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Several studies have shown that Helicobacter pylori eradication rates with standard 7-day triple therapy are unsatisfactory. A novel 10-day sequential treatment regimen recently achieved a significantly higher eradication rate. To improve the pharmacotherapeutic cost, we evaluated whether an acceptable eradication rate could be achieved in peptic ulcer patients by halving the dose of clarithromycin.

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.

Helicobacter pylori infection persists in a considerable proportion of patients after both first- and second-line current treatments. A standard therapy for re-treatment in such refractory patients is still lacking. This study aimed to evaluate the efficacy of a levofloxacin-amoxycillin combination in patients who previously failed two or more therapeutic attempts.

Background and objectivesHelicobacter pylori (HP) is an endemic pathogenic bacterium causing gastritis and gastroduodenal ulceration in humans and is linked to the development of gastric malignancies. These first human in vivo studies investigated the photoeradication of HP using laser and white light.Study design/materials and methodsIn 13 HP-positive volunteers, a zone of gastric antrum was irradiated with laser (410 nm, 50 J/cm(2)) or endoscopic white light (10 J/cm(2)) 45 minutes after oral 5-aminolevulinic acid (5-ALA) 20 mg/kg. HP-eradication was assessed by biopsy urease test and HP-culture from irradiated and control zones 5 minutes, 4 and 48 hours post-irradiation.ResultsA maximum eradication effect was achieved at 4 hours post-irradiation when 85% of biopsies in the monochromatic and 66% in the white light exposed zones, and 58 and 33% in the respective control zones were HP-negative.ConclusionsHP numbers were greatly reduced following exposure to 5-ALA and either laser or white light in vivo. Photoeradication appears feasible, but further light dosimetry and the development of convenient application methods is required.

El descubrimiento por Warren y Marshall, en 1982, del Helicobacter pylori, inicialmente denominado Campylobacter pylori, constituyó una revolución en el conocimiento de la fisiopatología de la úlcera gastroduodenal, al quedar demostrada su asociación causal. En la actualidad, se ha comprobado que este bacilo gramnegativo, espirilar y microaerofílico tiene una importancia patogénica como causante de úlcera gastroduodenal, gastritis, linfoma gástrico tipo MALT, además de incrementar nueve veces el riesgo de desarrollar un adenocarcinoma gástrico, elementos que han condicionado la necesidad de establecer un tratamiento erradicador de este microorganismo. Se revisan las terapéuticas erradicadoras actuales y se recomienda, para nuestro país, el uso de una pauta donde se combina un agente antisecretor (cimetidina o ranitidina) junto con dos antibióticos (metronidazol y tetraciclina) por su elevada tasa de erradicación y baja incidencia de efectos adversos.

A multicentre study was carried out in order to validate the E test in comparison with the reference agar dilution method for testing the susceptibility of Helicobacter pylori to amoxicillin, clarithromycin, and metronidazole. Ten clinical isolates and one control collection isolate ( Helicobacter pylori ATCC 43504) were tested blindly at four centres according to a uniform methodology. The E test showed excellent intra- and inter-laboratory correlations with the agar dilution method for amoxicillin and clarithromycin (>98% agreement within 2 log(2) dilution steps). For metronidazole, however, the E test revealed significantly higher minimum inhibitory concentration values (>2 log(2)) against 5 of the 10 Helicobacter pylori strains tested. Overall, neither method was found reliable for testing the susceptibility of Helicobacter pylori to metronidazole, since both tended to lack reproducibility.

