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Biomedical subjects

A Armuzzi

Publications and source records attributed to A Armuzzi.

At least 55 records · Page 3Linked to original sources

Extradigestive manifestations of Helicobacter pylori gastric infection.

In the past year, several studies have been carried out on the association between Helicobacter pylori infection and a miscellany of extradigestive diseases, such as cardiovascular, immunological, and various other pathologies. In particular, a higher prevalence of H pylori infection in patients affected by ischaemic heart disease has been described and there is growing evidence for an association between H pylori and some autoimmune diseases. Moreover, recent studies have shown that various helicobacter species have been detected in human bile; if confirmed, this finding could revise the diagnostic and therapeutic approach to diseases of the biliary tract.

Autoimmune Diseases↗

The role of Helicobacter pylori in cardiovascular and cerebrovascular diseases.

Classical risk factors for cardiovascular and cerebrovascular diseases do not fully coincide with the prevalence of these conditions. Emerging evidences show that new factors may be predisposing for the development of ischemic events. It has been demonstrated that atherosclerosis has a strong inflammatory background; such state of chronic inflammation may be related to the presence of persistent infectious agent. Helicobacter pylori (H. pylori), among other microorganisms, has been extensively investigated for its possible role. Many molecular mechanisms have been hypothesized to explain its eventual action. Epidemiological studies do not exclude a correlation between the infection and cardiovascular and cerebrovascular diseases. Many confounding factors, however, make difficult a definitive evaluation of the huge number of data present in the literature. Moreover, various therapeutic studies have been attempted to show if antibiotic treatment improves prognosis in patients affected by ischemic heart disease. Still, none of these trials focused specifically on the effects of H. pylori eradication on the clinical progression of vascular lesions.

Cardiovascular Diseases↗

One-week therapy for Helicobacter pylori eradication: ranitidine bismuth citrate plus medium-dose clarithromycin and either tinidazole or amoxycillin.

BACKGROUND: One-week ranitidine bismuth citrate (RBC)-based triple regimens may be effective for the eradication of Helicobacter pylori. We evaluated the efficacy of two short-term RBC-based eradicating therapies including RBC plus medium-dose clarithromycin and either tinidazole or amoxycillin. METHODS: Seventy consecutive patients, who underwent gastroscopy for dyspeptic symptoms and were found to be H. pylori-positive, were randomly subdivided into two groups receiving either RBC 400 mg b.d. plus clarithromycin 250 mg t.d.s. and tinidazole 500 mg b.d. (group RBCCT) or RBC 400 mg b.d. plus clarithromycin 250 mg t.d.s. plus amoxycillin 1 g b.d. (group RBCCA). H. pylori status was evaluated by means of histology and rapid urease test at entry, and by 13C-urea breath test alone 8 weeks after treatment. RESULTS: Sixty-nine out of 70 enrolled patients completed the study: 35/35 in group RBCCT and 34/35 in group RBCCA. One patient in group RBCCA was lost to follow-up. In group RBCCT, at the end of treatment, 32 of 35 patients were H. pylori-negative (per protocol analysis 91%, intention-to-treat analysis 91%; 95% CI: 77-98%). In group RBCCA, 31 of 34 patients returned H. pylori-negative (per protocol 91%; 95% CI: 76-98%, intention-to-treat 89%; 95% CI: 73-97%). Slight side-effects occurred in 3/35 patients (9%) in group RBCCT and in 3/34 (9%) in group RBCCA. CONCLUSIONS: One-week regimens consisting of RBC plus clarithromycin and either tinidazole or amoxycillin, combine high eradication rates with modest side-effects. No substantial difference was found between the two treatment regimens tested in this trial.

Adult↗

Importance of changes in epithelial cell turnover during Helicobacter pylori infection in gastric carcinogenesis.

