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Biomedical subjects

G Fedeli

Publications and source records attributed to G Fedeli.

At least 19 recordsLinked to original sources

Efficacy of a multistep strategy for Helicobacter pylori eradication.

BACKGROUND: Helicobacter pylori eradication therapies do not achieve 100% success rates. Antibiotic resistant strains are among the major causes of failure. Current recommendations concerning the management of treatment failures are not fully clear. AIM: To evaluate the efficacy of a multi-step therapeutic strategy in a large group of infected patients. METHODS: A total of 2606 H. pylori-positive patients were administered tinidazole, clarithromycin and a proton pump inhibitor for 1 week. Patients with continuing infection were then given a second 1-week course of amoxycillin, clarithromycin and ranitidine bismuth citrate. Patients still infected after the second course underwent upper gastrointestinal endoscopy with H. pylori culture, and then received a 1-week quadruple proton pump inhibitor-bismuth based scheme established on H. pylori antibiotic sensitivity. RESULTS: After the first step, eradication was achieved in 2063 out of 2413 patients [86% per protocol analysis (PP); 79% intention-to-treat analysis (ITT)]. First-step failures (350 out of 2413; 14.5% PP) showed second-step eradication rates of 82% (271 out of 329 patients, PP; 77% ITT). The specific quadruple therapy for second-step failures (58 out of 329, 18% PP) achieved 77% (30 out of 39 patients, PP) or 52% (ITT) success. This algorithm led to overall eradication rates of 99% (PP) or 91% (ITT). CONCLUSIONS: This multi-step strategy succeeded in a high percentage of H. pylori infected patients. Given the lack of precise guidelines on treatment failures, assessing H. pylori sensitivity to antibiotics only after failure of the second treatment could be suggested in clinical practice.

Algorithms↗

Prevalence and early diagnosis of coeliac disease in autoimmune thyroid disorders.

BACKGROUND AND AIMS: Coeliac disease is associated with several autoimmune disorders such as insulin-dependent diabetes, Sjogren's syndrome, Addison's disease and thyroid diseases. The aim of our study was to evaluate the prevalence of coeliac disease in patients affected by autoimmune thyroid diseases by means of anti-gliadin and anti-endomysial antibodies. PATIENTS: We studied 92 patients affected by autoimmune thyroid diseases (47 chronic autoimmune thyroiditis, 22 Hashimoto's thyroiditis and 23 Graves' disease). Ninety patients with non autoimmune thyroid disorders (51 multifollicular goitre, 28 solitary nodule and 11 papillary carcinoma) and 236 blood donors also took part in the study as control groups. METHODS: Total serum IgA were measured in all subjects to exclude selective IgA deficiency; then we measured anti-gliadin antibodies and anti-endomysial antibodies. In patients with anti-gliadin/anti-endomysial antibody positivity and/or with haematinic and laboratory signs of malabsorption we carried out gastrointestinal endoscopy with duodenal histological examination. RESULTS: Among the 92 patients with autoimmune thyroid disease, 4 (4.3%) showed anti-gliadin and anti-endomysial positivity and had coeliac disease; among the 90 patients with non autoimmune thyroid diseases, 1 (1.1%) had coeliac disease; finally, among the blood donors, 1 subject (0.4%) was anti-gliadin-anti-endomysium antibody positive and had coeliac disease. Those subjects presenting with only anti-gliadin antibody positivity did not have coeliac disease. CONCLUSIONS: These results show that the prevalence of coeliac disease in patients with autoimmune thyroid diseases is significantly increased when compared with the general population (p = 0.009) but not with patients affected by non autoimmune thyroid disorders (p = 0.18). We suggest a serological screening for coeliac disease in all patients with autoimmune thyroid disease measuring anti-endomysial antibodies, considering that early detection and treatment of coeliac disease are effective in preventing its complications.

Adult↗

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.

Aged↗

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↗

Disappearance of gastric mucosa-associated lymphoid tissue in coeliac patients after gluten withdrawal.