Helicobacter pylori urease activity is a potential source of ammonia in the stomach of patients with cirrhosis. However, the possible role of H. pylori in the pathogenesis of hepatic encephalopathy deserves further investigations. The current study evaluates the relationship among H. pylori infection, gastric juice ammonia concentrations, and arterial ammonia levels in patients with cirrhosis. Overall, 14 patients with cirrhosis with overt hepatic encephalopathy, 19 with subclinical hepatic encephalopathy, and 13 without encephalopathy were enrolled. All patients underwent upper endoscopy, and gastric biopsy specimens were taken for H. pylori assessment (rapid urease test, histology, and culture). A gastric juice sample and an arterial blood sample were obtained for ammonia level assessment. Patients with overt encephalopathy had both higher arterial ammonia levels and a more severe hepatic impairment than the remaining patients, whereas gastric juice ammonia concentrations did not differ among the three groups. H. pylori prevalence was similar among groups. Patients with H. pylori infection had significantly higher gastric juice ammonia concentrations than those without infection (2.3 +/- 1.3 vs. 0.9 +/- 0.6 mmol/L, respectively; p = 0.003); however, no difference in arterial ammonia levels emerged between the two groups (37.7 +/- 18.6 vs. 37.6 +/- 18.8 micromol/L, respectively). No significant correlation was found between gastric juice ammonia concentrations and arterial ammonia levels. The data suggest that liver impairment remains crucial in ammonia disposal in patients with cirrhosis, whereas H. pylori infection does not seem to play a major role in the pathogenesis of hyperammonemia in these patients.

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Moxifloxacin is a broad spectrum fluoroquinolone with single daily administration, currently used, above all, for respiratory tract infections.

Previous studies showed that either the urease activity possessed by H. pylori and the bacterial load may influence the results of the [13C] urea breath test. However, the correlation between urease activity and dyspepsia is unclear. The aim of our study was to evaluate whether the urease activity of the gastroduodenal tract may influence the severity of dyspeptic symptoms. In all, 2520 dyspeptic patients (1109 men, 1411 women; mean age 47 +/- 16 years) without gastroesophageal reflux disease, diabetes, vascular disorders, liver and biliary tract diseases, and tumors of the gastrointestinal tract and with a normal appearing abdominal ultrasonography were enrolled. All these patients underwent a [13C] urea breath test and filled out a questionnaire on dyspeptic symptoms. Subjects were divided in five different groups according to delta over baseline (DOB) values (group 1 < 3.5, group 2 = 3.5-6; group 3 = 6.1-11, group 4 = 11.1-23, group 5 > 23.1). The prevalence and intensity of dyspeptic symptoms were compared among groups. In all, 1688 patients (67%, 928 females and 760 males; mean age 48 +/- 15 years) were H. pylori-positive. The chi-squared test and analysis of variance showed increase of frequency and intensity of each dyspeptic symptom according to DOB values. In conclusion, Dyspepsia may parallel gastric urease activity. However, whether higher DOB values are related to higher bacterial load or, alternatively, to the presence of particular H. pylori strains able to produce larger amounts of urease is uncertain.

Chronic Helicobacter pylori infection and migraine: a case-control study" (Pinessi L, Savi L, Pellicano R, et al. Headache. 2000;40:836-839

Hepatitis C virus (HCV) has been localized in several extra-hepatic sites. Recent evidence suggests that the stomach can harbour HCV. We therefore evaluated the prevalence of gastric localization of HCV and its possible relationship with the chronic inflammatory response to Helicobacter pylori infection.

Several studies show that probiotics may prevent side effects during therapy against Helicobacter pylori (H. pylori). Other reports indicate competitive interaction between some probiotics and H. pylori. We compared efficacy of two different probiotics and one probiotic combination with placebo for preventing anti-H. pylori therapy-related side effects and for improving the eradication rate.

Background and objectivesHelicobacter pylori (HP) is an endemic pathogenic bacterium causing gastritis and gastroduodenal ulceration in humans and is linked to the development of gastric malignancies. These first human in vivo studies investigated the photoeradication of HP using laser and white light.Study design/materials and methodsIn 13 HP-positive volunteers, a zone of gastric antrum was irradiated with laser (410 nm, 50 J/cm(2)) or endoscopic white light (10 J/cm(2)) 45 minutes after oral 5-aminolevulinic acid (5-ALA) 20 mg/kg. HP-eradication was assessed by biopsy urease test and HP-culture from irradiated and control zones 5 minutes, 4 and 48 hours post-irradiation.ResultsA maximum eradication effect was achieved at 4 hours post-irradiation when 85% of biopsies in the monochromatic and 66% in the white light exposed zones, and 58 and 33% in the respective control zones were HP-negative.ConclusionsHP numbers were greatly reduced following exposure to 5-ALA and either laser or white light in vivo. Photoeradication appears feasible, but further light dosimetry and the development of convenient application methods is required.

