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Corticosteroid Metabolism in Liver Disease
HAROLD BROWN, M.D.;
EDWIN ENGLERT, JR., M.D.
Arch Intern Med. 1961;107(5):773-783.
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During the last decade the tremendous interest in the adrenocortical hormones has led to an appreciation of the central role of the liver in their metabolism. Early observations of corticoid metabolism in liver disease suggested that there was hyperactivity of the adrenal cortex.1-5 This conclusion was based largely on measurements of the urine corticoids by techniques which did not detect the conjugated metabolites, the largest fraction of the adrenocortical endproducts. Studies utilizing more specific methods for the metabolites in plasma and urine have furnished data which are not in keeping with the earlier reports.6-8
In man, the principal corticosteroids elaborated by the adrenal cortex are hydrocortisone (cortisol, 17-hydroxycorticosterone, pregn - 4 - ene -11β,17 ,21 - triol - 3,20- dione, Compound F), corticosterone (pregn-4ene-11β,21-diol-3,20-dione, Compound B), and aldosterone (pregn-4-ene-11β,21-diol-3, 20-dione-18-al). The largest fraction is hydrocortisone (Fig. 1). The Porter-Silber reaction9 measures the corticoids which react with phenylhydrazine because of their 17, 21-dihydroxy-20-ketone
. . . [Full Text PDF of this Article]
Author Affiliations
SALT LAKE CITY
From the Department of Medicine, University of Utah College of Medicine, and the Veterans Administration Hospital, Salt Lake City.
Footnotes
Submitted for publication Nov. 29, 1960.
Supported in part by U.S.P.H.S. Grant No. A-1310.
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