You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 136 No. 1, January 1976 TABLE OF CONTENTS
  Archives
  •  Online Features
  ARTICLES
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (47)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Serum Bile Acids in Primary Biliary Cirrhosis

Joseph R. Bloomer, MD; Rose M. Allen; Gerald Klatskin, MD

Arch Intern Med. 1976;136(1):57-61.


Abstract

Fasting serum bile acid levels were measured by gas-liquid chromatography in 56 patients with primary biliary cirrhosis. Of these, 52 (93%) had increased levels (>2µg/ml), including 14 of the 18 with normal serum bilirubin concentrations. The four patients with normal bile acid levels had early lesions as judged by histological and clinical criteria. With progression of the disease, as indicated by the histological features of the lesions, total bile acid levels increased, and the ratio of serum cholic-to-chenodeoxycholic acid decreased. Ratios of serum cholicto-chenodeoxycholic acid below 1 occurred predominantly in patients with advanced or termina! disease. These studies suggest that serial measurement of serum bile acids may aid in the evaluation of primary biliary cirrhosis.

(Arch Intern Med 136:57-61, 1976)



Author Affiliations

From the Department of Medicine, Yale University School of Medicine, New Haven, Conn.


Footnotes

Received for publication Feb 19, 1975; accepted March 17.

Reprint requests to 333 Cedar St, New Haven, CT 06510 (Dr. Bloomer).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Multiple Cyclin Kinase Inhibitors Promote Bile Acid-induced Apoptosis and Autophagy in Primary Hepatocytes via p53-CD95-dependent Signaling
Zhang et al.
J. Biol. Chem. 2008;283:24343-24358.
ABSTRACT | FULL TEXT  

Bile Acid Regulation of C/EBP{beta}, CREB, and c-Jun Function, via the Extracellular Signal-Regulated Kinase and c-Jun NH2-Terminal Kinase Pathways, Modulates the Apoptotic Response of Hepatocytes
Qiao et al.
Mol. Cell. Biol. 2003;23:3052-3066.
ABSTRACT | FULL TEXT  

Deoxycholic Acid (DCA) Causes Ligand-independent Activation of Epidermal Growth Factor Receptor (EGFR) and FAS Receptor in Primary Hepatocytes: Inhibition of EGFR/Mitogen-activated Protein Kinase-Signaling Module Enhances DCA-induced Apoptosis
Qiao et al.
Mol. Biol. Cell 2001;12:2629-2645.
ABSTRACT | FULL TEXT  

Enzymatic Fluorometry for Estimating Serum Total Bile Acid Concentration
Kobayashi et al.
JAMA 1979;241:2043-2045.
ABSTRACT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1976 American Medical Association. All Rights Reserved.