A multicentre in vitro survey was carried out in 1998 in 22 European centres in order to assess the variation in the prevalence of Helicobacter pylori resistance. The susceptibility of 1,274 isolates to metronidazole, clarithromycin and amoxicillin was determined by the E test. The mean rate of resistance to metronidazole was 33.1% (95% CI, 7.5-58.9), to clarithromycin 9.9% (95% CI, 0-28.1) and to amoxicillin 0.8% (95% CI, 0-8.9). Resistance to metronidazole was significantly higher in females (P<0.001), while resistance to clarithromycin was significantly higher in children and teens (P<0.05). Resistance to both agents also tended to be higher in strains isolated from patients from southern European countries than in those isolated from patients from central or northern Europe. Overall, these results emphasize the need for further surveys of Helicobacter pylori sensitivity to antibiotics at a national and regional level.

The aim of this study was to design and evaluate a modified Ussing chamber, that makes use of constant air suction (modified Ussing air suction chamber, MUAS) for fixation of biopsy specimens. Standard size forceps biopsies were taken from the descending part of duodenum from patients undergoing endoscopy. Short circuit current (SCC) and conductance (G) were measured during basal conditions and after addition of different sugars and secretagogues. Histologic examination was performed to determine the degree of tissue damage after study in the chamber. Basal SCC was 54.7 +/- 4.3 microA x cm(-2) and G was 58.7 +/- 4.7 mS x cm(-2) (mean +/- SEM, n=48) and steady values of these parameters were observed for at least 2 h. Reproducible and steady responses in SCC were obtained with D-glucose (SCCmax=172 +/- 22.1 microA x cm(-2); EC50=6.9 +/- 0.7 mM, n=5) and D-galactose (SCCmax=233 +/- 55.7 microA x cm(-2); EC50=9.2 +/- 0.7 mM, n=3), and secretory responses with 5-hydroxytryptamine, 100 microM (DeltaSCC= 16.1 +/- 3.8 microA x cm(-2), n=10), histamine, 100 microM (DeltaSCC=24.0 +/- 4.1 microA x cm(-2), n=10) and prostaglandin E2, 1 microM (DeltaSCC=30.3 +/- 5.4 microA x cm(-2), n=6). Experimental biopsy specimens showed intact surface epithelium by histologic examination and did not differ from controls apart from minor indications of edge damage. No difference in basal electrical parameters and D-glucose fluxes were found between Helicobacter pylori positive and negative patients. Our data suggests that the MUAS chamber represents a promising alternative approach to measure transport processes in intestinal endoscopic biopsies.

The aim of this study was to design and evaluate a modified Ussing chamber, that makes use of constant air suction (modified Ussing air suction chamber, MUAS) for fixation of biopsy specimens. Standard size forceps biopsies were taken from the descending part of duodenum from patients undergoing endoscopy. Short circuit current (SCC) and conductance (G) were measured during basal conditions and after addition of different sugars and secretagogues. Histologic examination was performed to determine the degree of tissue damage after study in the chamber. Basal SCC was 54.7 +/- 4.3 microA x cm(-2) and G was 58.7 +/- 4.7 mS x cm(-2) (mean +/- SEM, n=48) and steady values of these parameters were observed for at least 2 h. Reproducible and steady responses in SCC were obtained with D-glucose (SCCmax=172 +/- 22.1 microA x cm(-2); EC50=6.9 +/- 0.7 mM, n=5) and D-galactose (SCCmax=233 +/- 55.7 microA x cm(-2); EC50=9.2 +/- 0.7 mM, n=3), and secretory responses with 5-hydroxytryptamine, 100 microM (DeltaSCC= 16.1 +/- 3.8 microA x cm(-2), n=10), histamine, 100 microM (DeltaSCC=24.0 +/- 4.1 microA x cm(-2), n=10) and prostaglandin E2, 1 microM (DeltaSCC=30.3 +/- 5.4 microA x cm(-2), n=6). Experimental biopsy specimens showed intact surface epithelium by histologic examination and did not differ from controls apart from minor indications of edge damage. No difference in basal electrical parameters and D-glucose fluxes were found between Helicobacter pylori positive and negative patients. Our data suggests that the MUAS chamber represents a promising alternative approach to measure transport processes in intestinal endoscopic biopsies.