The role of Helicobacter pylori in gastric carcinogenesis is supported almost exclusively by epidemiological data and prospective histopathological studies. From biological and molecular points of view, there is no evidence that H pylori or its cytotoxic products have any mutagenic effects. Nevertheless, this infection is associated with profound changes in the pattern of epithelial cell turnover in gastric glands, though the importance of these changes in gastric carcinogenesis is still controversial. H pylori infection increases cell proliferation and alters the distribution of cycling cells within these glands, but these changes can be reversed by successful eradication of the infection. Apoptosis seems to be increased in gastric epithelial cells during H pylori infection, as shown by in vitro studies. There is some, though no conclusive, evidence that this finding also occurs in H pylori positive subjects. It seems that cagA status influences the effect of H pylori on epithelial apoptosis in infected patients. An association of in vitro H pylori induced apoptosis with changes in the expression of pro- and anti-apoptotic genes is reported in the literature, but further study is necessary to clarify the effect of H pylori infection on the molecular events of the apoptotic pathway.

Apoptosis↗

Epithelial cell turnover and apoptosis.

The homeostasis of gastric epithelial cells is maintained by the balance between cell proliferation and apoptosis. Alterations of these physiological cellular events in chronic pathological conditions of the stomach. As far as the proliferative pattern is concerned, an increase in the total number of epithelial proliferating cells and an abnormal distribution of the latter are frequently observed in chronic gastritis, gastric atrophy, intestinal metaplasia, gastric dysplasia and gastric cancer. Conversely, apoptosis has been found to be impaired in intestinal metaplasia, gastric dysplasia and cancer. Helicobacter pylori infection is associated with changes in epithelial-cell turnover, though their significance in gastric carcinogenesis is still controversial. An increase in overall epithelial cell proliferation and the upward shift of replicating cells toward the superficial part of the gastric pits are patterns usually observed during Helicobacter pylori infection and these changes can be reversed by successful eradication of the infection. However, it seems that this reversibility will be lost during progression through the steps of gastric carcinogenesis, such as intestinal metaplasia, probably representing the phenotypic expression of the true initiating phase of the carcinogenetic process. The influence of Helicobacter pylori infection on gastric epithelial apoptosis in humans is still controversial, since different results having been obtained by different authors. It seems that cagA status influences the effect of Helicobacter pylori on epithelial apoptosis, so that a different cagA make-up of the studied groups could explain these conflicting results. However, further studies are needed to elucidate this issue in humans.

Apoptosis↗

Epithelial-cell apoptosis and proliferation in Helicobacter pylori-related chronic gastritis.

BACKGROUND: Several studies have shown that Helicobacter pylori infection is associated with enhanced gastric epithelial-cell proliferation, which is thought to be involved in its apparent carcinogenicity. This hyperproliferation is believed to be related to the inflammatory effects of the bacterium. The role of Helicobacter pylori in gastric epithelial apoptosis, however, is less clear. AIM: We attempted to identify the effect of Helicobacter pylori infection on apoptosis in the gastric epithelium and its possible relation to epithelial-cell proliferation and mucosal inflammation. PATIENTS AND METHODS: We studied cell proliferation (via bromodeoxyuridine labelling), apoptosis (using in situ TdT-mediated dUTP-biotin nick end labelling of DNA strand breaks) and mononuclear and polymorphonuclear cell infiltrates (computer-assisted image analysis) in gastric antral biopsies obtained from 37 gastritis patients (20 Helicobacter pylori-positive, 17 Helicobacter pylori-negative). RESULTS: Helicobacter pylori-positives displayed significantly enhanced proliferation within the gastric epithelium that was positively correlated with both acute and chronic inflammatory-cell densities. Apoptotic indexes were similar in both groups and showed no correlation with any of the parameters under consideration. CONCLUSIONS: Enhanced epithelial cell proliferation and an altered distribution of cycling cells within the gastric glands are a common feature of chronic superficial gastritis caused by Helicobacter pylori. In vivo immunohistochemically detected apoptosis of gastric epithelial cells does not seem to be affected by Helicobacter pylori infection. Further study is needed to clarify the effect of this infection on programmed cell death within gastric glands.

Adult↗

Seroprevalence of hepatitis A virus and Helicobacter pylori infections in the general population of a developed European country (the San Marino study): evidence for similar pattern of spread.

