Role Of Helicobacter Pylori Infection Research Articles

The role of helicobacter pylori infection in autoimmune and allergic diseases

The role of H. pylori in the pathogenesis of variety gastric diseases such as chronic active gastritis, peptic ulcer disease, MALT lymphoma, and gastric adenocarcinoma is well established. In this pa per we re view the pathogenic mechanisms involved in some autoimmune and allergic diseases shown to be related to H pylori infection. Scripta Scientifica Medica 2010; 42(1):51-53

The role of Helicobacter pylori infection in children with chronic immune thrombocytopenic purpura

Helicobacter pylori infection has been associated with immune thrombocytopenic purpura in adults, however, the few studies concerning this issue showed conflicting results in the paediatric field. Therefore, authors prospectively investigated the incidence of Helicobacter pylori infection and the effect of Helicobacter pylori eradication on platelet count recovery in children with immune thrombocytopenic purpura. The study included 27 children with immune thrombocytopenic purpura (13 boys and 14 girls) with a median age of 8.2 years (range, 18 months-18 years). 38 healthy children (controls) were also enrolled (20 boys, 18 girls, median age, 9.6 years, range, 4-18 years). Helicobacter pylori infection was diagnosed using 13 C urea breath test. Eradication was assessed at 6 weeks following the end of the treatment by 13 C urea breath. 2 children out of 27 patients with immune thrombocytopenic purpura proved to be positive for Helicobacter pylori infection (7.7%) and were treated with combination therapy. Controls showed similar rate of Helicobacter pylori infection (3/38, 7.9%) in comparison to those with immune thrombocytopenic purpura. In the follow-up period (mean, 10 months, range, 6-14 months) platelets did not show any improvement in infected children following the eradication treatment and were identical to those of the uninfected patients. Eradication was successful in the 2 Helicobacter pylori infected patients with immune thrombocytopenic purpura. The results do not suggest a pathogenetic role of Helicobacter pylori infection in the etiology of immune thrombocytopenic purpura. Screening of Helicobacter pylori infection among paediatric patients with immune thrombocytopenic purpura is not recommended.

The response of Asian patients with functional dyspepsia to eradication of Helicobacter pylori infection

The role of Helicobacter pylori infection in functional dyspepsia (FD) remains controversial. Several randomized controlled trials involving populations in the West, observed no statistically significant advantage over placebo. However, none of these studies involved Asian populations which have high infection rates. A double blind, randomized, placebo-controlled trial of H. pylori eradication for FD was conducted in our Singapore-based Asian population. Forty-one patients received active treatment consisting of a 1-week course of omeprazole 20 mg once daily, clarithromycin 250 mg twice daily and tinidazole 500 mg twice daily whereas another 41 patients received matching placebo tablets. A dyspepsia score was derived by grading 5 dyspeptic symptoms on a Likert scale. Symptom assessment and urea breath test were repeated at 6 weeks, 6 and 12 months from the start of treatment. The primary end point was symptom resolution, defined as a dyspepsia score of 0 or 1 at the end of 12 months follow-up. On intention-to-treat analyses, symptom resolution was observed in 24% of patients on active treatment and 7% on placebo; the difference in proportion of patients with symptom resolution was statistically significant (P=0.02, 95% confidence interval: 1.1-17.7). H. pylori eradication rates perprotocol and intention-to-treat were 80.0 and 68.3%, on active treatment and 5.6 and 4.9% on placebo (both P values<0.0001). Among patients with H. pylori eradicated on active treatment the symptom resolution rate was 39% (10 of 26), whereas it was 3% (one of 35) among patients in the placebo group who had persistent H. pylori infection. In multivariate analysis, posttreatment H. pylori status was the only predictor of symptom resolution. The majority of patients, 91.5%, had ulcer-like dyspepsia; heartburn and acid regurgitation were uncommon, and no increase was observed after treatment. In contrast to Western populations, our results suggest that patients with FD in Asia would benefit from treatment for H. pylori infection with as much as a 13-fold increased chance of symptom resolution following its eradication.