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.

Following standard triple therapy, up to 20% of patients require further Helicobacter pylori eradication treatment. Data regarding the efficacy of re-treatment in these patients are scarce.

An increased risk for gastric cancer in patients with liver cirrhosis has recently been reported. This study was performed in order to determine gastric epithelial cell proliferation in cirrhotic patients and to evaluate the role of congestive gastropathy (CG) and Helicobacter pylori infection in this process. Thirty-six cirrhotic patients and 18 controls were enrolled in the study. All patients underwent endoscopy and three biopsies were performed in the antrum and three in the gastric body. The presence of H. pylori infection was assessed by a rapid urease test and histology. The antral biopsies were used for gastric cell proliferation assessment by an immunohistochemical analysis (Ki-67). There was no significant difference in epithelial cell proliferation between cirrhotics and controls. Gastric proliferation values were higher in patients with H. pylori infection compared with uninfected patients, both in cirrhotic (P = 0.003) and in control groups (P = 0.06). Among the cirrhotic group, we found a progressive increase in gastric cell proliferation values related to the degree of CG, the highest values being observed in cirrhotic patients with severe CG. Moreover, cirrhotics with both severe CG and H. pylori infection had the highest proliferation values when compared with all other subgroups. In conclusion, this study found that: (1) CG significantly affects epithelial cell proliferation in gastric mucosa in cirrhotic patients, (2) H. pylori infection plays a similar role in gastric cell proliferation in both cirrhotic and non-cirrhotic patients, and (3) CG and H. pylori could act synergistically in this process.

Although high prevalences of both chronic inflammation (carditis) and intestinal metaplasia at the gastric cardia have been reported, the pathogenesis is still unclear. This study assesses the role of Helicobacter pylori (H. pylori) infection and symptoms of gastroesophageal reflux disease (GERD) in these histological alterations.

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Iron-deficiency anaemia is a frequent finding in coeliac disease. Recent investigations have identified Helicobacter pylori infection as a factor responsible for iron deficiency. We investigated the potential relationship between H. pylori and iron-deficiency anaemia in patients with coeliac disease.

Helicobacter pylori plays a key role in production of reactive oxygen metabolites (ROMs). However, the importance of virulent CagA-positive H. pylori strains remains to be determined. The aim of this study was to assess ROMs production in gastric biopsies of patients infected by H. pylori. Results were correlated to CagA status and acute inflammatory infiltration.

Patients with insulin-dependent diabetes mellitus (IDDM) are often affected by chronic infections. H. pylori is one of the most common infection worldwide. Aim of the paper was to evaluate the prevalence of H. pylori infection, the efficacy of the most common H. pylori eradication therapies and the incidence of H. pylori reinfection after 12 months follow-up in IDDM and in a control group of dyspeptic patients matched for sex and age.

Disappearance of antiphospholipid antibodies syndrome after Helicobacter pylori eradication

Many new therapeutic strategies are studied to improve Helicobacter pylori eradication rate. Probiotics are live microorganisms which, upon administration, may interact with the human microflora and positively affect the health status. The use of probiotics in the field of H. pylori infection has been proposed for improving eradication rate and tolerability and for compliance of multiple antibiotic regimens used for the infection. Results from laboratory studies and from clinical trials seem to confirm the expectancies, but there is lack of standardization in terms of type of probiotic strain used, dosage and timing of supplementation. Before further ongoing trials and future studies will clarify these points, probiotics could remain a useful adjunct to standard anti-H. pylori therapies, but cannot take the place of other validated options.

