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R Fiocca

Publications and source records attributed to R Fiocca.

113 records · Page 7Linked to original sources
PubMedDate not supplied

[Pathogenesis of peptic ulcer: role of Helicobacter pylori gastritis and its course during antibiotic and/or antisecretory treatment].

A systematic investigation of the histologic pattern of antral and corpus gastritis has been carried out in 1177 patients with various clinical conditions. An increased rate and severity of antral mucosa gastritis activity as well as surface epithelium cytotoxic lesions and Helicobacter pylori colonization, coupled with low rates and severity of the same parameters in corpus mucosa gastritis (usually of superficial nature so as to spare the integrity of acidopeptic glands) were the main features associated with active gastroduodenal peptic ulcer or antroduodenal mucosal erosions. Simultaneous antisecretory (omeprazole) and antibiotic treatment of duodenal ulcer patients led to the eradication of Helicobacter in 54 to 82% of patients when amoxycillin alone was used as antibiotic, and up to 94% of patients, when metronidazole was added to amoxycillin, as against none of patients treated with omeprazole alone, despite effective healing of their ulcer lesion. Very low (usually less than 5% per year) recurrency rates are reported in the literature for patients undergoing bacterial eradication, as against 50 to 80% in non-eradicated patients whose ulcer was healed by short term antisecretory drug treatment.

Amoxicillin↗
PubMedDate not supplied

[Helicobacter pylori and gastro-duodenal pathology].

Helicobacter Pylori (HP) were found in 878 (73%) of 1205 patients undergoing upper G-I endoscopy with multiple biopsies for gastroduodenal diseases. HP were present in similar percentages among patients with active (89%) or healed (81%) peptic ulcer as well as in non ulcerous dyspeptics affected with gastritis (85%). 96% of active chronic gastritis were infected by HP as compared with 55% of quiescent gastritis. Antral gastritis was more frequently active in patients with ulcer diseases (76%) than in dyspeptic and asyntomatic patients (50%). Healed gastric and duodenal ulcers showed decreased incidence of active antral gastritis (69) as compared with active ulcers. Conversely body gastritis was more frequently active in healed (37%) than in overt (18%) duodenal ulcers. 95 histologically normal stomachs as well as 9 cases exhibiting type A gastritis were devoid of HP. High rates of infection were found in 610 cases of chronic gastritis without atrophy as well as in 151 atrophic antral (type B) gastritis. Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in HP-infected mucosa. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated HP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions.

Adult↗
PubMedDate not supplied

Morphological evidence of Campylobacter pylori pathogenicity in chronic gastritis and peptic ulcer.

Campylobacter pylori (CP) were found in 84% of 384 patients with chronic gastritis and in none of 49 subjects without inflammation. CP were present in similar percentages among patients with active (90%) or healed peptic ulcer (84%), as well as in non-ulcerous dyspepsia complicated by gastritis (91%). Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in CP-infected mucosa. In 100 cases with gastritis both intraepithelial granulocytes and epithelial lesions were prominent features of heavily CP-infected antral mucosa. The occurrence of some cases with abundant, adhering CP but lacking epithelial lesions is in keeping with the different ability of various CP-strains to produce cytotoxins. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated CP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions. These data provide further morphological evidence of direct cytotoxic activity of CP toward gastric mucosal cells.

Adult↗
PubMedDate not supplied

p53 gene mutations and protein nuclear accumulation are early events in intestinal type gastric cancer but late events in diffuse type.

We screened for p53 alterations in 71 early gastric cancers of differing histological types and growth patterns, 18 advanced cancers of diffuse type, 19 dysplastic lesions, and 12 extensive intestinal metaplasia cases. Tumors were investigated for gene mutations (exons 5-8) with PCR-based denaturing gradient gel electrophoresis and sequencing techniques, and for protein accumulation with immunohistochemical methods. Nontumor samples were studied with immunohistochemistry alone. Of the early cancers, intestinal tumors showed a much higher p53 mutation frequency (41%) than did diffuse cancers (4%). When comparing early and advanced tumors of the same type, we observed a similarity in mutation frequency (41 versus about 50%) for intestinal tumors, and a significant increase for diffuse tumors (from 4 to 33%). Immunopositive case distribution between tumor types and stages paralleled that of mutated cases. Immunohistochemical and genetic analysis gave concordant results for all samples with gene mutations. Eighteen of the 65 (28%) nonmutated tumors displayed significant immunoreactivity. Early tumors that massively penetrated the submucosa, i.e., the early tumors for which prognosis is worst, showed the highest frequency both of p53 gene mutation and of nonmutated protein accumulation. Twelve of 19 dysplastic lesions showed significant immunoreactivity, whereas intestinal metaplasias proved unreactive in all but a few cells. Our results yield two implications: that p53 alterations have a crucial and early role in gastric carcinogenesis of intestinal type, likely acting at the transition step between metaplasia and dysplasia; and that the alterations are mainly associated with tumor progression in cancer of diffuse type.

Adenocarcinoma↗