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Archived Comments for: Delayed-onset heparin-induced thrombocytopenia presenting with multiple arteriovenous thromboses: case report

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  1. Delayed-onset Heparin-Induced Thrombocytopenia

    HIKMAT ABDEL-RAZEQ, KING HUSSEIN CANCER CENTER

    10 December 2007

    Delayed-onset Heparin-Induced Thrombocytopenia

    Hikmat N. Abdel-Razeq, MD.

    American Board of Internal Medicine

    American Board of Hematology

    American Board of Medical Oncology

    Chief, Section of Hematology and Medical Oncology

    Chairman, Department of Internal Medicine

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    King Hussein Cancer Center

    P.O.Box 1269 Al-Jubeiha

    Amman 11941 Jordan

    Tel. (962 6) 5300460 Ext. 1000

    Fax. (962) 6 5353001

    e-mail: habdelrazeq@khcc.jo

    Delayed-onset Heparin-Induced Thrombocytopenia

    We read with interest the case report “Delayed-onset Heparin-Induced Thrombocytopenia presenting with multiple arteriovenous thrombosis” reported by SalehiOmran et al in your journal. We have the following comments that hopefully clarify few issues discussed in this case report.

    The authors used the term “delayed onset” heparin-induced thrombocytopenia to refer to thrombocytopenia occurring beyond the well-described golden 10 or 14 days upper limit of timing used to make such clinical diagnosis. However, making such diagnosis beyond this time interval is not that rare as stated by the authors. The problem here is where to draw your line. The patient under discussion had a platelet count of 139x103/ul on the eleventh postoperative day, this platelet count is relatively low and may well represent a 50% decline of the original platelet counts prior to the procedure which the authors failed to report. When discussing the timing of thrombocytopenia associated with heparin, one should refer to the elegant classification suggested by Warkentin in his recent review of the subject; he refered to “delayed-onset “ HIT to the situation where the platelet count begins to decrease after all heparins has been stopped. The term “rapid-onset” HIT, on the other hand, was used to describe a drop in the platelet counts within 24 hours of administering heparins while “spontaneous HIT” was used to describe clinical situation suggestive of HIT with positive confirmatory tests but with no history of prior heparin use.

    On the diagnostic issue, though we agree with the authors and do understand situations where such confirmatory tests can’t be performed, one should emphasize, like our authors did, the importance of making such diagnosis based on clinical ground, for that matter, it is important for readers to refer to the clinical scoring system described by Warkentin and his group (33). This “ 4-T” scoring system rely on the occurrence of Thrombocytopenia, Thrombosis, Timing of both and the absence of other causes to explain the presence of thrombocytopenia.

    On the management issue, we strongly disagree with the use of Warfarin in a patient with a clinical diagnosis of HIT and active venous and arterial thrombosis. Due to the depletion of vitamin K-dependent natural anticoagulants in a clinical sitting of hypercoagulable state, the use of Coumarins is considered contraindicated. Having said so, we do understand the situation where alternative anticoagulants like danparoids, lepirudin and argatruban may not be available in peripheral hospitals, and even if available, they need experienced physician to use and follow their anticoagulant effect. We recently reported our experience with similar situation. The absence of alternative non-heparin anticoagulant forced us to use unconventional methods to bridge anticoagulation process with warfarin. For our patient, we used plasmapheresis with albumin rather than fresh-frozen plasma to deplete coagulation factors enough to elevate aPTT to levels safe enough to introduce Warfarin.

    The recently introduced direct antithrombin inhibitor, Fondaparinux, may be a reasonable alternative anticoagulant that can be used safely in HIT as reported by many short series. The simplicity of its administration (fixed dose ) and the no need to monitor its anticoagulant effect make this drug an attractive agent for further study and utilization for this indication.

    References:

    1. Warkentin TE. Heparin-Induced Thrombocytopenia. Hematol Oncol Clin N Am. 2007;21: 589-607

    2. Wester JP, Leyte A, Oudemans-van Straaten HM, Bosman RJ, Van der Spoel JI, Haak EA, Procelijn L, Zandstra DF. Low-dose fondaparinux in suspected heparin-induced thrombocytopenia in the critically ill. Neth J Med. 2007; 65(3):101-8.

    3. Warkentin TE, Cook RJ, Marder VJ, Sheppard JA, Moore JC, Eriksson BI, Greinacher A, Kelton JG. Anti- platelet factor 4/heprain antibodies in orthopedic surgery patients receiving antithrombotic prophylaxis with fondaparinux or enoxaparin. Blood 2005; 106 ( 12 ): 3791-6.

    4. Kuo Kh, Kovacs MJ. Fondaparinux: a potential new therapy for HIT. Hematology. 2005; 10(4):271-5.

    5. Kovacs MJ. Successful treatment of heparin induced thrombocytopenia (HIT) with fondaparinux. Thromb Haemost. 2005; 93(5)999-1000.

    6. Abdel-Razeq HN, Bajouda AA, Khalil MM, Ashmeg AK. Treating heparin-induced thrombocytopenia. The unconventional way! Saudi Med J. 2004; 25(9):1258-60

    Competing interests

    None

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