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: 3122
Function: getPubMedXML
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
Current approved medical therapies for endometriosis rely on drugs that suppress ovarian steroids and induce a hypoestrogenic state, which determines the atrophy of the ectopic endometrium. Gonadotropin-releasing hormone analogs such as danazol, progestogens and estrogen-progestin combinations have all proven effective in relieving pain and reducing the extent of endometriotic implants. However, symptoms often recur after discontinuation of therapy and hypoestrogenism-related side effects limit the long-term use of most medications. Recently, knowledge of the pathogenesis of endometriosis, particularly at the molecular level, has grown substantially, providing a rational basis for the development of new drugs with precise targets that may be safely administered over the long term.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2217/17455057.2.2.297 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!