Role of Helicobacter pylori in refractory iron deficiency anaemia

The role of Helicobacter pylori infection in the development of iron deficiency anaemia has been the focus of attention over the past decade. However, confirmation of a relationship has not confirmed the pathophysiological mechanisms involved in the phenomenon. The aim of the present work is to study the levels of fasting gastric acidity (free and total) as well as the level of tumour necrosis factor-α (TNFα) in male refractory iron deficiency anaemia patients seropositive for H. pylori infection versus those who are seronegative. Thirty adult patients with iron deficiency anaemia and gastroduodenitis were subdivided into two groups of matched age and haemoglobin value. Group l was H. pylori-seropositive for infection and these patients did not receive prior treatment for eradication of H. pylori infection. Group 2 comprised patients seronegative for H. pylori infection (control group). Patients with active bleeding or previous medical problems were excluded from the study. All patients and controls were subjected to the following at presentation: history taking and thorough clinical examination, complete blood picture, reticulocytes (%), assessment of serum iron, total iron binding capacity, serum ferritin, IgG anti-Helicobacter antibody and TNFα, stool for occult blood and measurement of gastric acidity (total and free). Upper endoscopy was performed and multiple biopsies were taken and tested for expression of cytotoxin-associated gene A (cagA) by the polymerase chain reaction (PCR). Results showed significantly higher values of free and total gastric acidity as well as TNFα levels in Group 1 compared to controls (Group 2). Among those in Group 1, higher TNFα levels were seen in seven H. pylori cagA-positive patients than in eight cagA-negative patients. Haemoglobin values were inversely correlated with TNFα levels. Thus, elevated serum TNFα in the H. pylori-seropositive group may be one of the underlying pathophysiological mechanism for iron deficiency anaemia observed in these patients.

H. pylori should be eradicated in chronic liver disease patients with peptic ulcer

Although the role of Helicobacter pylori infection in peptic ulcer [1], gastric cancer [2], congestive gastropathy [3], and hepatic encephalopathy [4] has been investigated in patients with liver cirrhosis, available data are still scanty and conflicting. Therefore, the study from Jung et al. published in this issue is welcome [5]. Basically, following standard triple therapy, H. pylori eradication was achieved in a large number (N=191) of peptic ulcer patients with chronic liver disease, without a statistically significant difference between 7-day and 14-day therapy (82.9% vs.

Possible pathogenetic role of Helicobacter pylori infection in cardiac syndrome X

The diagnosis of cardiac syndrome X (CSX) is often a diagnosis of exclusion and hence requires a systematic and comprehensive assessment of each patient to rule out more common causes of chest discomfort. The definitive technique for the diagnosis of CSX is not currently available. Many patients with chest pain and normal coronary angiograms have neither metabolic nor hemodynamic evidence of myocardial ischemia. Causes of nonischemic chest pain such as esophageal dysfunction, pulmonary hypertension, and mitral valve prolapse, should also be considered and pursued. Although chronic inflammation induced by Helicobacter pylori infection might play a part in the pathophysiology of CSX, one can conclude that nonischemic chest pain resulting from gastrointestinal disease such as esophagitis, gastritis cannot be completely excluded in the patients with CSX. We believe future large scale prospective cohort studies will be needed to solve that dilemma.

Helicobacter pylori, inflammation, oxidative damage and gastric cancer: a morphological, biological and molecular pathway

Gastric carcinogenesis is a complex, multistep and multifactorial event, characterized by progressive cyto-histological dedifferentiation, in which the role of Helicobacter pylori infection has been established. Among the pathways relevant to gastric carcinogenesis and correlated with H. pylori infection, it has been demonstrated that the production of reactive oxygen species, with damage to the DNA, may be quite important. Oxidative damage, alone and/or in combination with exogenous and endogenous factors, induces several molecular changes. The assumption is that, in precancerous lesions, these molecular changes belong to the same biological spectrum as their invasive counterpart. The molecular profile of these preneoplastic lesions is heterogeneous, however, and there are still no molecular markers enabling the distinction between atypical hyperplastic lesions and low-grade noninvasive neoplasia (NiN) or between high-grade NiN and early invasive neoplasia. Indeed, within the spectrum of morphological changes characterizing this multistep evolution, dysplasia (NiN) is the lesion coming closest to the development of invasive adenocarcinoma. Several of the genetic and epigenetic alterations reported in gastric precancerous lesions affect DNA repair system genes, tumor suppressor genes, oncogenes, cell cycle regulators, growth factors, and adhesion molecules. Although we await reliable molecular markers, it is best to monitor patients harboring NiN closely with endoscopy and extensive bioptic sampling, and to eradicate any H. pylori to prevent the accumulation of oxidative DNA damage and its consequent progression. The growing body of evidence of the regression of precancerous changes and the high prevalence of superficial gastric carcinoma demonstrated in long-term follow-up studies on NiN make this approach mandatory.

