Skip Navigation


Rheumatology Advance Access originally published online on July 10, 2007
Rheumatology 2007 46(8):1221-1222; doi:10.1093/rheumatology/kem148
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
46/8/1221    most recent
kem148v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Tzioufas, A. G.
Right arrow Articles by Moutsopoulos, H. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tzioufas, A. G.
Right arrow Articles by Moutsopoulos, H. M.
Related Collections
Right arrow Systemic Lupus Erythematosus and Autoimmunity
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


EDITORIALS

Predicting autoimmune congenital heart block: is it feasible and how?

A. G. Tzioufas and H. M. Moutsopoulos

Department of Pathophysiology, Medical School, University of Athens, Greece

Correspondence to: A. G. Tzioufas. E-mail: agtzi@med.uoa.gr

The first 150 words of the full text of this article appear below.

Autoimmune congenital heart block (CHB) is the most serious complication of neonatal lupus syndrome (NLS), a rare disorder afflicting fetuses of mothers with circulating autoantibodies to Ro/SSA and La/SSB ribonucleoproteins. The syndome is considered a model of passively acquired autoimmunity since during pregnancy maternal autoantibodies are transferred across the placenta, bind onto tissues of the developing fetus and eventually produce the pathology of NLS. NLS develops in 2–5% of fetuses of Ro/SSA and La/SSB autoantibody-positive pregnant women. Two thirds of mothers have Sjögren's syndrome, systemic lupus erythematosus or undifferentiated connective tissue disease and the remainder are asymptomatic. Although NLS can affect the skin, liver, blood cells and heart, almost all extra-cardiac manifestations subside when the maternal autoantibodies are cleared from the circulation of the offspring [1]. NLS has certain characteristics that distinguish it from other autoimmune diseases. These include a unique causative factor (antibodies against Ro/SSA and La/SSB), . . . [Full Text of this Article]

Functional studies

Immunological studies


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?