Migraine is a commonly unilateral throbbing headache, which has been associated with disorders of the vascular tone. Helicobacter pylori, the most relevant cause of gastritis and peptic ulcer, has been recently associated with a typical functional vascular disorder such as primary Raynaud phenomenon. The aim of this study was to assess the prevalence of H. pylori for patients affected by migraine and the effects of H. pylori eradication on migraine symptoms.

Among the suspected bacterial causes of cancer, H. pylori is the agent more consistently linked to malignancy. After its discovery in 1983 and the later confirmation as the leading cause of chronic gastritis, several studies were performed to prove an association between H. pylori infection and gastric carcinoma. The epidemiological data have been so strong that in 1994 the International Association for Research on Cancer stated that "there was sufficient evidence" to classify H. pylori as a group I carcinogen in humans. However, the exact mechanisms underlying the link between H. pylori infection and gastric carcinoma remain still to be elucidated. The natural history of H. pylori infection shows that, although roughly half of the world's human population bears the organism, only a minority of individuals develop clinically important outcomes (e.g. peptic ulcer, lymphoproliferative diseases, atrophic gastritis and gastric carcinoma): host's genetic make-up, duration of infection, diet and differences between H. pylori strains have been proposed as factors potentially able to influence the outcomes in different individuals. The damaging agents by which H. pylori could promote gastric carcinogenesis are produced either by the organism or as a consequence of the host inflammatory response to the infection. Gastric mucosal chronic damage may, therefore, lead to changes in the pattern of epithelial cell kinetic (increase in cell proliferation and induction of apoptosis) in gastric glands which may induce DNA injury with irreversible genetic lesions. Finally, a direct association between H. pylori infection and the induction of gastric carcinoma has been recently demonstrated in an animal model, giving further credence to the role of this organism in gastric carcinogenesis.

One-week triple therapy is currently regarded as the reference of anti-Helicobacter pylori treatment. However, antibiotic-associated gastrointestinal side effects are among the major pitfalls of such regimens. Probiotic supplementation may be regarded as a therapeutic tool to prevent or reduce these troublesome drug-related manifestations.

Helicobacter pylori (H. pylori) infection is one of the most common gastrointestinal diseases. An increasing number of people undergo different treatment options. Unfortunately, H. pylori therapy may be troublesome for drug side effects and inefficacious for resistance to antibiotics.

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The mechanism by which Helicobacter pylori causes hypergastrinaemia is not completely understood.

Although triple therapy regimens suggested in the Current European guidelines give fairly good results, several studies have reported an unsatisfactory Helicobacter pylori eradication rate (< 80%).

Intestinal type metaplasia plays a role in intestinal type gastric carcinoma development. Ascorbic acid demonstrates a protective effect against gastric carcinogenesis, due to its ability to inactivate oxygen free-radicals as well as its nitrite-scavenging effects.

Factors influencing Helicobacter pylori infection recurrence still have not been fully clarified. The aim of this study was to determine whether, after eradication of H. pylori, any clinical or histologic features could yield information on infection relapse. We enrolled in the study 72 patients successfully treated for H. pylori infection by either dual (n = 49) or triple (n = 23) therapy. H. pylori eradication was defined as a negative bacterial finding by rapid urease test and histologic assessment at least 4 weeks after cessation of therapy. Upon eradication, gastritis grading was performed and patients were asked to return for an endoscopic control 6-8 months later. The recurrence of H. pylori infection was observed in 12 of 72 (16.7%) patients. The infection recurrence rate resulted significantly higher in nonulcer dyspepsia patients (p = 0.01 ) and in women (p = 0.03), whereas infection relapse did not differ between patients treated with dual or triple therapy. There was a strong (p = 0.0001 ) relationship between the persistence of chronic active gastritis after H. pylori eradication and recurrence of infection, whereas gastritis grade and metaplasia were not related to recurrence. In conclusion, this study found that H. pylori infection recurrence after successful dual or triple therapy is fairly high and that gastroduodenal disease, gender, and gastritis activity seem to affect infection relapse.

