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,17α,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
BROWN H, ENGLERT E. Corticosteroid Metabolism in Liver Disease. Arch Intern Med. 1961;107(5):773–783. doi:10.1001/archinte.1961.03620050139015
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