Beneficial effects of Helicobacter pylori eradication on idiopathic chronic urticaria

Helicobacter pylori, the most important cause of gastritis and peptic ulcer, recently has been associated with several extradigestive diseases. The aim of this study was to assess the prevalence of Helicobacter pylori infection and the effects of bacterium eradication in 42 consecutive patients affected by idiopathic chronic urticaria. Helicobacter pylori was assessed by [13C]urea breath test. Amoxicillin, clarithromycin, and lansoprazole were given to infected patients for seven days. Urticaria and gastrointestinal symptoms were assessed on enrollment and after eradication. Fifty-five percent of patients proved to be infected by Helicobacter pylori. Prevalence of gastrointestinal symptoms did not differ between infected and uninfected patients. Eighty-eight percent of infected patients in whom the bacterium was eradicated after therapy showed a total or partial remission of urticaria symptoms. Conversely, symptoms remained unchanged in all uninfected patients. In conclusion, Helicobacter pylori affects a high percentage of patients with idiopathic chronic urticaria; however, typical gastrointestinal symptoms do not identify infection status. Bacterium eradication is associated with a remission of urticaria symptoms, suggesting a possible role of Helicobacter pylori in the pathogenesis of this skin disorder.     

Prevalence of Helicobacter pylori infection and gastric mucosal abnormalities in chronic pancreatitis

OBJECTIVE: Chronic pancreatitis is often associated with abnormal gastric acid secretion. However, previous studies have taken into consideration neither the potential role of Helicobacter pylori (H. pylori) infection nor histological features of the gastric mucosa in this context. The aim of this study was to analyze the prevalence of H. pylori infection as well as the pattern of gastritis in patients with chronic pancreatitis. METHODS: Forty patients with chronic alcoholic pancreatitis were included in the study: 40 patients with alcoholic liver cirrhosis and normal exocrine pancreatic function and 40 asymptomatic nonalcoholic subjects matched for age and sex used as control subjects. Endoscopy was performed in all patients, and five biopsy specimens from the antrum (three from the gastric body and two from the cardia) were taken for histological grading of gastritis and H. pylori assessment. RESULTS: Prevalence of H. pylori infection was similar in subjects with chronic pancreatitis (38%), asymptomatic subjects (28%) and liver cirrhosis (30%). Topography and expression of H. pylori-associated chronic gastritis was also not different among the three groups of subjects. In H. pylori-negative subjects, the presence of moderate to severe chronic antral gastritis was significantly more common in patients with chronic pancreatitis (40%) than in subjects with liver cirrhosis (18%) and in asymptomatic subjects (14%) (p < 0.05). No difference was found among the three groups of patients with regard to gastritis activity, atrophy, and intestinal metaplasia in the various gastric regions. The chronicity grade of gastritis did not correlate with the severity of pancreatic insufficiency. CONCLUSION: Prevalence of H. pylori infection is not different in patients with chronic pancreatitis as compared with subjects alcoholic liver cirrhosis and asymptomatic subjects. A severe H. pylori-negative chronic gastritis is more common in patients with chronic pancreatitis. This chronic inflammation of the gastric mucosa could contribute to determining the changes in gastric physiology described in patients with chronic pancreatitis.     

Association of virulent Helicobacter pylori strains with ischemic heart disease

BACKGROUND: Previous studies have reported an association between chronic Helicobacter pylori infection and ischemic heart disease. However, it is not clear whether this association is really due to the virulence of the bacterium or is merely the result of confounding factors (in particular, age and social class). METHODS AND RESULTS: We assessed the prevalence of infection by Helicobacter pylori and by strains bearing the cytotoxin-associated gene-A (CagA), a strong virulence factor, in 88 patients with ischemic heart disease (age, 57+/-8 years; 74 men) and in 88 age- and sex-matched controls (age, 57+/-8 years; 74 men) with similar social background. Prevalence of Helicobacter infection was significantly higher in patients than in controls (62% versus 40%; P=.004), with an odds ratio of 2.8 (95% CI, 1.3 to 7.4; P<.001) adjusted for age, sex, main cardiovascular risk factors, and social class. Patients with ischemic heart disease also had a higher prevalence of CagA-positive strains (43% versus 17%; P=.0002), with an adjusted odds ratio of 3.8 (95% CI, 1.6 to 9.1; P<.001). Conversely, prevalence of CagA-negative strains was similar in patients and controls (19% versus 23%), with an adjusted odds ratio of 0.8 (95% CI, 0.4 to 1.4). CONCLUSIONS: The association between Helicobacter pylori and ischemic heart disease seems to be due to a higher prevalence of more virulent Helicobacter strains in patients. These results support the hypothesis that Helicobacter pylori may influence atherogenesis through low-grade, persistent inflammatory stimulation.     

