Example sentences of "[prep] [letter] pylorus " in BNC.

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1 As the acid secretory capacity does not change after H pylori eradication , it would seem that the former is the more important determinant factor in the development of gastric metaplasia and the H pylori related inflammatory process is of less importance .
2 Patients who were comparatively deficient in vitamin C with plasma concentrates below about 30 µmol/l did not secrete much ascorbate into gastric juice even after H pylori eradication .
3 Detection of H pylori by at least two of these was considered as a true positive , and its absence in all biopsy specimens as a true negative .
4 The low cost and convenience of these techniques encouraged some workers to recommend their use in the diagnosis and management of H pylori associated ulcers , without the need for endoscopy .
5 The Pyloriset detects IgG antibodies by agglutination , using Latex particles coated with acid extracted antigen of H pylori .
6 Table II shows the prevalence of H pylori , as detected by the various tests , in patients with histological and endoscopic abnormalities .
7 It is also worth noting that the prevalence of H pylori in patients treated with NSAID was 34 of 64 ( 53% ) compated with 43 of 60 ( 72% ) ( p<0.05 ) in patients not taking NSAID , using the standard tests ( see Table III ) .
8 Several factors have recently been identified as being capable of influencing the performance of H pylori serological tests : these include the patients ' age , histological findings , H pylori antigens , and , as suggested by this study , NSAID intake .
9 However , it is worth noting that our findings refer to the presence of H pylori in the antrum , the commonest site of such infection , and atrophy of the gastric body of our patients can not , therefore , be excluded .
10 A relatively high frequency of false positive and false negative results has been observed in studies using whole extracts of H pylori as antigens .
11 More recently , higher sensitivity and specificity values have been reported when antibodies were raised against certain components of H pylori organisms such as partially purified urease enzyme or high molecular weight cell associated proteins , and the 25 kDa antigen of H pylori .
12 More recently , higher sensitivity and specificity values have been reported when antibodies were raised against certain components of H pylori organisms such as partially purified urease enzyme or high molecular weight cell associated proteins , and the 25 kDa antigen of H pylori .
13 Another factor that needs to be considered is the fate of the antibody titres once their formation has been triggered by one or more of H pylori antigens .
14 These observations , like chemical gastritis , might also help us understand the low specificity of our tests , especially in patients treated with NSAID , who have a low prevalence of H pylori .
15 Despite being directed against relatively specific components of H pylori , their sensitivity ( excluding that of Bio-Rad GAP Test ) and their specificity values are lower than some of the recently published data .
16 The lower specificity of Pyloriset Latex , Helico-G , and Biolab Malakit tests in NSAID patients could be explained by the presence of chemical gastritis and the low prevalence of H pylori in these patients , as found by this study and by thers .
17 The latter could be related to the impairment , by NSAID , of the gastric nucus layer , which is considered the natural habitat of H pylori organisms .
18 Threfore , accurate diagnosis of H pylori in these patients is at least as important as it is in patients not taking NSAID .
19 These results could be related to the histological findings , the dynamic nature of H pylori infection , the types of the antigens tested , NSAID intake , or some weaknesses in the manufacturers ' instructions .
20 More than 90% of patients with duodenal ulcer are carriers of H pylori .
21 Due to the high prevalence of H pylori infection in DU disease the numerous previous studies of the pathogenesis of DU have consisted almost entirely of patients with H pylori related DU .
22 Although the 12 such patients were identified for more than 400 patients with DU examined , this may not represent the true prevalence of H pylori negative patients with DU as not all the 400 patients with DU had their H pylori state determined with the same stringency .
23 The six patients with chronic DU disease in whom there was no evidence of H pylori or other explanation for their ulceration are of particular interest .
24 More recent studies , however , have shown that H pylori infection raises serum pepsinogen I. The fact that two of our patients with idiopathic DU had serum pepsinogen I concentrations that were considerably higher than those in any of the H pylori positive patients with DU or H pylori positive healthy controls suggests that there is an association between hyperpepsinogenaemia I and DU disease independent of H pylori .
25 Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori .
26 Eating stimulated a noticeable rise in G17 but little change in G34 , both in the presence and absence of H pylori .
27 Studies to date have produced conflicting evidence concerning changes in acid secretion after eradication of H pylori and lowering of the serum gastrin concentration .
28 To clarify this , we have examined the different circulating forms of gastrin in duodenal ulcer patients , basally and in response to eating , and both before and after eradication of H pylori .
29 Chromatographic analysis was performed on serum samples obtained 20 minutes postprandially before and after eradication of H pylori in six patients .
30 This was undertaken to determine the contribution of G17 and G34 to the total immunoreactive gastrin in the presence and absence of H pylori .
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