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
We present a report on two sisters who have 17 alpha-hydroxylase deficiency with hyperaldosteronism. They have hypertension and hypergonadotropic hypogonadism. The steroid profiles suggest that they have 17 alpha-hydroxylase deficiency. In contrast to the classical biochemical findings in 17 alpha-hydroxylase deficiency, both of these patients have hyperaldosteronism. Thus this report describes a new variant of 17 alpha-hydroxylase deficiency with hyperaldosteronism. Dexamethasone suppressed the mineralocorticoid excess, including aldosterone, and improved their hypertension. In the untreated state, ACTH, instead of the renin-angiotensin system, regulated plasma aldosterone levels, but during dexamethasone treatment the renin-angiotensin system regulated these levels.
Download full-text PDF |
Source |
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http://dx.doi.org/10.1507/endocrj1954.36.315 | DOI Listing |
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