Effect of Helicobacter pylori eradication on intestinal metaplasia and gastric epithelium proliferation

Gastric epithelial turnover increase in Helicobacter pylori infection has been demonstrated by interventional and non interventional methods for proliferating cell detection. We have observed a progressive hyperproliferation with the progression of Helicobacter pylori-induced mucosal lesions until the development of intestinal metaplasia. A similar result has been reported in other studies in the succession from normal mucosa to gastric carcinoma even if interventional techniques show less conspicuous differences in comparison to non interventional ones, which give an overestimated picture of proliferation. Later studies show that Helicobacter pylori-related hyperproliferation reverses after eradication. We have observed that this reversibility does not occur in areas of intestinal metaplasia, where the oncoprotein ras p21, involved in early gastric carcinogenesis, is expressed. This finding agrees with that demonstrating that hyperproliferation in intestinal metaplasia or gastric cancer is not affected by Helicobacter pylori. Other oncogenetic changes in intestinal metaplasia (i.e., p53 mutation) may further explain the persistently modified proliferative pattern of the epithelium. Recent studies suggest a lack of reversibility of intestinal metaplasia after Helicobacter pylori eradication, but this problem remains controversial. Our experience suggests that the persistence of the bacterium may increase the extent of this lesion. In conclusion the development of intestinal metaplasia is associated with an impaired regulation of gastric epithelial proliferation. Nevertheless, from the biological point of view, the progression towards carcinoma requires further DNA changes. Moreover, many questions need to be answered in order to establish clear guidelines for the clinical management.     

Helicobacter mustelae and Helicobacter pylori bind to common lipid receptors in vitro

Helicobacter pylori is a recently recognized human pathogen causing chronic-active gastritis in association with duodenal ulcers and gastric cancer. Helicobacter mustelae is a closely related bacterium with similar biochemical and morphologic characteristics. H. mustelae infection of antral and fundic mucosa in adult ferrets causes chronic gastritis. An essential virulence property of both Helicobacter species is bacterial adhesion to mucosal surfaces. The aim of this study was to determine whether H. mustelae binds to the same lipids shown previously to be receptors for H. pylori adhesion in vitro. By using thin-layer chromatography overlay and a receptor-based enzyme-linked immunosorbent assay, H. mustelae was found to bind the same receptor lipids as H. pylori, namely, phosphatidylethanolamine and gangliotetraosylceramide. In addition, both H. pylori and H. mustelae bound to a deacylplasmalogen phosphatidylethanolamine. In contrast to H. pylori, H. mustelae binding to receptors was unaffected by motility or viability. Murine monoclonal and bovine polyclonal antibodies against exoenzyme S, and exoenzyme S itself (from Pseudomonas aeruginosa), inhibited binding of H. mustelae to phosphatidylethanolamine and gangliotetraosylceramide. These findings show that H. mustelae binds in vitro to the same lipid receptors as H. pylori and suggest that the adhesion of H. mustelae to such species is mediated by preformed, surface-exposed adhesins which include an exoenzyme S-like protein.     