The relation between Helicobacter pylori infection and cardiac syndrome X: A preliminary study

Cardiac syndrome X is defined by an angina pectoris with normal or near normal coronary angiogram.We evaluated the association of Helicobacter pylori (HP) infection with cardiac syndrome X (CSX). We studied 30 patients with CSX, 30 cases with stable angina and also 30 healthy controls. All three groups underwent urea breath test (UBT). Fifty percent (15 out of 30) of CSX patients had positive UBT result (> = 200 dpm), while two other groups did not have the positive results. Regarding high prevalence of HP infection in patients with CSX in our study and probable causative effect of chronic infection in coronary artery diseases, possible role of HP infection in the pathogenesis of CSX is suggested. However well designed clinical trial studies are needed to confirm this preliminary result.

No Association Between Helicobacter pylori Infection or CagA-bearing Strains and Glaucoma

Accumulating evidence indicates that a variety of infections contribute to the pathogenesis of glaucoma. The role of Helicobacter pylori infection in glaucoma is controversial. Prospective, population-based study. Patients with various types of glaucoma and a control group of patients with cataract. We evaluated seropositivity to H. pylori and to its cytotoxin-associated gene A (CagA) product in patients with various types of glaucoma and compared the findings to those of a control group of patients with cataract. H. pylori infection and CagA seropositivity were detected in 31/51 (60.8%) and 26/51 (51%) glaucoma patients compared with 22/36 (61.1%) and 19/36 (52%) control patients, respectively (P=0.88, 0.67, not significant). Similar rates of H. pylori infection and CagA-positive strain were found in all glaucoma subgroups, and none of them was statistically different from those of controls. Neither H. pylori infection nor seropositivity for virulent CagA-bearing H. pylori strains have significant association with the occurrence of glaucoma of any type.

Vascular Risks and Complications in Diabetes Mellitus: The Role of Helicobacter Pylori Infection

Patients with diabetes mellitus (DM) are at risk for Helicobacter pylori infection. This infection has been linked to atherosclerosis and its vascular complications. The aim of this study was to evaluate the: (1) prevalence of H pylori infection in patients with DM; (2) association between diabetic vascular complications and H pylori infection; and (3) influence of H pylori infection on atherosclerosis and inflammatory biomarkers. In this study, we evaluated 80 patients with DM for atherosclerosis; cardiac, cerebral, and peripheral vascular diseases; retinopathy; neuropathy; and nephropathy. We estimated the blood levels of glucose, glycosylated hemoglobin, complete blood cell count, erythrocytic sedimentation rate, lipid profile, tumor necrosis factor-alpha, interleukin (IL)-6, and anti-H pylori IgG antibodies. H pylori infection was detected in 85% of patients versus 76.7% for control subjects. Carotid artery intima-media thickness was significant in H pylori-infected patients. IL-6 and tumor necrosis factor-alpha were significantly associated with H pylori infection. In multivariate analysis, blood glucose, triglycerides, erythrocytic sedimentation rate, IL-6, and tumor necrosis factor-alpha increased the odds for atherothrombotic cause of cerebral ischemia in H pylori infection. We concluded that H pylori infection is common in DM and seems to be linked to the presence of atherosclerosis and ischemic cerebrovascular stroke. This effect could be mediated by increasing cytokine levels.

