AJCN Tufts Nutrition Symposium, Boston Sept 24-26
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pandit, A.
Right arrow Articles by Bhave, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pandit, A.
Right arrow Articles by Bhave, S.
Agricola
Right arrow Articles by Pandit, A.
Right arrow Articles by Bhave, S.

American Journal of Clinical Nutrition, Vol 63, 830S-835S, Copyright © 1996 by The American Society for Clinical Nutrition, Inc

REVIEW ARTICLES

Present interpretation of the role of copper in Indian childhood cirrhosis

A Pandit and S Bhave
Department of Pediatrics, KEM Hospital, Pune, India.

A common killer disease of the past, Indian childhood cirrhosis (ICC), which became preventable and treatable in the early 1990s, is now rare. ICC must be clearly distinguished in Indian children from other chronic liver disorders including Wilson disease. Grossly increased hepatic, urinary, and serum copper concentrations are characteristic of ICC. These increased concentrations are easily demonstrated histologically with orcein-rhodanine staining. Environmental ingestion of copper appears to be the most plausible explanation for ICC, as shown by feeding histories, the prevention of ICC is siblings and in the Pune district by a change in feeding vessels, and the dramatic reduction in incidence of ICC throughout India. The nature and role of a second factor in the causation of ICC remains unclear, although an inherited defect in copper metabolism is strongly suspected. ICC, however, does not appear to be a straightforward early onset of Wilson disease because ceruloplasmin is consistently normal and clinical and histologic recovery is maintained in the long term despite withdrawal of D-penicillamine therapy. Descriptions of an ICC-like illness in the West suggest that different mechanisms (environmental, genetic, or both) can lead to the same end-stage liver disease: copper-associated childhood cirrhosis. ICC probably represents a specific form of copper- associated childhood cirrhosis that requires high environmental copper ingestion for its full expression.


This article has been cited by other articles:


Home page
 Am. J. Clin. Nutr.Home page
J. R Turnlund, W. R Keyes, S. K. Kim, and J. M Domek
Long-term high copper intake: effects on copper absorption, retention, and homeostasis in men
Am. J. Clinical Nutrition, April 1, 2005; 81(4): 822 - 828.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by The American Society for Nutrition