CASE REPORTS
JOURNAL ARTICLE
Desvenlafaxine as a possible cause of acquired hemophilia.
General Hospital Psychiatry 2010 November
OBJECTIVE: Acquired hemophilia A (AHA) is characterized by the depletion of Factor VIII mediated by specific autoantibodies. While the cause is unknown in 50% of the cases, an association with malignancy, peripartum period, autoimmune disease and the use of drugs has been described. We report a case of AHA possibly induced by desvenlafaxine.
CASE REPORT: Mr. P, a 70-year-old Caucasian male with alcohol and opioid dependence in remission, was started on 50 mg of desvenlafaxine for a moderate depressive episode. After 10 weeks, he developed an ecchymosis of the right upper extremity, in the absence of past or family history of bleeding disorder. He had a prolonged activated partial thromboplastin time (74.5 s) not corrected on performing mixing study, decreased Factor VIII activity (< 1%) and detectable Factor VIII inhibitor (30 Bethesda units) confirming a diagnosis of AHA. After all other causes were ruled out, desvenlafaxine was discontinued and the patient was infused with Factor VIIa followed by a 6-week prednisone taper with which he achieved remission.
DISCUSSION: While serotonin inhibitors are known to impair platelet aggregation leading to bleeding, abnormalities in the coagulation cascade have not been described so far. Desvenlafaxine appears to be the probable cause of AHA given the temporal association, remission after withdrawal of the drug and the lack of any other probable cause. New-onset abnormalities of the coagulation cascade such as AHA should be considered in the context of bleeding events with desvenlafaxine and perhaps other serotonin inhibitors, given the significant mortality rates when untreated.
CASE REPORT: Mr. P, a 70-year-old Caucasian male with alcohol and opioid dependence in remission, was started on 50 mg of desvenlafaxine for a moderate depressive episode. After 10 weeks, he developed an ecchymosis of the right upper extremity, in the absence of past or family history of bleeding disorder. He had a prolonged activated partial thromboplastin time (74.5 s) not corrected on performing mixing study, decreased Factor VIII activity (< 1%) and detectable Factor VIII inhibitor (30 Bethesda units) confirming a diagnosis of AHA. After all other causes were ruled out, desvenlafaxine was discontinued and the patient was infused with Factor VIIa followed by a 6-week prednisone taper with which he achieved remission.
DISCUSSION: While serotonin inhibitors are known to impair platelet aggregation leading to bleeding, abnormalities in the coagulation cascade have not been described so far. Desvenlafaxine appears to be the probable cause of AHA given the temporal association, remission after withdrawal of the drug and the lack of any other probable cause. New-onset abnormalities of the coagulation cascade such as AHA should be considered in the context of bleeding events with desvenlafaxine and perhaps other serotonin inhibitors, given the significant mortality rates when untreated.
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