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An acquired inhibitor that produced a delay of fibrinopeptide B release in an asymptomatic patient

^* Hemostasis Unit, Hematology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
^# Laboratory of Inflammation Mediators, Institute of Research, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain

Correspondence: Montserrat Borrell, Hematology laboratory, Hospital de la Santa Creu i Sant Pau, Avda. St Antoni M^a Claret 167. 08024 Barcelona, Spain, E-mail: mborell{at}santpau.es, Tel: 34932919193 Fax: 34932919192

An asymptomatic, 29-year-old woman was referred to our hospital before surgery because in the basic study of hemostasis she showed a prolonged thrombin time (TT) and a normal reptilase time (RT). She had not received any anticoagulants so, to account for these abnormal results the presence of an inhibitor or a dysfibrinogenemia was suspected. A 1:1 mixture of the patient’s plasma with control plasma did not correct the TT. Dysfibrinogenemia was excluded because the defibrinated plasma retained the inhibitory activity when mixed with normal plasma. When 0.02 mg/ml of Protamine Sulphate (a concentration that neutralizes 1 U/mL of heparin in normal plasma) was added to the patient’s plasma, the inhibitory activity did not disappear. IgG from the patient and from normal serum was isolated. The patient’s IgG was able to prolong the TT of a normal plasma and of a purified fibrinogen. The patient IgG did not impair the catalytic activity of thrombin, because no difference was observed in the hydrolysis of S-2238 by 1 U NIH human thrombin with normal or patient IgG. The time course of the thrombin–mediated fibrinopeptide-release from normal fibrinogen with the patient’s IgG, showed a delay in the fibrinopeptide B (FPB) release without affecting the fibrinopeptide A (FPA) release. This patient has an IgG antibody that delays fibrinopeptide B release of fibrinogen

Key words: Acquired inhibitors, Fibrinopeptide B, Thrombin time, Dysfibrinogenemia.