Helicobacter pylori infection in patients with chronic pancreatitis and duodenal ulcer

BACKGROUND: The prevalence of duodenal ulcer is high in patients with chronic pancreatitis. Patients with simple duodenal ulcer without chronic pancreatitis are mostly Helicobacter pylori-infected, and the prevalence of IgG seropositivity is > 95%. The prevalence of H. pylori infection in patients with chronic pancreatitis is not known. METHODS: IgG antibodies against H. pylori were measured in a cross-sectional survey of consecutive patients who had their exocrine pancreas function examined with a Lundh meal test in the period 1988-95 and in a control group of patients with simple duodenal ulcer. RESULTS: Twenty-seven per cent of the patients with chronic pancreatitis had duodenal ulcer during the observation period. The prevalence of IgG antibodies against H. pylori was 22% in patients with chronic pancreatitis without duodenal ulcer as compared with 27% with non-organic abdominal pain. The prevalence of IgG antibodies against H. pylori was 60% in patients with chronic pancreatitis complicated by duodenal ulcer as compared with 86% in controls with simple duodenal ulcer. CONCLUSIONS: H. pylori infection contributes but may not be the only cause of duodenal ulcer in patients with chronic pancreatitis.     

Helicobacter canis isolated from a dog liver with multifocal necrotizing hepatitis

On the basis of biochemical, phenotypic, and 16S rRNA analysis, a novel gram-negative bacterium, isolated from normal and diarrheic dogs as well as humans with gastroenteritis, has been recently named Helicobacter canis. A 2-month-old female crossbred puppy was submitted to necropsy with a history of weakness and vomiting for several hours prior to death. The liver had multiple and slightly irregular yellowish foci up to 1.5 cm in diameter. Histologically, the liver parenchyma contained randomly distributed, occasionally coalescing hepatocellular necrosis, often accompanied by large numbers of mononuclear cells and neutrophils. Sections of liver stained by the Warthin-Starry silver impregnation technique revealed spiral- to curve-shaped bacteria predominantly located in bile canaliculi and occasionally in bile ducts. Aerobic culture of liver was negative, whereas small colonies were noted on Campylobacter selective media after 5 days of microaerobic incubation. The bacteria were gram negative and oxidase positive but catalase, urease, and indoxyl acetate negative; nitrate was not reduced to nitrite, and the organism did not hydrolyze hippurate. The bacteria were also resistant to 1.5% bile. Electron microscopy revealed spiral-shaped bacteria with bipolar sheathed flagella. By 16S rRNA analysis, the organism was determined to be H. canis. This is the first observation of H. canis in active hepatitis in a dog and correlates with recent findings of Helicobacter hepaticus- and Helicobacter bilis-related hepatic disease in mice. Further studies are clearly warranted to ascertain whether H. canis-associated hepatitis is more widespread in canines as well as a cause of previously classified idiopathic liver disease in humans.     

Characterization of a cb-type cytochrome c oxidase from Helicobacter pylori

Helicobacter pylori is a microaerophilic Gram-negative spiral bacterium residing in human stomach. A cb-type cytochrome c oxidase that terminates the respiratory chain was purified to near homogeneity by solubilizing the membranes with Triton X-100 and applying anion exchange, Cu-chelating, and gel filtration chromatographies. Redox- and CO-difference spectra and pyridine ferrohaemochrome analysis showed the enzyme to contain three haems C, one low-spin protohaem, and one high-spin protohaem that probably forms a dioxygen-reducing bimetalic center with a copper atom. The enzyme actively oxidizes soluble cytochrome c from this bacterium (TNmax of about 250 s-1) with a Km of 0.9 microM. Yeast cytochrome c and N,N,N',N'-tetramethyl p-phenylenediamine (TMPD) are also oxidized at similar maximal velocities with larger Km's. Oxygen pulse experiments on resting cells in the presence of ascorbate plus TMPD or L-lactate indicated that this sole terminal oxidase pumps H+, although the H+ pumping activity by proteoliposomes reconstituted from the enzyme and P-lipids was low. Two main bands with haem C at 58 and 26 kDa were observed upon polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and succeeding protein and haem staining. Sequencing of the operon encoding the subunits of the enzyme revealed the presence of ccoNOQP. N-terminal analysis of the 58 kDa band showed 15 or 13 amino acids coinciding with the amino acid sequences deduced from the DNA of ccoN and ccoO. CcoN, the largest subunit bearing two protohaems and copper, and ccoO, a mono-haem cytochrome subunit form a protein complex with an apparent molecular mass of 58 kDa, even in the presence of sodium dodecyl sulfate. The 26 kDa band is tentatively assumed to be ccoP with two haems C.     

