A Circulating Anticoagulant Against Factor V

Nilsson, Inga Marie; Hedner, Ulla; Ekberg, Mats; Denneberg, Torsten

doi:10.1111/j.0954-6820.1974.tb08099.x

Journal of Internal Medicine

1974

DOI: 10.1111/j.0954-6820.1974.tb08099.x

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A Circulating Anticoagulant Against Factor V

Inga Marie Nilsson

Ulla Hedner

Mats Ekberg

et al.

Abstract: A 65-year-old man who developed a potent circulating anticoagulant directed against factor V is described. After prostatectomy he went into a septic shock and received treatment with cephalothin. After 12 days' treatment he developed severe bleedings and signs of drug allergy. Coagulation studies showed a factor V level of 0% and a circulating anticoagulant against factor V in high titre. The anticoagulant belonged to the IgG class. After treatment with cyclophosphamide in large doses and withdrawal of cephalo… Show more

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Cited by 16 publications

(1 citation statement)

References 26 publications

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“…Such anticoagulants have been demonstrated in patients with various autoimmune diseases, such as SLE, rheumatoid arthritis, drug allergy, in women after childbirth and sometimes in apparently healthy middle-aged and elderly persons (2,4,6,9,18,21,26). The anticoagulants may be directed against factors V, VIII, IX, XI, XII, prothrombin and thromboplastin.…”

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confidence: 99%

Intrauterine Death and Circulating Anticoagulant (“Antithromboplastin”)

Nilsson

Åstedt

Hedner

et al. 1975

Journal of Internal Medicine

Self Cite

276

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A report is presented of a young, otherwise apparently healthy, woman who had had three pregnancies which for some unknown reason terminated in intrauterine death (macerated foetuses). During the third pregnancy a coagulation defect was diagnosed, which was characterized by prolonged coagulation times and prolonged one‐stage prothrombin time. This defect disappeared after the end of the pregnancy, but returned during the fourth pregnancy. This time a circulating anticoagulant was found, which inhibited the action of thromboplastin. The values found for the various coagulation factors were normal. The anticoagulant titre rose during the pregnancy from 1/2 to 1/10. Leucocyte agglutinating as well as Iymphocytotoxic antibodies directed against the husband's cells were demonstrated in the patient during the pregnancy. In this case, by passage of cell fragments and thromboplastic substances to the mother, the foetus had probably induced the development of antibodies against the foetal tissues. The foetus may be regarded as an incompatible transplant. The fourth pregnancy was terminated by caesarean section in the 34th week. The child weighed 1440 g and, after three exchanges of blood, did very well. The placenta was severely infarcted. It is postulated that the development of antithromboplastin during pregnancy may be a contributory cause of intrauterine death.

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mentioning

confidence: 99%

Intrauterine Death and Circulating Anticoagulant (“Antithromboplastin”)

Nilsson

Åstedt

Hedner

et al. 1975

Journal of Internal Medicine

Self Cite

276

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show abstract

Hemorrhagic death associated with a high titer factor V inhibitor

1978

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An acquired bleeding diathesis was first noted in a 51-year-old patient 11 days following an exploratory laparotomy. Laboratory studies indicated the cause of bleeding to be the development of a circulating anticoagulant which inhibited factor V activity. The inhibitor, an immunoglobulin of the IgG class, was separated by use of Sephadex G-200 filtration, disc electrophoresis, and isoelectric focusing. Despite vigorous immunosuppressive, antifibrinolytic, and replacement therapy, including the use of a "prothrombin complex" and plasmaphoresis, the bleeding diathesis could not be reversed and the patient died of hemorrhage. Although inhibitors to factor V are not usually associated with major life-threatening hemorrhage, this case demonstrates that the development of such an inhibitor can be an ominous finding. The use of an aminoglycoside antibiotic in this and other patients so reported may be one of the contributing causes to the development of such an inhibitor.

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Rapid elimination of a high-titer spontaneous factor V antibody by extracorporeal antibody-based immunoadsorption and immunosuppression

et al. 1995

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We report on the rapid elimination of a potent spontaneous factor V antibody of undetermined etiology by extracorporeal immunoadsorption on sepharose-bound polyclonal sheep antibodies to human immunoglobulins (Ig-Therasorb, Baxter) in combination with immunosuppressive treatment. A 68-year-old woman presented with severe hematuria. Severe factor V deficiency (< 1%) caused by an antibody to factor V (26 BU/ml) was found. Extracorporeal immunoadsorption (8.245 +/- 553 ml plasma processed per session) led to an average reduction of the antibody titer by 75% per session. The procedure was well tolerated without any side effects. Hematuria ceased after three immunoadsorptions and complete elimination of the antibody was achieved after seven sessions (day 15), followed by a rapid increase of the factor V activity to normal levels. Treatment with cyclophosphamide and prednisone was started on day 6 and continued for 2 months. The patient remains in remission at 6 months. Extracorporeal immunoadsorption is a highly effective method for eliminating antibodies to factor V (or other clotting factors) in selected cases, i.e., in patients with severe bleeding tendency, high antibody titer, and low probability of a rapid spontaneous remission.

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A Circulating Anticoagulant Against Factor V

Cited by 16 publications

References 26 publications

Intrauterine Death and Circulating Anticoagulant (“Antithromboplastin”)

Intrauterine Death and Circulating Anticoagulant (“Antithromboplastin”)

Hemorrhagic death associated with a high titer factor V inhibitor

Rapid elimination of a high-titer spontaneous factor V antibody by extracorporeal antibody-based immunoadsorption and immunosuppression

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