New Aspects of Regulatory Signaling Pathways and Novel Therapies in Pancreatic Cancer

Pancreatic cancer is an exceptionally devastating and incurable disease, the treatment of which has largely been unsuccessful due to higher resistance of pancreatic tumor cells to conventional approaches including surgery, radiation and/or chemotherapy. Therefore, there is a need for development of new and effective chemotherapeutic agents which can target multiple signaling pathways to induce responsiveness of pancreatic cancer cells to death signals. Although crucial advances in our understanding of the molecular pathogenesis of the disease have been made, the exceptional aggressiveness of pancreatic cancer remains largely unexplained. Investigators have actively investigated to elucidate molecular mechanisms involved in the oncogenesis, growth, invasion and metastasis of this malignancy. Pancreatic tumor cells have developed remarkable defense mechanisms to evade apoptosis and to increase their resistance to several drugs. All the typical signs of apoptosis are the final results of a complex biochemical cascade of events, whose proper function is regulated by growth and transcriptional factors, hormones and other molecules affecting the intracellular signal transduction. Understanding these complex mechanisms has created new hopes concerning pancreatic cancer in the last years and has evoked new therapeutic approaches, many of which undergo clinical trials with promising results to date. The present review provides a comprehensive description of the molecular signaling mainly of the apoptotic pathways implicated in the pathogenesis of pancreatic cancer, an incentive on the potential pathogenetic role of Helicobacter pylori infection and an appraisal of the most recent therapeutic strategies aiming at the repair of molecular lesions and applied at a cell biochemical level.

Clinical Featues and Role of Helicobacter pylori Infection in Children with Idiopathic Thrombocytopenic Purpura

小児特発性血小板減少性紫斑病 (ITP) 87例の臨床的検討を行なった。初発時の臨床像として，発症年齢は0～4歳が71.3%，血小板数は1×104/μl未満が49.4%と，多くの症例が年少児で著しい血小板減少を伴っていた。初発時治療は，大量グロブリン療法が60例 (69.0%)，ステロイド療法が10例 (11.5%)，無治療が17例 (19.5%)であった。血小板数2×104/μl未満の症例では90%以上が治療を受けていたが，2×104/μl以上の症例では無治療観察が多かった。頭蓋内出血など重篤な出血はなかった。慢性型の頻度は17例 (19.5%) であった。慢性型の平均年齢は6歳3か月で，急性型 (2歳8か月) より有意に高かったが，性別や血小板数や初発時治療では有意な差はなかった。慢性型と診断された症例でも35.3%はその後血小板数が正常化した。現在も5×104/μl未満の症例は全症例の3.4%，慢性型の17.6%で，小児ITPの生活の質を含めた予後は良好であった。Helicobacter Pylori (H. pylori) 感染が認められたのは慢性型の7.1%，急性型の5.3%で，除菌療法なしでも血小板数は改善しており，小児ITPにおけるH. pylori感染の関与は低かった。

The Prevalence and Risk Factors of Reflux Esophagitis Among Adult Chinese Population in Taiwan

Risk factors of reflux esophagitis among Chinese in Taiwan are at present not clear and the role of Helicobacter pylori infection in the development of reflux esophagitis is still controversial. The aim of this study was to examine the prevalence of reflux esophagitis, and to identify risk factors associated with reflux esophagitis in a multivariate context and to evaluate if H. pylori is a predictive factor for reflux esophagitis. A total of 482 physical check-up subjects who underwent upper gastrointestinal endoscopy were investigated. The severity of esophagitis was evaluated by Los Angeles classification. H. pylori status was assessed by serology. Twelve percent (58/482) demonstrated reflux esophagitis with 87% of grade A or B. Of those with reflux esophagitis, 48.3% had reflux symptoms whereas 17.4% of those with reflux symptoms had reflux esophagitis. Univariate analysis identified hiatal hernia, male sex, smoking, alcohol drinking, and overweight as risk factors associated with reflux esophagitis. Multivariable logistic regression showed that hiatal hernia [odds ratio (OR)=12.2, 95% confidence interval (CI)=5.0-29.9, P<0.0001], male sex (OR=4.2, 95% CI=1.9-9.0, P<0.001), and chronic obstructive pulmonary disease sufferers (OR=3.4, 95% CI=1.1-10.9, P<0.05) were 3 independent risk factors for development of reflux esophagitis. The prevalence of reflux esophagitis in Taiwanese is 12% and most are mild grade and free from reflux symptoms. Hiatus hernia, male sex, and chronic obstructive pulmonary disease are 3 independent risk factors for development of reflux esophagitis. H. pylori infection did not protect subjects from reflux esophagitis.

