AJCN North Carolina Research Campus
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by SULLIVAN, J. F.
Right arrow Articles by HEANEY, R. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by SULLIVAN, J. F.
Right arrow Articles by HEANEY, R. P.
Agricola
Right arrow Articles by SULLIVAN, J. F.
Right arrow Articles by HEANEY, R. P.

American Journal of Clinical Nutrition, Vol 23, 170-177, Copyright © 1970 by The American Society for Clinical Nutrition, Inc.

Zinc Metabolism in Alcoholic Liver Disease

JAMES F. SULLIVAN M.D.1 and ROBERT P. HEANEY M.D.1

1 From the Medical Service, Creighton University School of Medicine, and Veterans Administration Hospital, Omaha, Nebraska 68105

Zinc metabolism was studied in 10 alcoholic cirrhotic patients following intravenous injection of zinc 65. Kinetic analysis was performed assuming a two-compartment open system. Values for miscible zinc pool, renal zinc clearance, total zinc turnover, endogenous zinc excretion, and "internal loss" were determined. Comparison with available kinetic data in normal subjects suggests a diminution in pool size and a slower turnover of zinc in these cirrhotic patients. Thus the kinetic data are compatible with the concept of zinc deficiency as a consistent abnormality in this type of cirrhosis. All patients studied had severe hepatic dysfunction but there was little correlation of clinical status with the measurements of zinc metabolism except for the serum zinc level that was within normal limits in the least ill patients. An increased renal clearance of zinc was found in all patients regardless of serum level. A consistent lag period between isotopic equilibrium in urine and plasma suggests that the urinary zinc is more a product of renal cellular zinc turnover than of glomerular filtration.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1970 by The American Society for Nutrition