Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
Objective: To assess proliferation in the columnar-lined esophageal mucosa before and after antireflux surgery.
Summary Background Data: Intestinal metaplasia persists in Barrett's mucosa after reflux control. It remains at risk for uncontrolled cellular proliferation and adenocarcinoma formation.
Methods: Forty-five patients with Barrett's esophagus had a mean follow-up of 4 years after a Collis-Nissen gastroplasty. Proliferative activity was assayed immunohistochemically for Ki-67 expression in 73 preoperative and 176 postoperative biopsies. Correlation with manometric and 24-hour pH results was obtained.
Results: The Collis-Nissen gastroplasty restored the median lower esophageal sphincter gradient from 5.5 mmHg before surgery to 14.5 mmHg at 24 months and 12.9 mmHg at 48 months after surgery. The median esophageal acid exposure was reduced from 8% to 1% and 1% of recording time, respectively. The median Ki-67 labeling index increased from 28.5% before surgery to 36.1% at 12 to 23 months. It returned to preoperative level (26.9%) at 24 to 47 months. After surgery, abnormal intraesophageal acid exposure was documented in 12 patients but could not be correlated with sphincter pressure. After surgery, the pattern of proliferation in patients with acid exposure less than 4% in their esophagus showed significant differences when compared with the proliferation pattern of patients where abnormal intraesophageal acid exposure was recorded. New present dysplasia was observed only in patients with abnormal acid exposure.
Conclusions: In Barrett's mucosa, from preoperative values, proliferation peaked early after surgery and then decreased to preoperative levels. Despite sphincter restoration and global reflux control, abnormal esophageal acid exposure persisted in 12 patients. Patients with abnormal esophageal acid exposure displayed more proliferation and more dysplasia.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1422003 | PMC |
http://dx.doi.org/10.1097/00000658-200108000-00006 | DOI Listing |
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