OBJECTIVE: To evaluate the role of faecal-oral transmission in the spread of Helicobacter pylori. DESIGN: A cross-sectional comparison of the patterns of hepatitis A and H. pylori seropositivity. METHODS: At interview, blood samples and questionnaire data were collected from a random sample of 1528 healthy subjects aged 20-85 years from the Republic of San Marino. Serum samples from each subject were then tested for anti-H. pylori and anti-hepatitis A antibodies. RESULTS: Overall, 529 of 670 H. pylori-seropositive subjects (78.9%) and 460 of 858 H. pylori-seronegative subjects (53.6%) were hepatitis A seropositive (P<0.01; odds ratio=3.2; confidence interval 95%=2.6-4.1). This association remained after adjustment by a multiple logistic regression analysis for the confounding effect of age and length of schooling, as surrogate for socio-economic status (OR=2.0; CI 95%=1.3-3.3). The age-specific prevalence curves for H. pylori and hepatitis A infections showed a parallel increase by age, although to a lesser extent for H. pylori. CONCLUSION: These findings provide evidence that in the community studied H. pylori may have spread in a manner similar to that of hepatitis A.

Adult↗

Anti-CagA antibodies are associated with atrophic gastritis in a population at high gastric cancer risk: a morphometric study by computerized image analysis.

BACKGROUND: CagA-positive Helicobacter pylori strains appear to increase the risk for atrophic gastritis. AIM: To verify the association between CagA status and atrophic gastritis in the general population by means of computerized image analysis. SUBJECTS: Forty-five subjects were chosen out of a representative sample of a population at high gastric cancer risk. METHODS: Helicobacter pylori status was assessed by IgG ELISA, rapid urease test and histology. Serum anti-CagA antibodies were detected by western blotting. Subjects were subdivided into 3 groups: 15 subjects Helicobacter pylori positive CagA-positive, 15 Helicobacter pylori positive CagA-negative and 15 controls Helicobacter pylori negative. Biopsies were studied using the Sydney System score. A computerized image analysis was used to count inflammatory cells in the lamina propria and to measure the area of the gastric glands. RESULTS: Anti-CagA antibodies were associated with reduction of gland area (126,671 +/- 81,032 mu 2/mm2 vs 231,384 +/- 54,159; p = 0.0001), with increasing both of polymorphonuclear cells (426 +/- 238 cell/mm2 vs 136 +/- 69; p = 0.0001) and mononuclear cells (8675 +/- 1304 cell/mm2 vs 7141 +/- 1230; p = 0.003). CONCLUSIONS: The association of anti-CagA antibodies with a high grade of gastric atrophy further supports the hypothesis that Helicobacter pylori CagA-positive strains can promote the multifactorial process of gastric carcinogenesis.

Adult↗

Prevention and treatment of low-grade B-cell primary gastric lymphoma by anti-H. pylori therapy.

Mucosa-associated lymphoid tissue (MALT) showing a follicular structure can develop in the gastric mucosa as a response to Helicobacter pylori infection. We emphasize the importance of anti-H. pylori antibiotic therapy in the elimination of acquired MALT. Of the 200 patients studied, acquired MALT was found in 70 of the 151 H. pylori-positive patients, whereas it was present in only five of the 49 H. pylori-negative patients. Thirty-eight H. pylori-positive and MALT-positive patients were treated with antibiotic therapy and reevaluated after 6 months: 21 patients were H. pylori negative/MALT negative, 12 were H. pylori positive/MALT positive, four were H. pylori negative/MALT positive, one was H. pylori positive/MALT negative. In the control group (n = 20), H. pylori and acquired MALT were still present at follow-up. One patient with histological and immunohistochemical evidence of low-grade B-cell gastric MALT lymphoma underwent antibiotic treatment and was reexamined after 8, 12, and 24 weeks: histological examination of biopsy samples showed regression of the MALT lymphoma in tandem with the disappearance of H. pylori colonization. Our data confirm the correlation between H. pylori infection and acquired MALT, as documented by the ability of antibiotic therapy to induce the disappearance of acquired MALT and regression of MALT lymphoma. Considering the potential evolution of MALT into low-grade B-cell MALT lymphoma, H. pylori eradication should play a role in the prevention of this tumor.

Adolescent↗

Efficacy and tolerability of antibiotics in patients undergoing H. pylori eradication.