BACKGROUND: Mucosa-associated lymphoid tissue (MALT) develops in gastric mucosa in response to chronic antigenic stimulation, such as Helicobacter pylori infection. However, reactive lymphoid follicles have been found also in the stomach of H. pylori-negative coeliac patients, suggesting that other environmental factors may be involved in MALT genesis. The aim of our study was to evaluate the effects of gluten withdrawal in H. pylori-negative coeliac patients with gastric MALT. METHODS: We studied 23 H. pylori-negative untreated coeliac patients with gastric MALT. All patients underwent determination of antigliadin (AGA) and antiendomysium antibodies (EMA) and upper endoscopy with multiple biopsies in duodenum, gastric corpus, and antrum. Lymphoid follicles and H. pylori status were assessed by histopathologic and enzymatic analysis. All patients were started on a gluten-free diet and were reevaluated after 12 months. To consider their adherence to the gluten-free diet we relied on direct patient questioning. Thirteen patients who had strictly adhered to the gluten-free diet constituted our study group. Ten patients who had not strictly adhered to gluten withdrawal from their diet constituted the control group. RESULTS: Regression of MALT was obtained in 9 of 13 (69%) patients who strictly followed the gluten-free diet; in the control group MALT disappeared in 2 of 10 (20%) patients (P=0.0361). DISCUSSION: Disappearance of reactive lymphoid follicles in the gastric mucosa of H. pylori-negative coeliac patients after gluten withdrawal suggests that antigens related to alimentary gluten may constitute persistent stimuli for development of gastric MALT in coeliac patients.

Adult↗

Helicobacter pylori infection and ischaemic heart disease.

Helicobacter pylori infection is probably one of the most widely spread infectious diseases in man and a growing body of knowledge provides evidence in favour of a causal link between this infection and the majority of upper gastrointestinal conditions. For example, we now know that peptic ulcer disease is an infectious disease; if the infection is diagnosed and treated, ulcer can be cured. On the other hand, in recent years, a number of epidemiological studies have focused on the possible relation between ischaemic heart disease and several infectious disorders, such as chronic dental infections, Cytomegalovirus, Coxsackie viruses, Chlamydia and, finally Helicobacter pylori. The results of studies on the association between ischaemic heart disease and Helicobacter pylori have, in particular, often been contradictory, and only some studies adjusted the results for confounding factors, and the adjustment of the results in some cases modified the association. In conclusion, even if coronary atherosclerosis may now be considered as an inflammatory process, according to several histologic and pathophysiologic studies, we cannot, for the moment, be sure that it is an infectious disease.

Antigens, Bacterial↗

Effect of moderate and heavy alcohol consumption on intestinal transit time.

BACKGROUND: Alcohol abusers frequently have gastrointestinal symptoms, such as diarrhea, nausea and vomiting. In the genesis of these symptoms multiple mechanisms are involved, including alteration of gastrointestinal motility. The aim of our study was to investigate oro-cecal transit time (OCTT) using the H2-breath test (H2-BT) in moderate and heavy drinkers. MATERIALS AND METHODS: We studied 40 chronic drinkers: 20 with heavy alcohol consumption (> or = 60 g/day for men and > or = 40 g/day for women) and 20 with moderate alcohol intake (< 60 g/day for men and < 40 g/day for women). The control group consisted of 20 teetotal subjects. All subjects underwent a lactulose H2-BT to assess OCTT. RESULTS: OCTT in heavy alcohol drinkers ranged from 100 to 240 min, with a mean of 149.5 min, while OCTT in moderate drinkers ranged from 70 to 140 min, with a mean of 109 min. In the control group the mean OCTT was 100 mins, ranging from 70 to 130 min. The difference between alcohol abusers and controls was statistically significant; on the contrary, there was no statistically significant difference between moderate alcohol drinkers and teetotallers. CONCLUSIONS: Our study shows that only in chronic heavy alcohol drinkers is OCTT clearly increased. Multiple mechanisms are hypothesized to explain motility disorder, such as visceral autonomic neuropathy, inflammation and loss of contractile proteins of smooth muscle layer of the small intestine.

Adolescent↗

The growth of primary low-grade B-cell gastric lymphoma is sustained by Helicobacter pylori.

