Evidence suggests that Helicobacter pylori causes chronic active gastritis. 1 Furthermore, a correlation between H. pylori infection and intestinal metaplasia in the stomach has been found, 2±4 with recent studies showing an estimated 4.5±9-fold increased risk of intestinal metaplasia in patients with this bacterial infection. 5±7 Moreover, the presence of chronic atrophic gastritis together with intestinal metaplasia is widely recognized as being the most prevalent precursor of intestinal type gastric carcinoma. 8 Three variants of intestinal metaplasia have been identi®ed, namely`small intestinal' metaplasia (types I and II) and`colonic' metaplasia (type III). 9 In general, it has been suggested that intestinal type metaplasia is the result of a reaction to the in¯ammatory process which tends to regress following healing of gastritis. 10 Despite this, other studies have reported no signi®cant change in intestinal metaplasia presence at long-term follow-SUMMARY Background: Intestinal type metaplasia plays a role in intestinal type gastric carcinoma development. Ascorbic acid demonstrates a protective effect against gastric carcinogenesis, due to its ability to inactivate oxygen free-radicals as well as its nitrite-scavenging effects. Aim: To assess whether long-term ascorbic acid administration following Helicobacter pylori eradication could affect intestinal metaplasia regression in the stomach. Methods: Sixty-®ve patients were included in the study. The inclusion criterion was the presence of intestinal metaplasia on the gastric mucosa after H. pylori eradication. An upper gastrointestinal endoscopy was performed and 3 biopsy specimens were taken in the antrum, 3 in the gastric body, and 2 in the incisura angularis. Patients were randomized to receive 500 mg of ascorbic acid o.d., after lunch (32 patients) for 6 months or no treatment (33 patients). All patients underwent to endoscopic control at the end of the 6 months.
The occurrence of carcinoembryonic antigen (CEA) was studied in 45 cases of gastric tumors by the immunoperoxidase technique. CEA-positive staining was found in 48.8% of tumors. A correlation was found between preoperative CEA values and tumor CEA staining. All patients with serum CEA values below 2.5 ng/ml showed CEA-negative staining of tumor. In patients with serum CEA values between 2.6 and 10 ng/ml, the tumors showed a minority of CEA-positive cells; but in patients with serum CEA values above 10 ng/ml, the tumors contained a majority of CEA-positive cells. CEA-positive staining was found in 34.4% of tumors of the diffuse type, and in 75% of tumors of the intestinal type. A high percentage of CEA positivity was seen in well-differentiated tumors (87.7%) compared to the moderately differentiated (69.2%), and to the undifferentiated (28.7%). A faint CEA-positivity was observed in intestinal metaplasia, while normal gastric mucosa was CEA-negative.
In order to demonstrate a prognostic value of preoperative CEA levels, we have tried to define a correlation between CEA and histologic stage of tumor in 124 patients with colorectal carcinoma. CEA concentration has been evaluated by radioimmunologic assay and the histologic stage following Dukes' classification. The results show a 25.0% positivity rate for patients in stage A, 48.2% for stage B, 61.1% for stage C, and 85.7% for stage D. The mean CEA values are 7.8 ng/ml in the first group, 30.3 ng/ml in the second, 58.1 ng/ml in the third, and 134.3 ng/ml in the last group. Furthermore, we have tried to relate the histopathologic grade of the tumor (G) with CEA levels in 54 patients of the 124. We conclude that preoperative CEA has a prognostic value, and it is useful in the staging of colorectal cancer patients. A low concentration indicates an early stage of the tumor, while a high concentration indicates a wide spread of disease; on the other hand, there are not significant correlations with cancer grading.
Factors influencing Helicobacter pylori infection recurrence still have not been fully clarified. The aim of this study was to determine whether, after eradication of H. pylori, any clinical or histologic features could yield information on infection relapse. We enrolled in the study 72 patients successfully treated for H. pylori infection by either dual (n = 49) or triple (n = 23) therapy. H. pylori eradication was defined as a negative bacterial finding by rapid urease test and histologic assessment at least 4 weeks after cessation of therapy. Upon eradication, gastritis grading was performed and patients were asked to return for an endoscopic control 6-8 months later. The recurrence of H. pylori infection was observed in 12 of 72 (16.7%) patients. The infection recurrence rate resulted significantly higher in nonulcer dyspepsia patients (p = 0.01 ) and in women (p = 0.03), whereas infection relapse did not differ between patients treated with dual or triple therapy. There was a strong (p = 0.0001 ) relationship between the persistence of chronic active gastritis after H. pylori eradication and recurrence of infection, whereas gastritis grade and metaplasia were not related to recurrence. In conclusion, this study found that H. pylori infection recurrence after successful dual or triple therapy is fairly high and that gastroduodenal disease, gender, and gastritis activity seem to affect infection relapse.
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