Helicobacter pylori, Anemia, and Iron Deficiency

Attempts to understand determinants of anemia and iron deficiency have led researchers to examine the role of Helicobacter pylori infection. The current study assessed determinants of anemia and iron deficiency, including H. pylori, in Alaska Native children. In 1999, a population-based survey was conducted among 86 children (67% response rate), mean age of 43.7 months (standard deviation = 16.8 months). Samples of breath, stool, and venous blood were obtained from children for measures of anemia, iron deficiency, H. pylori, fecal blood loss, and current inflammation. Standardized interviews with parents provided information on demographics, illness, and intake of dietary iron, iron-absorption inhibitors, and enhancers. Of the 86 children studied, 17.4% were anemic and 38.6% were iron deficient. Forty-one percent of the cohort had H. pylori-specific IgG antibodies, 86% tested positive by the urea breath test (UBT), and 80% tested positive by the stool antigen test. Presence of H. pylori antibodies emerged as a significant risk factor for anemia and iron deficiency in adjusted analyses controlling for demographic factors, current inflammation, and antibiotic use. In contrast, children with positive UBT or stool antigen results were significantly less likely to have anemia or iron deficiency than those with negative results. Results from different measures of H. pylori may reflect different stages of infection. Relationships between H. pylori and anemia/iron deficiency may depend on the phase of infection measured, with serologic tests reflecting established H. pylori infection associated with anemia/iron deficiency, and UBT and stool antigen results reflecting an earlier stage of infection.

Matrix metalloproteinase 2 (MMP2) polymorphism, Helicobacter pylori (HP) infection and esophageal adenocarcinoma (EA) risk

10553 Background: Epidemiologic studies suggest that HP infection protects against EA risk, as HP-mediated chronic atrophic gastritis reduces acid reflux. Genetic variations may modify the host response to HP infection and alter this risk. MMP2 expression is commonly upregulated in HP infections. We hypothesize that a functional MMP2 promoter polymorphism (-C1306T) that abolishes a Sp1 binding site and decreases promoter activity will also reduce the protective effects of HP infections in EA risk. Methods: HP status was determined in 98 EA patients and 101 age and gender matched healthy controls, using a commercially available serum immunoblotting kit (Helicoblot 2.1, Genelabs Diagnostics) that measures ever, current, CagA+ and VacA+ HP infections. Genotyping was performed using TaqMan. Data were analyzed using unconditional logistic regression. Results: 39% of cases and 44% of controls (P=0.69) had MMP2 variants (T/T or C/T). 36% of cases and 42% of controls were ever HP infected (P= 0.35). In individuals carrying the MMP2 wild type (CC) genotype, ever HP infection was strongly protective against EA [Odds Ratio (OR) 0.32: 95% CI, 0.13–0.75; P=0.008]. In contrast, in individuals carrying the MMP2 variants that are associated with lower promoter activity, this protective effect was lost (OR 1.76; 95% CI, 0.06–5.2; P= 0.30). Similar results were found when evaluating the MMP2 and current, CagA or VacA infection. Statistical interactions between MMP2 genotype and ever HP infection (P=0.027) and between MMP2 genotype and VacA+ infection (P= 0.035) were significant. Conclusions: We are the first to report that host factors such as the MMP2 polymorphism modulate the role of HP infection in EA susceptibility. No significant financial relationships to disclose.

Critical role of Helicobacter pylori in the pattern of gastritis and carditis in residents of an area with high prevalence of gastric cardia cancer

