Clinical Picture and Outcome of Transthyretin-Related Familial Amyloid Polyneuropathy (FAP) in Japanese Patients : Clinical Chemistry and Laboratory Medicine

www.degruyter.com uses cookies, tags, and tracking settings to store information that help give you the very best browsing experience.
To understand more about cookies, tags, and tracking, see our Privacy Statement
I accept all cookies for the De Gruyter Online site

Jump to ContentJump to Main Navigation

Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Schlattmann, Peter / Tate, Jillian R. / Tsongalis, Gregory J.


IMPACT FACTOR 2014: 2.707
Rank 6 out of 30 in category Medical Laboratory Technology in the 2014 Thomson Reuters Journal Citation Report/Science Edition

SCImago Journal Rank (SJR) 2014: 0.741
Source Normalized Impact per Paper (SNIP) 2014: 1.011
Impact per Publication (IPP) 2014: 2.310

VolumeIssuePage

Issues

30,00 € / $42.00 / £23.00

Get Access to Full Text

Clinical Picture and Outcome of Transthyretin-Related Familial Amyloid Polyneuropathy (FAP) in Japanese Patients

Shu-ichi Ikeda

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 40, Issue 12, Pages 1257–1261, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2002.217, June 2005

Publication History

Published Online:
2005-06-01

Abstract

Familial amyloid polyneuropathy (FAP) was once considered to be a disease peculiar to endemic areas, but it is now recognized that FAP kindreds exist in worldwide places. The amyloid precursor of FAP is a variant form of transthyretin (TTR) with one amino acid substitution, which is ascribed to a mutation of TTR gene. Corresponding to the variety of the clinical phenotypes of FAP, more than 80 mutations have been identified as causative gene abnormality in this disease. Since the vast majority of TTR in serum is produced in the liver, liver transplantation has become widely accepted as a valuable treatment for FAP.

Citing Articles

Here you can find all Crossref-listed publications in which this article is cited. If you would like to receive automatic email messages as soon as this article is cited in other publications, simply activate the “Citation Alert” on the top of this page.

[1]
Satheesh K. Palaninathan, Nilofar N. Mohamedmohaideen, William C. Snee, Jeffery W. Kelly, and James C. Sacchettini
Journal of Molecular Biology, 2008, Volume 382, Number 5, Page 1157
[2]
Yoshiki Sekijima, R. Luke Wiseman, Jeanne Matteson, Per Hammarström, Sean R. Miller, Anu R. Sawkar, William E. Balch, and Jeffery W. Kelly
Cell, 2005, Volume 121, Number 1, Page 73
[3]
Yves Ingenbleek
Clinical Chemistry and Laboratory Medicine, 2002, Volume 40, Number 12
[4]
Morie A Gertz
Future Rheumatology, 2008, Volume 3, Number 4, Page 369
[5]
David Agudo, Francisco Gómez-Esquer, Gema Díaz-Gil, Fernando Martínez-Arribas, José Delcán, José Schneider, María Angustias Palomar, and Rafael Linares
PROTEOMICS, 2005, Volume 5, Number 18, Page 4946

Comments (0)

Please log in or register to comment.