Endoscopic findings and clinical patterns are not useful for distinguishing low from high grade gastric MALT lymphoma.
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Biomedical subjects
Publications and source records attributed to G Fedeli.
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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.
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.
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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.
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.
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OBJECTIVES: Mucosa-associated lymphoid tissue (MALT) can develop in gastric mucosa after Helicobacter pylori infection, but not all H. pylori-positive patients develop acquired MALT, probably because of different levels of individual susceptibility against H. pylori-antigens. Our aim was to conduct long-term follow-up in MALT-positive and MALT-negative patients after H. pylori had been eradicated to determine what happens after H. pylori reinfection. METHODS: We studied 30 H. pylori-positive patients, 15 MALT-positive patients (group A), and 15 MALT-negative patients (group B). After the eradication of H. pylori and disappearance of acquired MALT in group A, follow-up was conducted by repeated endoscopic biopsies every 4-6 months for a mean period of 30.6 months (31.6 months for group A, 29.4 for group B). RESULTS: During follow-up, three group A patients were reinfected by H. pylori, and MALT recurred. Moreover, in each patient, it was the same grade of acquired MALT that had previously been diagnosed (grade 2 in two patients and grade 3 in one). A second course of anti-H. pylori treatment resulted both in eradication of H. pylori and the disappearance of MALT. Conversely, none of the group B patients with H. pylori reinfection developed MALT. However, in those patients, too, a second course of treatment eradicated the H. pylori. CONCLUSIONS: Our study shows that acquired MALT appears after reinfection with H. pylori only in patients who previously had that condition. Moreover, the grade of acquired MALT that reappears is the same as previously diagnosed. These findings demonstrate that not only H. pylori infection but also individual susceptibility may be important in determining both the presence of acquired MALT and its grade. However, strict follow-up is not advisable in MALT-positive patients, because no patient developed MALT-lymphoma during follow-up.
Some studies have suggested that low-grade MALT lymphoma may regress after eradication of Helicobacter pylori infection. This case report describes a Helicobacter pylori-positive patient with very extensive ulcerated polypoid lesions involving gastric antrum and prepyloric region, diagnosed by histology, pathological analysis and staging procedures as low-grade MALT lymphoma of EI1 stage. The patient received eradication therapy with a one-week course of omeprazole plus amoxicillin plus clarithromycin and was seen at follow-up after 3, 6 and 15 months. At follow-up, Helicobacter pylori eradication appeared to be in resolution of the macroscopic and histological features of the lymphoma, as confirmed by endoscopic, histological and molecular findings. Until now, only a few cases with a large gastric MALT lymphoma has successful treatment of Helicobacter pylori resulted in regression. Although additional follow-up is needed, it would appear that Helicobacter pylori infection cure may be effective also for large low-grade stage EI1 MALT lymphoma.
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AIM: To evaluate and compare two 1-week low-dose triple therapies based on lansoprazole, amoxycillin and a macrolide in eradicating Helicobacter pylori. METHODS: Seventy consecutive patients, suffering from dyspeptic symptoms with H. pylori infection, were randomly allocated to one of two treatment groups: (A) (LAC; n = 35) lansoprazole 30 mg once daily, amoxycillin 1000 mg b.d., clarithromycin 250 mg b.d., all for 7 days; and (B) (LAA; n = 35) lansoprazole 30 mg once daily and amoxycillin 1000 mg b.d., both for 7 days, plus azithromycin 500 mg once daily for only 3 days. The H. pylori status was evaluated by means of histology and rapid urease test at entry and 8 weeks after treatment. RESULTS: Three patients did not complete the treatment: one in the LAC group was withdrawn owing to severe side-effects; two patients in the LAA group stopped the treatment prematurely. H. pylori eradication was obtained in 28 of 34 (82%; 95% CI = 66-93%) patients in the LAC group and in 20 of 33 (61%; 95% CI = 42-77%) patients in the LAA group. The difference is significant (P < 0.029). On intention-to-treat analysis, the rates of eradication were (28 of 35 patients, 80% in the LAC group and 20 of 35 patients, 57% in the LAA group. Side-effects occurred in nine (26%) and six (18%) patients in the LAC and LAA groups, respectively. CONCLUSIONS: Low-dose lansoprazole plus amoxycillin and clarithromycin is more effective than low-dose lansoprazole plus amoxycillin and azithromycin, but it gave a greater incidence of side-effects.
With regard to the role of dental plaque in the transmission of Helicobacter pylori infection, data from the literature vary greatly, owing to differences in sample collection and H. pylori-detecting techniques. Using the polymerase chain reaction (PCR), we have determined the incidence of H. pylori colonization in the dental plaque of 31 consecutive patients who underwent gastroscopy. The patients were divided into two groups on the basis of H. pylori infection, determined by Giemsa stain and the rapid urease test: group A made up of 21 H. pylori-positive patients and group B with 10 H. pylori-negative patients. Our PCR assay of dental plaque samples proved negative in all group A subjects but was positive in only one patient in group B. In our study, we found that H. pylori had a low prevalence (3.2%) in the oral cavity, with no significant relationship between gastric mucosa and dental plaque colonization. More comprehensive studies are needed to determine whether dental plaque is an important reservoir in the epidemiology of H. pylori-induced gastric disease.
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BACKGROUND: The aim of our study was to compare two 1-week, low-dose triple therapies for Helicobacter pylori eradication. METHODS: One hundred consecutive patients, suffering from dyspeptic symptoms with H. pylori infection, were randomly allocated to 7 days of treatment with omeprazole 20 mg o.m. plus clarithromycin 250 mg b.d. and either tinidazole 500 mg b.d. (group A: n = 50, 19 with peptic ulcer) or amoxycillin 1000 mg b.d. (group B: n = 50, 20 with peptic ulcer). H. pylori-status was evaluated by means of histology, culture and urease test, at entry and 8 weeks after treatment. RESULTS: Three patients did not complete the treatment. H. pylori eradication was obtained in 35 patients from group A (73%) (95% CI, 55-82%) and in 40 patients from group B (82%) (95% CI, 66-90%). On intention-to-treat analysis, the rates of eradication were similar. Side-effects occurred in seven patients from group A (14.58%) and in four patients from group B (8.33%), but none discontinued therapy because of side-effects. CONCLUSION: Both triple 1-week, low-dose omeprazole therapies gave good eradication rates with infrequent side-effects.
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