Idiopathic autoantibody that inhibits fibrin monomer polymerization

Abstract

A 73-year-old female was found to have prolonged thrombin and reptilase times in the immediate post-operative period. These abnormalities were not corrected by the addition of normal plasma. They were subsequently shown to be due to an IgG immunoglobulin which inhibited fibrin monomer polymerization. The IgG immunoglobulin activity could be neutralized completely by prior incubation with either patient or normal fibrinogen, uncrosslinked fibrin monomers or IgG antisera. No inhibitory effect on thrombin activity, fibrinopeptide A release or on the fibrin cross-linking reaction of factor XIIIa could be detected. Purified patient fibrinogen was functionally normal as demonstrated by normal fibrinogen-fibrin polymerization and fibrinopeptide A release. No underlying cause for this phenomenon was found. The presence of the inhibitor was associated with excessive blood loss during the post-operative period.

RAREACQUIREDBLEEDINGDISORDERS

“…Similar coagulation screening tests were reported for a girl with ulcerative colitis and liver disease due to an IgG inhibitor of fibrin polymerization (2). Ghosh et al (3) investigated an inhibitor with similar characteristics in an elderly woman with postoperative bleeding. In these last two instances there was no inhibition of factor XIII, in contrast to other reports where bleeding has been associated with inhibitors reactive with factor XIII.…”

Diagnosis of factor XIII deficiency

“…31,32 In routine assay of clot solubility, if the level of FXIII is higher than 5%, patients with FXIIID are falsely considered as normal. 32,33 The ISTH recommends the following algorithm for diagnosis and classification of FXIIID 11 :…”

Acquired dysfibrinogenemia caused by monoclonal production of immunoglobulin light chain

“…13 There are also examples of anti-fibrinogen antibodies developing spontaneously for no determined reason. [14][15][16] Anti-fibrinogen alloantibodies are equally rare, but there have been reports of their appearance in afibrinogenemic patients who have received fibrinogen replacement therapy. [17][18][19] Another patient developed alloantibodies against fibrinogen, thrombin and factor V after receiving bovine topical thrombin as a hemostatic agent.…”