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Helicobacter pylori-related extradigestive diseases and effects of eradication therapy

A 42-year-old man with chest pain was found to have ST depression in leads V1 through V4. The coronary arteries appeared normal on angiography. Positive results of ventricular pacing and acetylcholine test led to a diagnosis of syndrome X. Other studies revealed gastritis due to CagA-positive Helicobacter pylori. Classic therapy for angina did not resolve chest pain, but eradication of H. pylori led to disappearance of symptoms and negative test results.

To assess the variability and sensitivity of morphometric measures of gastric mucosal lymphocyte and plasma cells to determine a systematic procedure for evaluating the density of these mononuclear inflammatory cells (MNC).

The role of Helicobacter pylori (H. pylori) infection as a cause of hepatic encephalopathy is still debated. This study focused on the relationship between H. pylori, plasma ammonia levels, and intellectual function in cirrhotic patients.

It has been suggested that short-term triple therapy comprising a proton pump inhibitor, plus clarithromycin and amoxycillin be used as first choice in treating H. pylori infection, while eradication failure patients should be further treated with a quadruple therapy. Nevertheless, conflicting results have been reported using these treatment regimens in different countries.

Helicobacter pylori resistance to antimicrobial agents is of particular concern because it is a major determinant in the failure of eradication regimens. Antimicrobial drug resistance has been reported to occur for nitroimidazoles, macrolides, fluoroquinolones, rifampin and tetracyclines. Resistance to nitroimidazoles is the most common, in the range of 30-40% on the average in Europe while the overall prevalence rate of resistance to macrolides is lower, probably ranging between 2-10% in most countries. Development of secondary (acquired) resistance to nitroimidazoles and to the macrolides usually occurs as a rule (> 70-100%) in case of failed eradication therapy. Data available from several centres seems however to indicate that a significant shift towards increasing resistance to metronidazole and to the macrolides might have possibly occurred in many countries over the last years. Resistances to both metronidazole and to clarithromycin are the most significant ones because they influence the success of the treatments although this seems to be less marked and more dependent on the treatment regimens considered in the case of metronidazole resistance than in the setting of clarithromycin resistance. These differences may in part relate to methodological variations and to the inherent difficulties in assessing the susceptibility of H. pylori to metronidazole. It is possible that different resistance cut-off might also have to be considered for metronidazole depending on the treatment regimens administered. The mechanisms of resistance have been well defined for the macrolides and are beginning to be unraveled for the nitroimidazoles. In all cases, resistance of H. pylori to antimicrobial agent seems to be due to the development of single mutational events in chromosomal genes rather than to the acquisition of exogenous resistance genes. Owing to the restricted ability of microbiology laboratories with expertise in H. pylori culture and the lack of standardised meth

Different invasive and non-invasive diagnostic tests are available for the diagnosis of H. pylori in the individual patient. In practice, endoscopic tests are best for a primary diagnosis of H. pylori infection because endoscopy allows assessment of treatment indications. The new rapid urease tests may help the clinician in treatment decision-making. Culture is currently not recommended for routine evaluation, but it is becoming increasingly important in certain populations with higher prevalence of drug resistance, since it allows testing for susceptibility to antibiotics. Serological testing has been recommended for initial pre-endoscopy or pre-treatment screening in dyspeptic patients. However, several current 'in-office' tests appear insufficiently accurate or would need further validation before being recommended for use in clinical management strategies at a primary care level. The urea breath tests are best suited to confirm eradication early after treatment, while laboratory serology tests are of limited use, since 6 months are required before a result can be obtained. The serological office tests cannot be used for post-treatment assessment of H. pylori status.