BACKGROUND/AIMS: 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. METHODOLOGY: One hundred and ninety-three (193) H. pylori-positive patients were randomly assigned to one of the following 7-day treatments: Group A (N = 64): amoxicillin, clarithromycin and rabeprazole; Group B (N = 64): tinidazole, clarithromycin and ranitidine bismuth citrate; Group C (N = 65): tinidazole, clarithromycin and rabeprazole Eradication was assessed by 13C-Urea Breath Test 6-8 weeks after the end of the therapy. Not-eradicated patients underwent a second cycle with tinidazole, tetracycline, bismuth and rabeprazole. All patients were asked to complete a validated questionnaire regarding presence and intensity of drug side effects. RESULTS: One hundred and eighty-eight out of the 193 H. pylori-positive patients (96%) completed therapy. No significant difference in eradication rates was observed among the three groups both in intention to treat analysis and in per protocol analysis. No significant difference in incidence of side effects occurred among groups after the first-line regimens: 48% in group A, 44% in group B and 46% in group C. Twenty-two out of the 193 enrolled subjects (11%) were not eradicated after the first-line therapy. Among them, 86% were successfully eradicated by the tinidazole, tetracycline, bismuth and rabeprazole therapy. Moreover, during quadruple therapy, a higher prevalence and intensity of side effects than in each one of the groups submitted to the first-line triple therapy was observed. CONCLUSIONS: This study shows that triple rabeprazole-based eradicating regimens are effective and safe. Incidence of side effects seems low and similar in different three-drug regimens used. Quadruple therapy, which appear highly efficacious as a second line therapy, is associated with a significantly higher incidence of side effects when compared to first-line treatment.

Adult↗

[Helicobacter pylori and gastric carcinoma].

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.

Helicobacter Infections↗

Pharmacological approaches to the management of alcohol addiction.

Alcohol abuse and alcoholism represent a world-wide problem, both from a medical and a social point of view. In the past the therapy for patients affected by alcoholism was based mainly on the psychological approach. In recent years the use of pharmacotherapy together with psychosocial interventions have enhanced the percentage of success in maintaining alcoholic patients in remission. The present review discusses the main drugs experimented both in preclinical and clinical studies. Pharmacotherapy of alcohol dependence seems to be effective in both alcohol-related emergencies and prevention relapse. However, pharmacotherapy should not be considered as the only form of treatment but as an integrated part of a multimodal approach including psychological and social support.

Alcohol Deterrents↗

Antibodies to Saccharomyces cerevisiae: are they useful in clinical practice?

BACKGROUND/AIMS: Antibodies to Saccharomyces cerevisiae are associated with Crohn's disease. The aim of this study was to assess the sensitivity and specificity of antibodies to Saccharomyces cerevisiae for Crohn's disease in an Italian population and to evaluate their clinical role. METHODOLOGY: Antibodies to Saccharomyces cerevisiae serum levels were assessed in 72 inflammatory bowel disease patients (30 Crohn's disease; 42 ulcerative colitis) and 35 age-matched controls. Patients were divided into subgroups on the basis of disease behavior and clinical feature were evaluated. RESULTS: Antibodies to Saccharomyces cerevisiae sensitivity and specificity for Crohn's disease patients were 50% (31-68) and 91% (77-98), for IgG and 56% (37-64) and 94% (80-99), respectively, for IgA. No correlation was observed between the presence of antibodies to Saccharomyces cerevisiae and clinical features. Antibodies to Saccharomyces cerevisiae were more prevalent in Crohn's disease than in ulcerative colitis patients (IgA: 57% vs. 26%; IgG: 50% vs. 17%; p < 0.05). Interestingly, in Crohn's disease patients, the prevalence of antibodies to Saccharomyces cerevisiae was higher in patients with small bowel involvement than in patients with pure colonic disease (IgA: 66% vs. 17%; IgG: 58% vs. 17%). No difference in antibodies to Saccharomyces cerevisiae prevalence was observed between ulcerative colitis and pure colonic Crohn's disease patients. CONCLUSIONS: Our data show an association between Crohn's disease and antibodies to Saccharomyces cerevisiae. However, it does not seem useful in discriminating between ulcerative colitis and colic Crohn's disease.

Adult↗

13C-breath tests in the study of mitochondrial liver function.

