SummaryThe contribution of Helicobacter pylori (HP) infection to the risk of myocardial infarction was evaluated. The role of fibrinogen and its genetic control as a possibile mechanism by which HP may influence myocardial infarction risk was explored in this context. A case-control study was performed in 101 patients with myocardial infarction and in 101 controls.HP infection was associated with an increased risk of myocardial infarction independently for confounding variables (OR 4.1, CI95: 1.8-9.4). HP infection was significantly associated with higher levels of fibrinogen, both in cases and in controls. Furthermore, there was an additive effect of HP infection and B2 allele of BclI fibrinogen poly-morphism in increasing fibrinogen levels. HP infection showed a stronger effect on the risk of myocardial infarction in B2 allele carriers (OR 7.6, CI95: 1.8-31.6) as compared to subjects carrying the B1B1 genotype (OR 3.3, CI95: 1.2-9.2).We showed that a previous HP infection is a risk factor for myocardial infarction. An increase in fibrinogen levels is a possible mechanism by which HP may act. Concomitant conditions, like a genetic predisposition in increasing fibrinogen levels, seem to further increase the effect of HP on myocardial infarction risk.
The morphological and histochemical features of colonic mucosa adjacent to 142 adenomas and 31 hyperplastic polyps were studied. Three predominant patterns were identified: (1) normal mucosa, showing normal histological architecture and secretion of sulphomucins; (2) N+ type, histologically normal mucosa with predominance of sialomucins; (3) transitional mucosa; hyperplastic mucosa secreting sialomucins. Hyperplastic changes were observed in the immediate neighbourhood or at the base of adenomas and were more frequent and extensive near large adenomas than around smaller lesions. Sialomucins were often predominant in the mucosa adjacent to large adenomas, but N+ type mucosa was also seen near minute adenomas and hyperplastic polyps and remote from polypoid lesions. Moreover, both hyperplastic and secretory changes were more frequent in the left colon than in the right. These findings seem to suggest that mucosal hyperplasia more likely represents a local change, parallel with or secondary to tumour development rather than a pre-adenomatous lesion. Secretory modifications are widespread and may result from the action of various factors among which carcinogens cannot be excluded.
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