FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Volume 304:857-861 April 9, 1981 Number 15 Next

	Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited PubMed Citation

Abstract

A 13-year-old girl with chronic aggressive hepatitis, postnecrotic cirrhosis, ulcerative colitis, and a coagulation defect acquired an antibody that specifically interfered with fibrin formation. We sought to characterize the antibody and determine the mechanism of its inhibitory activity. The patient's purified fibrinogen was functionally normal; however, the antibody inhibited the self-assembly of fibrin and prolonged the clotting times of the patient's plasma. This antibody, which belonged to the IgG class of immunoglobulins, acted early in the polymerization process to inhibit the association of fibrin monomers, as indicated by a prolonged lag time and a decreased slope in the polymerization curves. It did not inhibit fibrinopeptide cleavage or fibrin cross-linking. Affinity chromatography indicated that the antibody bound strongly to both fibrinogen and fibrin monomer.

This article has been cited by other articles:

• Dear, A., Brennan, S.O., Sheat, M.J., Faed, JM., George, P.M. (2007). Acquired dysfibrinogenemia caused by monoclonal production of immunoglobulin {lambda} light chain. haematol 92: e111-e117 [Abstract] [Full Text]  
• Llobet, D., Borrell, M., Vila, L., Vallve, C., Felices, R., Fontcuberta, J. (2007). An acquired inhibitor that produced a delay of fibrinopeptide B release in an asymptomatic patient. haematol 92: e17-e19 [Abstract] [Full Text]