Epidemiology and pathogenesis of Helicobacter pylori infection]

In 1982 a spiral gram-negative bacterium was first cultured from human gastric mucosa. Helicobacter pylori causes chronic active gastritis, which is the most common chronic infectious disease worldwide. The fact that this bacterial infection is furthermore linked to the majority of all duodenal and gastric ulcers is now commonly accepted after initial scepticism. Some fundamentals of this infectious disease like the extrahuman reservoir of pathogens and the mode of transmission are only partially understood. Some of the bacterial virulence factors allowing mucosal colonization and inflammation have been described. So are some details in the bacterial interaction with the host's immune system. The specific feature of this infection is the inability of the immune system to eliminate H. pylori. Finally no immunity but lifelong chronic infection results. The question, why some individuals infected will have merely gastritis, while others will suffer from peptic ulcer disease, or even gastric carcinoma cannot be answered sufficiently by now. Environmental factors may play a role as well as varying pathogenicity of bacterial strains. Furthermore the age at which infection was acquired and genetic differences in the host's susceptibility to disease are of importance.     

Granulocyte activation by Helicobacter pylori

Helicobacter pylori-associated gastritis (HAG) is characterized by granulocytic and mononuclear cell infiltrates within infected gastric mucosa. Since the bacterium does not invade the epithelial layer, it must be assumed that components or products of the pathogen which permeate the epithelial barrier may initiate chemotaxis and activation of neutrophils. The aim of this study was to evaluate the effect of H. pylori water soluble protein (WSP) components on the induction of granulocyte adherence and activation. The results show that H. pylori WSP led to enhanced expression of the beta 2-integrin CD11b/CD18 on the granulocyte surface. Following upregulation of this adhesion molecule, activated granulocytes demonstrated increased adhesion to human endothelial cells (HUVEC) in culture. These observations support the hypothesis that in vivo neutrophil activation may be a direct result of H. pylori constituents promoting transendothelial migration into the lamina propria of infected gastric mucosa.     

A standardized mouse model of Helicobacter pylori infection: introducing the Sydney strain

BACKGROUND & AIMS: Currently available Helicobacter pylori models show variable and, in some instances, poor colonization. There is a need for a strain with high colonizing ability to act as a standard for animal studies. METHODS: After screening a range of fresh clinical isolates and long-term adaptation in mice, a strain of H. pylon has been isolated with a very good colonizing ability. RESULTS: This strain, named the Sydney strain of H. pylori (strain SS1), is cagA and vacA positive. High levels of colonization (10(6)-10(7) colony-forming units/g tissue) were achieved consistently in C57BL/6 mice. Colonization levels varied depending on the mouse strain used with BALB/c, DBA/2, and C3H/He, all being colonized but in lower numbers. In all strains of mice, bacteria were clearly visible at the junctional zone between the antrum and the body. The phenotype was stable with colonizing ability remaining after 20 subcultures in vitro. The bacterium attached firmly to gastric epithelium. During 8 months, a chronic active gastritis slowly developed, progressing to severe atrophy in both C57BL/6 and BALB/c mice. CONCLUSIONS: The Sydney strain of H. pylori is available to all and will provide a standardized mouse model for vaccine development, compound screening, and studies in pathogenesis.     

Beneficial effects of Helicobacter pylori eradication on migraine

BACKGROUND/AIMS: 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. METHODOLOGY: Two-hundred and twenty-five patients were consecutively enrolled between October 1996 and January 1997. H. pylori was assessed by 13C-urea breath test. Infected subjects were eradicated of the bacterium; frequency, intensity and duration of attacks of migraine were assessed during a 6 month follow-up period. RESULTS: H. pylori was detected in 40% of the patients. Eighty-three percent of the patients who underwent therapy were eradicated. Intensity, duration and frequency of attacks of migraine were significantly reduced in all eradicated patients. CONCLUSIONS: H. pylori is common in subjects with migraine. Bacterium eradication causes a significant decrease in attacks of migraine. The reduction of vasoactive substances produced during infection may be the pathogenetic mechanism underlying the phenomenon.     