Breath tests for "dynamic" liver function evaluation have been proposed several years ago. A variety of carbon-labelled breath tests for the assessment of mitochondrial, microsomal and cytosolic liver function have been described with the aim to increase data on liver disease staging, prognosis, and response to therapy. In the last years a great interest is developed about the use of breath test for liver mitochondrial function evaluation since it results impaired in a wide range of liver diseases either of genetic or acquired origin. In these cases mitochondrial oxidative metabolism of some substrates, as far as recovery of the hepatic energy state after a metabolic insult, results impaired because of the disfunction of the electron transport chain and/or ATP synthesis. Ketoisocaproic acid and methionine are the best studied carbon-labelled substrates for the investigation of mitochondrial functional damages related to structural alterations that occur in many liver diseases. Although these tests are simple, cost-effective and safe, to date there is still not general approval for their usefulness in clinical settings since they should fulfill several requirements to overcome the drawbacks of traditional quantitative tests. On the other hand, this field is relatively young and further studies are needed in order to assess the suitable substrate for the evaluation of the complex mitochondrial metabolism both in healthy subjects and in patients with liver disease.

Breath Tests↗

13C-breath tests in the study of microsomal liver function.

Conventional liver tests can be used to estimate a mixture of injury and function but none of these may be regarded as a reliable marker either to quantify functional hepatic reserve or to reflect life-threatening complications of acute and chronic liver diseases. To overcome this limit, many dynamic tests have been developed in order to evaluate the "hepatic functional mass". Among these tests we can include breath tests with 13C-labeled substrates undergoing different metabolic pathways. As concerning the evaluation of microsomal function, two main categories of breath tests have been developed based on the limiting step in the different substrates metabolism. The first group include aminopyrine, caffeine and diazepam, all substrates with a metabolism independent from hepatic blood flow and dependent almost exclusively from the enzymatic activity of different cytochromes P450. The other group is composed of substrates with flow dependent metabolism like methacetin, phenacetin, erythromycin. The aim of this review is to describe the clinical applications of microsomal liver breath tests in different hepatic diseases.

Acetamides↗

Infliximab in the treatment of steroid-dependent ulcerative colitis.

BACKGROUND AND OBJECTIVES: Infliximab has proven efficacious in the treatment of Crohn's disease. Limited and contrasting data are available on effectiveness of anti-TNF alpha therapy in ulcerative colitis. We evaluated the efficacy of infliximab in the management of steroid-dependent ulcerative colitis. METHODS: We report preliminary data from a randomized, open-label, methylprednisolone-controlled trial of infliximab in the induction and maintenance of remission of patients with moderate to severe steroid-dependent ulcerative colitis. Twenty patients received either three infusion of infliximab (5 mg/kg) at 0, 2 and 6 weeks and thereafter every 8 weeks (group A) or methylprednisolone (0,7-1 mg/kg) daily for one week followed by a tapering regimen up to the minimal dose to maintain a symptom-free condition (group B). Clinical remission was defined as a DAI score less than 3. RESULTS: Ten patients in group A (DAI: 8.9+/-1.4) achieved remission after the first infusion (DAI: 1.6+/-0,7; p = 0.005) and steroids were progressively discontinued. At present (mean follow-up: 9.8+/-1.1 months), 9 out of 10 patients maintain clinical remission, while one patient relapsed at 3 months. Ten patients in group B (DAI: 8.7+/-1.4) reached clinical remission at one week (DAI: 1.9+/-0.3; p = 0.005). Eight out of 10 patients were maintained at a minimal steroid dosage without any relapse at 9.7+/-1.0 months follow-up. Two patients relapsed at 6 and 8 months, respectively. CONCLUSIONS: Infliximab seems to be as effective as steroids in the management of moderate to severe steroid-dependent ulcerative colitis. These preliminary data suggest the potential efficacy of repeated treatment with infliximab for short-term maintenance of remission and steroid withdrawal in glucocorticoid-dependent ulcerative colitis.

Adult↗

A novel pathogenic role for microvasculature in inflammatory bowel disease.

Crohn's disease (CD) and ulcerative colitis (UC) are the two major forms of inflammatory bowel disease (IBD). Although their etiology is still unknown, the pathogenic mechanisms underlying intestinal inflammation have made impressive progress in our understanding. In particular, the abnormalities underlying IBD pathogenesis are not restricted to those mediated by classical immune cells such as T and B lymphocytes, macrophages and dendritic cells, but also nonimmune cells. Interestingly, endothelium has become one of the major areas of investigation in gut inflammation.

Animals↗