Coagulopathy due to an acquired factor V inhibitor and subsequently thrombosis

George, Sushil; Nagabhushana, M. S.; Cyran, Elizabeth M.

doi:10.1002/ajh.2830490122

Cited by 21 publications

(14 citation statements)

References 5 publications

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“…Although there is no consistently effective treatment reported for FV inhibitors, most patients have achieved a clinical response to platelet transfusions, except for one case with dual antibodies to both thrombin and FV [1][2][3][4][5][6]. Theories about possible mechanisms of the response include the following.…”

Section: Discussionmentioning

confidence: 99%

“…In three cases, the platelet transfusions led to the cessation of the bleeding episode [1][2][3], and partial correction of the coagulation parameters was found in two of these three cases. The impact of the platelet transfusions in the other two cases is not clear since the patients received other treatments at the same time, including corticosteroids, intravenous immunoglobulins, packed red blood cell transfusions, and cryoprecipitates [4,5]. One patient with antibodies to both thrombin and FV did not respond to platelet transfusions [6].…”

Section: Introductionmentioning

confidence: 99%

“…Treatment options include corticosteroids, transfusions with fresh-frozen plasma, prothrombin complex concentrate, activated factor VII, intravenous immunoglobulin, plasmapheresis, and immunosuppressive therapy. Platelet transfusions were given in a few cases of acquired FV inhibitor with hemorrhagic tendency, with mostly favorable responses [1][2][3][4][5][6]. In three cases, the platelet transfusions led to the cessation of the bleeding episode [1][2][3], and partial correction of the coagulation parameters was found in two of these three cases.…”

Section: Introductionmentioning

confidence: 99%

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Platelet factor V supports hemostasis in a patient with an acquired factor V inhibitor, as shown by prothrombinase and tenase assays

Perdekamp

Rubenstein

Jesty³

et al. 2006

Blood Coagulation &Amp; Fibrinolysis

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A woman with gross hematuria was shown to have a severe isolated factor V deficiency due to a factor V inhibitor of 200 U/ml titer. Hematuria persisted despite multiple infusions of plasma but, after one transfusion with 1 U platelets, urine red blood cells decreased by more than 98%. To evaluate the patient's platelet function we performed prothrombinase and tenase assays with platelets from the patient and from normal donors. By prothrombinase assay, ionophore-activated patient platelets showed 42% of the activity of normal platelets in their ability to support prothrombin activation by activated factor X; whereas in a 'tenase' assay, which measures the platelets' ability to support factor X activation by activated factor IX + activated factor VIII, their activity was 117% of normal. The addition of excess bovine activated factor V to the prothrombinase assay fully corrected the defect. The results demonstrate the benefit of platelet transfusion and indicate that in this case the platelets are the primary source of factor V for hemostasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Platelet factor V supports hemostasis in a patient with an acquired factor V inhibitor, as shown by prothrombinase and tenase assays

Perdekamp

Rubenstein

Jesty³

et al. 2006

Blood Coagulation &Amp; Fibrinolysis

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show abstract

“…The remaining six patients were treated with heparin (LMWH or unfractionated heparin) during the initial phase followed by anti-vitamin K or oral anticoagulants. [6,[13][14][15] The treatment with heparin helped towards a favorable evolution of thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Transient FV inhibitor of unknown origin in difficult clinical situation

Pointeau

Marot

Suhl

et al. 2017

CRIM

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Acquired Factor V inhibitors are a rare condition, associated frequently with at times severe bleeding. Patients can show no symptoms and in exceptional cases thrombosis can be reported. In this article we report two cases of acquired FV inhibitors associated with thrombosis. We systematically reviewed the literature on FV inhibitors and thrombosis. A patient had acquired FV inhibitors and thrombosis. He had no bleeding and was treated with anticoagulant. Despite initial improvement, he died from legionaire's disease. The second patient had septicemia, acquired FV inhibitors and deep vein thrombosis. The patient's condition improved with anticoagulation and antibiotic therapy. Ten case reports were considered in the systematic review. The median age at admission was 67. Seven patients had bleeding episodes. The median peak inhibitor titer was 2.7 BU (0.62-8) while the median FV activity was 2% (1-75). Except for 2 patients, all recovered. FV has two activities: a procoagulant action activating prothrombin, as well as an anticoagulant action activating protein C. This property could be associated with thrombosis activity. Inhibitor could also have a through effect on activated protein C. In our study, because of underlying diseases, it was not possible to clearly demonstrate that inhibitors give thrombosis. Immunosuppressive therapies were administered in cases of severe bleeding. Heparin seemed efficient for thrombosis without major bleeding. The prognosis of acquired FV inhibitors appeared to be related to the underlying disease.

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“…To the best of our knowledge, our first patient is the second published case of bleeding associated with a factor V inhibitor followed by thrombosis. However, in the previously reported case, the thrombosis appeared after disappearance of the inhibitor [11], while in our case the thrombosis developed at low normal factor V levels and laboratory evidence of the inhibitor still being present. Whether the thrombotic event can be attributed to rituximab therapy remains unanswered.…”

mentioning

confidence: 99%