Helicobacter pylori attachment to gastric cells induces cytoskeletal rearrangements and tyrosine phosphorylation of host cell proteins

The consequences of Helicobacter pylori attachment to human gastric cells were examined by transmission electron microscopy and immunofluorescence microscopy. H. pylori attachment resulted in (i) effacement of microvilli at the site of attachment, (ii) cytoskeletal rearrangement directly beneath the bacterium, and (iii) cup/pedestal formation at the site of attachment. Double-immunofluorescence studies revealed that the cytoskeletal components actin, alpha-actinin, and talin are involved in the process. Immunoblot analysis showed that binding of H. pylori to AGS cells induced tyrosine phosphorylation of two host cell proteins of 145 and 105 kDa. These results indicate that attachment of H. pylori to gastric epithelial cells resembles that of enteropathogenic Escherichia coli. Coccoid H. pylori, which are thought to be terminally differentiated bacterial forms, are capable of binding and inducing cellular changes of the same sort as spiral H. pylori, including tyrosine phosphorylation of host proteins.     

Therapy of Helicobacter pylori infection using Lactobacillus acidophilus

INTRODUCTION: In vitro experiments with Lactobacillus acidophilus have revealed its inhibitory effect on Helicobacter pylori and its application in treatment of Helicobacter pylori positive gastritis was examined. MATERIAL AND METHODS: 15 patients have undergone gastroscopy with biopsy and by histopathological examination. Helicobacter pylori positive gastritis was detected. During a two-month period these patients took acidophilus milk (3 x 250 ml a day) prepared according to a special protocol and which contained 4 x 10(9)-1 x 10(10) live cells of Lactobacillus acidophilus at the moment of preparation. Lactobacillus acidophilus strain NAS, gained from lyophilized preparation Bio-Nate (Natren Inc. USA) was used as a test organism. Control gastroscopy was performed 2 months later. RESULTS: 14 patients have completed the examination. All of them were satisfied with the taste of acidophilus milk and could stand it well, whereas in 6 out of 14 Helicobacter pylori was eradicated. DISCUSSION: Helicobacter pylori eradication therapy is recommended in all cases of Helicobacter pylori positive gastritis associated with peptic ulcer, as well as in absence of ulcer when subjective difficulties occur. Antibiotic therapy is often unsuccessful and most often associated with risks of significant adverse effects, being the consequence of intestinal microflora disorders. The aim of using Lactobacillus acidophilus in the therapy is to reduce risks of adverse effects. In our study, by using acidophilus milk only, without other therapy, eradication of Helicobacter pylori was achieved in 6 out of 14 patients. All patients could stand the therapy well and were satisfied with the taste of the preparation. The number of examinees was small in regard to making conclusions, but the results are encouraging and show that apart from established in vitro effect. Lactobacillus acidophilus has a potential in vivo effect.     

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 degrees 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.     

Inhibitory actions of glycyrrhizic acid on arylamine N-acetyltransferase activity in strains of Helicobacter pylori from peptic ulcer patients

Arylamine N-acetyltransferase (NAT) activities with 2-aminofluorene (2-AF) and p-aminobenzoic acid (PABA) as substrates were determined in Helicobacter pylori, collected from patients with peptic ulcers. The NAT activity was determined using an acetyl CoA recycling assay and high pressure liquid chromatography. Inhibition of growth studies from H. pylori demonstrated that glycyrrhizic acid elicited dose-dependent bactericidal effect in H. pylori cultures, i.e.; the greater the concentration of glycyrrhizic acid, the greater the inhibition of growth of H. pylori. Cytosols or suspensions of H. pylori with and without selected concentrations of glycyrrhizic acid co-treatment showed different percentages of 2-AF and PABA acetylation. The data indicated that there was decreased NAT activity associated with increased glycyrrhizic acid in H. pylori cytosols and intact cells. For the cytosol and intact bacteria examinations, the apparent values of Km and Vmax were decreased after co-treated with 80 M glycyrrhizic acid. This report is the first demonstration of glycyrrhizic acid inhibition of arylamine NAT activity and glycyrrhizic acid inhibition of growth in the bacterium H. pylori.     

