How Exactly Does E-64 Perform?

6?years younger than cagA-negative patients (p?=?0.04) and smokers (p?=?0.02). No significant differences were found for age, sex or other clinical and lifestyle characteristics analysed. Bacterial load was much higher in patients with the virulence cagA gene: median cagA-positive antrum 345.4 (interquartile rank (IR) 1710.5); median cagA-negative antrum 58.4 (IR 297.8) p?=?0.002; median cagA-positive corpus 446.6 (IR 5190.6); median cagA-negative corpus 26.1 (IR 191.8) p?E-64 (scarce, moderate and abundant), with a very significant dose�Cresponse pattern: crude odds ratio for the highest category (ORH) in the antrum 4.28 (95% CI 1.5�C12.7), p trend?=?0.009; ORH corpus 12.5 (95% CI 3.0�C52.5), p trend?R428 associations became more marked after adjusting for age, sex, upper digestive tract haemorrhage and prior antibiotic treatment (see Table 1). Table 2 shows the associations between digestive tract morbidity, cagA and bacterial load adjusted for each other. CagA is more closely associated with the consumption of proton pump inhibitors than is the bacterial load: adjusted OR cagA 3.11 (95% CI 1.0�C9.6); ORH bacterial load 2.34. In relation to clinical presentation of upper digestive tract haemorrhage, although none of them yielded statistical significance, association was higher for bacterial load (ORH 2.34, 95% CI 0.6�C8.5) than for cagA (OR 1.12). However, consumption of NSAIDs (OR 8.99) or male sex (OR 3.26) is more closely associated with upper digestive tract haemorrhage than with cagA gene or bacterial load. In the case of a history of complicated ulcer, male sex is the factor most strongly associated (OR 7.20). Our data show that the cagA gene is detected in JQ1 younger people and it is statistically associated at high bacterial loads with a clear, significant dose�Cresponse (p trend) relationship between H.?pylori load and presence of cagA. These data suggest that both parameters combine to produce clinically significant lesions, as compared with colonization by strains of low virulence that multiply very little in the gastric mucosa and so do not cause significant damage [5]. These data are corroborated by the great variability in bacterial load values obtained. In some patients the number of microorganisms in the gastric mucosa was very small and therefore it is unlikely in these cases that the microorganism had an important influence on the patient��s pathology [6,7]. Our results suggest that the cagA gene is a risk factor independent of bacterial load in patients with a history of consumption of proton pump inhibitors (OR 3.11). This association could be explained by the fact that the virulence gene cagA produces greater gastric symptomatology, thus fomenting consumption of proton pump inhibitors.