BACKGROUND: The growth of primary low-grade B-cell gastric mucosa-associated lymphoid tissue (MALT) lymphoma is an antigen-dependent process CASE: We were able to document the influence of Helicobacter pylori on the natural history of primary low-grade B-cell gastric MALT lymphoma in a case investigated by means of polymerase chain reaction for IgH rearrangement. In this case the presence or absence of the bacterium appeared to affect both clinical manifestations and histologic features of the neoplasia, with an acceleration or a slowing down of the neoplastic expansion, respectively. CONCLUSIONS: We identified H. pylori as an antigenic stimulus that supports the growth of MALT-type lymphoma. This finding enables us to make some considerations about the management of the disease.

Aged↗

Gastric mucosa-associated lymphoid tissue in autoimmune thyroid diseases.

BACKGROUND: There is increasing evidence for a link between Helicobacter pylori infection and the development of lymphoid follicles in the gastric mucosa. It is not known whether other factors may also play a role. The aim of this study was to investigate the role played by the host with peculiar immunogenic disorders, in the presence or absence of a known antigenic stimulus such as H. pylori. For this, we studied patients with autoimmune thyroid diseases. METHODS: Thirty patients with autoimmune thyroid diseases and 30 dyspeptic patients without a history of thyroid disorders (as control group) underwent upper endoscopy. Lymphoid follicles and H. pylori status were assessed by histopathologic and enzymatic analysis. RESULTS: Organized mucosa-associated lymphoid tissue was found in 73.3% of the patients and in 33.3% of control group. Lymphoid follicles were found in 87.5% of the H. pylori-positive patients and in 57.1% of the H. pylori-negative patients (P = NS). In the control group these follicles were present in 50% of H. pylori-positive subjects and in 14.3% of those who were H. pylori-negative. CONCLUSIONS: lYMPHOID follicles in the gastric mucosa are common in autoimmune thyroid diseases. Besides H. pylori infection, other factors (environmental, unknown infectious agents) or mechanisms related to the underlying disease may play a causal role.

Adult↗

[Intestinal permeability].

Intestinal mucosa has an absorptive function and acts also as a selective barrier against potential antigenic, toxic and carcinogenic substances. Intestinal permeability can be defined as the capacity of mucosal surface to be penetrate by specific substances through unmediated diffusion. There are two theories about molecular permeation routes: the first one hypothesizes a transcellular (through small pores), a paracellular (through big channels) and a lipophilic pathways; the second one gives a key role only to paracellular tight-junctions. In many diseases we can find changes in intestinal permeability evaluable by simple and non invasive tests, administering "per os" probe molecules. These substances cross the epithelium in different way and amount according to their physicochemical features and mucosal integrity; then they reach circulation and are eliminated in urines where they can be detected. The most frequently molecules used are mono/disaccharides, 51Cr-labelled ethylenediaminetetraacetate (51Cr-EDTA) and polyethylene glycol (PEG). This simple method has become more and more used for diagnostic and speculative aims. These intestinal permeability tests have a low specificity so they cannot be used for a definitive diagnosis of intestinal disease; nevertheless, the high sensitivity for intestinal mucosal damage could make them a necessary method to evaluate mucosal integrity after therapy, to select patients with a specific symptoms and to support, particularly in pediatric populations, more specific and invasive diagnostic tests.

Humans↗

[The modes of transmission of Helicobacter pylori infection].

Helicobacter pylori plays an essential role in the development of several both acid-related and neoplastic gastroduodenal pathologies. There are still uncertainties about the transmission routes and the sources of H. pylori infection. Man is the only well established "reservoir" of H. pylori, while the role of other mammalians (cat, pig, primates), as sources of infection, is still controversy. Literature data suggest four different modalities of transmission of the infection: faeco-oral, oro-oral, gastro-oral, gastro-gastric. By faeco-oral route, the bacterium, excreted with faeces, might colonize water sources, becoming so available to be transmitted to man and other mammalians. By oro-oral route, H. pylori, which colonizes dental plaque and saliva, may be transmitted by saliva to other individuals. The gastro-oral route is the typical modality of transmission in the childhood, when H. pylori uses the mucous achlorhydric vomitus of the children to infect a new host. Finally, by gastro-gastric route the bacterium might be transmitted by endoscopic procedures. In conclusion, we believe the different modalities of transmission may be contemporaneously involved, since none per se is able to explain the widespread occurrence of H. pylori infection.

Disease Susceptibility↗