We have investigated the role of Helicobacter pylori infection and of other risk factors of gastritis and carditis in residents of a high-risk area for gastric cardia cancer. During a national population-based endoscopic survey, 508 randomly-selected participants aged > or =40 were enrolled. Mucosal biopsies were obtained from six standard sites. Polymorphonuclear (PMN) and mononuclear (MN) infiltration and combined inflammatory scores (CIS) for chronic gastritis and H.pylori were assessed. Relationships of H.pylori and reflux esophagitis with these variables were calculated for cardia and non-cardia subsites. Both PMN and MN infiltrations correlated strongly with H.pylori infection. For PMN the relationship was maximum for the antrum (odds ratio (OR) = 9.4 (5.2-17.1)) and minimum for the gastric body (OR = 1.7 (1.0-2.9)). There was a significant relationship between carditis and H.pylori (OR = 2.8 (1.7-4.9)). A similar relationship was obtained for MN infiltration. In 56% of subjects the mean MN score for the corpus was equal to or greater than that for the antrum. For 59% of subjects the MN score for the cardia was greater than or equal to the antral score. Use of logistic regression revealed that was the main risk factor for gastritis and carditis in all sites. There was an inverse relationship between reflux esophagitis and carditis. H.pylori is the main risk factor for gastritis for all sites of the stomach including the cardia; but this relationship is stronger for the antrum and cardia than for the body. Continuous cardia inflammation may contribute to the high incidence of gastric cardia cancer in this region.

Role of Helicobacter pylori Infection and Chronic Inflammation in Gastric Cancer in the Cardia

Helicobacter pylori-induced gastritis is an important factor for gastric carcinogenesis. However, it is still controversial whether it is also applicable for cardiac cancer development. Recently, we reported that H. pylori is an important factor for the induction of cardiac inflammation. We examined the status of H. pylori-induced gastritis in patients with cardiac cancer. Seventy-five Japanese patients (58 men; mean age, 64.2 years) with cardiac cancer were studied. Cardiac cancer was defined as that mainly located within 2 cm from the squamo-columnar junction (SCJ). Histological gastritis including the cardiac region was evaluated using the biopsy or surgically resected sections. Cardiac inflammation was evaluated at 1 cm distal from SCJ in lesser curvature. Sera were collected and several markers were evaluated. The status of H. pylori infection was evaluated by histology and serum antibodies. Expressions of cytokeratins were examined by immunohistochemical analysis. Out of 75 patients with cardiac cancer, H. pylori was positive in 71 (95%) patients. The cardiac inflammation was examined in 30 patients (26 with H. pylori and four without H. pylori infection) and we found cardiac inflammation was present in all cases with H. pylori infection. Histologically, H. pylori-related gastritis was also found in the gastric corpus and antrum. Serological data were consistent with the presence of chronic atrophic gastritis. Intestinal metaplasia was found in 18 cases in the cardiac mucosa, and their cytokeratin 7/20 pattern was judged as a gastric pattern in all cases. H. pylori infection is closely associated with cardiac cancer.

Role of Helicobacter pylori infection and use of NSAIDs in the etiopathogenesis of upper gastrointestinal bleeding

Non-steroid antiinflammatory drugs (NSAIDs) and Helicobacter pylori (Hp) infection are two most important independent risk factors involved in the etiopathogenesis of gastroduodenal mucosal injury with a clear and critical role in both uncomplicated and complicated peptic ulcer disease. It is estimated that upto 90% of all peptic ulcers result from the effect of one or both of these factors. To determine the frequency of NSAIDs use and Hp infection in patients with acute upper gastrointestinal bleeding. Study evaluated data from 500 patients in whom esophagogastroduodenoscopy was performed following presentation in emergency unit with acute upper gastrointestinal bleeding. Anamnestic data was collected together with detailed information on previous salicilates and/or NSAIDs use. Hp status was determined and anatomic localisation of bleeding lesion was also registered. Acute upper GIT bleading was caused solely by NSAIDs in 55 (11%), by aspirin in 66 (13.2%), while combined NSAID/aspirin therapy was identified in 19 (3.8%) of patients. In total NSAID and/or aspirin use were diagnosed in 139 (27.8%). while in 122 (24.4%) only Hp infection was diagnosed. Both risk factors were identified in 144 (28.8%) patients (Hp+NSAIDs in 12.2%, Hp+aspirin in 10.8% and Hp+aspirin+NSAIDs in 5.8%). In 19.8% of the cases (14% of males and 27% of females) neither NSAID/aspirin use nor presence of Hp infection was noted. Out of 500 patients enrolled, 63% were mails. In females, bleeding lesion was most frequently localized in gastric mucosa, while males had equal chance of bleeding from either gastric or duodenal mucosa. Fortunatelly, only 5 to 7% of patients were bleeding from both gastric and duodenal lesion. Prevention of acute upper gastrointestinal bleeding can be achieved trough strict and limited use of aspirin and NSAIDs, eradication of Hp infection and use of gastroprotective therapy in well-defined risk patients that need chronic NSAIDs and/or aspirin therapy. In all patients starting long-term NSAID and/or aspirin therapy and all patients already on long-term aspirin therapy test and treat strategy for Hp infection should be used. On the other hand, only in high risk patients (more than 65 years, history of peptic ulcer disease, concomitant corticosteroid, aspirin, clopidogrel or warfarin therapy) already on chronic NSAID therapy long-term PPI therapy should be prescribed after testing and treating of Hp infection.

