were correlated with corresponding variations in Hp bacterial load. In conclusion, between the different biochemical parameters evaluated, PGC showed the highest clinical efficiency. © 1996 Wiley-Liss, Inc.     

The prevalence of Helicobacter pylori: are emergency medicine residents at risk?

Helicobacter pylori is strongly associated with peptic ulcer disease and gastric cancer. It is a cause of chronic active gastritis. Our hypothesis was that Emergency Physicians might be at increased risk for infection due to their exposure to gastric contents from procedures performed in the Emergency Department. Our goal was to test a group of Emergency Physicians for H. pylori infection. In this cross sectional study, we tested a group of volunteers from an Emergency Medicine residency program for H. pylori infection by serum analysis for IgG. A matched control group was also tested. Forty-five subjects were enrolled; one subject's sample was lost. Three of 44 subjects (6.8%) were positive for H. pylori antibodies. Seven of 44 controls (15.9%) tested positive. Thus, Emergency Physicians do not have increased H. pylori infection rates and may be at less risk than the general population. Routine testing is not recommended.     

An observational study of upper gastrointestinal bleeding in intensive care units: is Helicobacter pylori the culprit?

OBJECTIVE: Upper gastrointestinal bleeding (UGIB) related to stress ulcers was formerly a fearsome complication of intensive care. The incidence of this event has decreased over the years. However, the morbidity, mortality, and causes of UGIB, particularly the etiologic role of Helicobacter pylori infection, are still controversial. Therefore, we prospectively assessed the incidence of UGIB in the intensive care unit (ICU) and evaluated the role of H. pylori infection. DESIGN: A prospective observational study followed by a case-control study. SETTING: Seven ICUs in the Paris area, five of them located in teaching hospitals. PATIENTS: All patients admitted consecutively to seven ICUs during a 1-year period were monitored for signs of clinically relevant UGIB. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Only cases of endoscopically confirmed UGIB were analyzed. Patients whose hemorrhage originated from the stomach and/or duodenum were tested for H. pylori infection, by means of serology, histologic examination, and stool antigen detection. The possible association between H. pylori and UGIB was examined in a case-control study. Twenty-nine of the 4,341 patients admitted to the seven ICUs during the study period had clinically relevant, endoscopically confirmed UGIB (incidence, 0.67%; 95% confidence interval, 0.56%-0.77%). Ulcers were most frequently observed endoscopically. Patients who bled had a higher Simplified Acute Physiology Score (SAPS II) at admission (mean +/- sd, 47 +/- 14 vs. 36 +/- 28; p < .001). Despite a higher in-ICU mortality rate among patients who bled (73% vs. 16%; p < .001), death was never due to bleeding. H. pylori infection was more frequent in patients who bled than in matched controls (36% vs. 16%; p = .04). CONCLUSIONS: Clinically relevant, endoscopically confirmed UGIB is a rare event in the ICU setting and tends to occur in severely ill patients. H. pylori infection is more frequent in patients with gastroduodenal hemorrhage than in nonbleeding patients.     

Geographical Pathology of Helicobacter pylori Infection: Is There More than One Gastritis?

Helicobacter pylori is the aetiological agent of chronic gastritis and a major causative factor in duodenal and gastric peptic ulcer disease; a strong association also exists with gastric cancer and primary gastric lymphoma. The prevalence of infection in adults ranges from less than 15% in developed countries to virtually 100% in less developed areas. If H. pylori infection alone was responsible for the development of gastritis, peptic ulcer disease, gastric carcinoma and primary gastric lymphoma, one would expect the frequency of all these conditions to parallel closely the prevalence of H. pylori infection. This is clearly not the case: therefore, genetic, environmental and cultural factors must act in concert with H. pylori to induce different outcomes of the infection.

This paper outlines the geographic approach to the study of disease and discusses the possible application of this methodology to the inquiry into the relationship between H. pylori, atrophic gastritis and gastric cancer. Preliminary results of a study showing great variation in the prevalence of intestinal metaplasia in duodenal ulcer patients from different geographic origin are presented and briefly discussed.