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Advances and dilemmas in factor XI

¹Division of Hematology Research, Jewish Hospital of St. Louis, Washington University Medical Center, MO 63110, USA.

Current Opinion in Hematology

|September 1, 1994

Summary

Factor XI deficiency causes bleeding issues that depend on severity and challenge location. New research suggests factor XI (FXI) may consolidate clots rather than initiate hemostasis.

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Area of Science:

Hematology
Hemostasis and Thrombosis
Molecular Biology

Background:

Factor XI (FXI) is crucial for intrinsic blood coagulation in vitro.
Clinical bleeding in FXI deficiency poorly correlates with in vitro assays, questioning its in vivo hemostatic role.

Purpose of the Study:

Investigate the role of factor XI in in vivo hemostasis.
Clarify the mechanisms of bleeding in factor XI deficiency.

Main Methods:

Characterization of point mutations causing FXI deficiency in Ashkenazi Jews.
Epidemiologic studies of FXI deficiency.
Review of recent studies on FXI activation pathways.

Main Results:

Bleeding severity in FXI deficiency is situational, depending on deficiency extent and challenge location.
Coexisting hemostatic disorders, like von Willebrand's disease, influence clinical presentation.
Factor XII deficiency does not cause bleeding, suggesting alternative FXI activation pathways.

Conclusions:

Factor XI's role in hemostasis may be in clot consolidation, not initiation.
Thrombin and FXI autoactivation are potential alternative activators of FXI.
Understanding FXI function is critical for managing bleeding disorders.

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