Frequency of Helicobacter pylori infection in patients with liver cirrhosis

Ulcer disease occurrence is increased among patients with liver cirrhosis. It is widely accepted that Helicobacter pylori infection is important in aetiology of ulcer disease. The role of Helicobacter pylori infection in pathogenesis of ulcer disease in patients with liver cirrhosis has not been satisfactorily explored yet. The aim of this study was to determine frequencies of Helicobacter pylori infection in patients with liver cirrhosis in relation to the aetiology of cirrhosis, clinical stage and concomitant ulcer disease. We studied 50 patients with liver cirrhosis analysing the aetiology of liver cirrhosis, clinical stage, presence of ulcer disease, and existence of Helicobacter pylori infection. Results were thoroughly analysed and compared. Among 50 studied subjects, 37 were male (average age 56.62 +/- 10.47 years), while 13 were female (average age 60.69 +/- 6.51 years). In 32 (64%) patients, liver cirrhosis was related to alcohol abuse, whereas in remaining 16 (36%) subjects, cirrhosis was due to chronic viral infection. Ulcer disease, determined by endoscopy, was present in 8 (16%) patients, although 18 (36%) subjects were Helicobacter pylori positive. There were no significant differences in occurrences of Helicobacter pylori infection amongst the patients with and without ulcer disease (chi2 = 0.923; p > 0.05). No significant difference was found for the clinical stage and type of ulcer disease (chi2 = 0.869; p > 0.05). The difference in presence of Helicobacter pylori infection and aetiology of liver cirrhosis appeared to be of no significance, either (F = 0.540; p > 0.05). The presence of Helicobacter pylori infection in different clinical stages seemed to be of statistical significance (chi2 = 7.0; p < 0.05). The obtained results indicate that the prevalence of Helicobacter pylori infection in patients with liver cirrhosis is lower compared to general population, and that is of no significance for ulcer disease in these subjects. Moreover, it is likely that the frequency of Helicobacter pylori infection in patients with liver cirrhosis is not related to the aetiology of cirrhosis, while this infection seems to be more frequently present in severe clinical forms of hepatic cirrhosis.

Helicobacter felis Infection Causes an Acute Iron Deficiency in Nonpregnant and Pregnant Mice

The role of Helicobacter pylori infection in iron deficiency during pregnancy is limited. The aim of the present study was to assess the relationship between Helicobacter infection and levels of iron stores in pregnant mice. Female C57BL/6 mice were either inoculated with 10(8) H. pylori, Helicobacter felis or water. In the nonpregnant study, 15 mice from each group were sacrificed after 4 and 20 weeks of infection. In the pregnancy study, after 6 weeks of infection all female mice were mated and approximately 2 weeks after mating, half of the pregnant mice (n = 9/group) from each group were sacrificed. The remaining mice were allowed to give birth, and approximately 4 weeks after birth, mice were asphyxiated with CO2, followed by heart puncture, and killed by cervical dislocation. Serum ferritin and iron were determined with a micro-particle enzyme immunoassay method and by a timed-endpoint method. Serum iron levels in mice infected with H. felis were significantly (p < .05) lowered compared to control (24%) and H. pylori (27%)-infected mice at 4 weeks of infection. Serum iron in the control, H. pylori and H. felis groups were significantly (p < .05) elevated at 20 weeks by 39, 26 and 77%, respectively, compared to 4 weeks of infection. H. felis-infected mice had a significantly (p < .05) decreased serum ferritin level during pregnancy (61%) compared to H. pylori-infected mice. These results suggest that H. felis but not H. pylori infection causes an acute iron deficiency in normal and pregnant mice.