Superoxide dismutase activity in Helicobacter pylori-positive antral gastritis in children

Reactive oxygen metabolites have been implicated in gastric mucosal injuries. Superoxide dismutase, a scavenger of superoxide radical, is a key enzyme in gastric mucosal protection against several damaging factors. This study was aimed at investigating the relationship of superoxide dismutase activity to Helicobacter pylori-induced antral gastritis in children. Two groups of 11 children each, one positive and the other negative for Helicobacter pylori, were studied. Biopsies from the antrum and corpus were obtained for evaluation of Helicobacter pylori by CLOtest and histology as well as for superoxide dismutase activity (cytochrome c method). Erythrocytic and serum superoxide dismutase levels were determined as well. Superoxide dismutase activity was significantly higher only in the antrum of children with Helicobacter pylori-induced antral gastritis. There was no significant difference in superoxide dismutase activity in the corpus, erythrocytes, or serum of both groups. These findings may suggest a pathogenic relationship between the presence of Helicobacter pylori and oxygen radicals in inducing antral mucosal injury.     

A possible role of Helicobacter pylori infection in the etiology of chronic laryngitis

In order to study a possible role of Helicobacter pylori infection in chronic laryngitis, we performed endoscopic and histological assessments in addition to a urease test for the bacterium in 35 patients with chronic hoarseness. Six of the patients investigated (17.1%) revealed a positive urease test of the laryngeal biopsy (four male and two female patients). These H. pylori-positive patients were treated with omeprazole and an antibiotic regimen using clarithromycin and metronidazole. This led to an eradication of the H. pylori and resolution of clinical signs and symptoms. These findings show a possible role of H. pylori infection in the etiology of chronic laryngitis in certain patients and can be important for clinical diagnosis and treatment.     

Epidemiology of peptic ulcer disease in cirrhotic patients: role of Helicobacter pylori infection

OBJECTIVE: The aim of this study was to investigate the clinical and epidemiological factors associated with the appearance of peptic ulcer in patients with cirrhosis and, in particular, the role of Helicobacter pylori infection. METHODS: A total of 201 of 220 consecutive patients included in a prospective study that aimed to evaluate the effect of dietary intervention on cirrhotic complications and survival underwent upper gastrointestinal endoscopy. At entry, an epidemiological and clinical questionnaire was completed and the presence of peptic ulcer disease or esophageal varices at endoscopy was prospectively collected. Sera were obtained and stored at -70 degrees C until analyzed, being tested afterward for Helicobacter pylori antibodies using a commercial ELISA kit. RESULTS: Eleven of 201 patients had borderline anti-Helicobacter pylori IgG titers and were excluded from further analysis. In the remaining 190 patients, point prevalence of peptic ulcer was 10.5% and lifetime prevalence 24.7%. Multivariate analysis selected male sex (OR 2.3; 95%CI 1.09-4.89) and Helicobacter pylori seropositivity (OR: 1.7, 95%CI 1.02-2.81) as the variables independently related to peptic ulcer disease. CONCLUSIONS: Male sex and seropositivity for Helicobacter pylori are the major risk factors for peptic ulcer in cirrhosis.     

One-day therapy for treatment of Helicobacter pylori infection

The present study evaluated the effect of a one-day high-dose combined therapy on Helicobacter pylori infection. Thirty-two consecutive patients (suffering from either peptic ulcer or nonulcer dyspepsia) with Helicobacter pylori infection received omeprazole (40 mg) + bismuth subcitrate (240 mg x 4) + amoxicillin suspension (2000 mg x 4) + metronidazole (500 mg x 4), for only one day. Endoscopy, histology, culture, and susceptibility studies were done at entry and 30 and 90 days after the treatment day. Successful eradication was obtained in 23/32 (72%) patients and gastritis had resolved in 95% of these. Side effects were induced by the treatment in 6/32 (19%) patients, but these were all self-limiting, short-lasting, and did not require any specific treatment. Development of bacterial resistance to metronidazole occurred in 6/9 (67%) non-eradicated patients. These data suggest that one-day treatment with high doses of amoxicillin, metronidazole, bismuth, and omeprazole represents an effective, safe, and inexpensive therapeutic approach for the treatment of H. pylori infection.