Thrombocytopenia medical therapy
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Treatment
Treatment is guided by etiology and disease severity. The main concept in treating thrombocytopenia is to eliminate the underlying problem, whether that means discontinuing suspected drugs that cause thrombocytopenia, or treating underlying sepsis. Diagnosis and treatment of serious thrombocytopenia is usually directed by a hematologist.
Specific treatment plans often depend on the underlying etiology of the thrombocytopenia.
Thrombotic thrombocytopenic purpura (TTP)
Treatment of thrombotic thrombocytopenic purpura is a medical emergency, since the hemolytic anemia and platelet activation can lead to renal failure and changes in the level of consciousness. Treatment of TTP was revolutionized in the 1980s with the application of plasmapheresis. According to the Furlan-Tsai hypothesis [1] [2] , this treatment theoretically works by removing antibodies directed against the von Willebrand factor cleaving protease, ADAMTS-13. The plasmapheresis procedure also adds active ADAMTS-13 protease proteins to the patient, restoring a more physiological state of von Willebrand factor multimers. Patients with persistent antibodies against ADAMTS-13 do not always manifest TTP, and these antibodies alone are not sufficient to explain the how plasmapheresis treats TTP.
ITP
In many cases, ITP is self-limited, and does not require treatment. Platelet counts less than ten thousand per mm3 usually require treatment (less than fifty thousand requires treatment, less than ten thousand is a potentially dangerous situation) and patients with significant bleeding and thrombocytopenia due to ITP are also usually treated. The threshold for treating ITP has decreased since the 1990s, and hematologists recognize that patients rarely bleed with platelet counts greater than ten thousand, though there are documented exceptions to this observation. Treatments for ITP include:
Thrombopoetin analogues have been tested extensively for the treatment of ITP. These agents had previously shown promise but had been found to stimulate antibodies against endogenous thrombopoeitin or lead to thrombosis.
A medication known as AMG 531 was found to be safe and effective for the treatment of ITP in refractory patients. [3] AMG 531 is a peptide that bears no sequence homology with endogenous human thrombopoeitin, so it is not as likely to lead to neutralizing antibodies as previous peptide thrombopoeitin analogues. [4]
Heparin-induced thrombocytopenia and thrombosis (HITT)
Discontinuation of heparin is critical in a case of HITT. Beyond that, however, care must be taken to avoid a thrombosis, and patients started directly on warfarin after a diagnosis of HITT are at excess risk of venous limb gangrene. For this reason, patients are usually treated with a type of blood thinner called a direct thrombin inhibitor such as the FDA-approved lepirudin or argatroban. Other blood thinners sometimes used in this setting that are not FDA-approved for treatment of HITT include bivalirudin and fondaparinux. Platelet transfusions are not a routine component of the treatment of HITT, since thrombosis, not bleeding, is the usual associated problem in this illness.
Contraindicated medications
Thrombocytopenia is considered an absolute contraindication to the use of the following medications:
References
- ↑ Furlan M, Lämmle B (2001). "Aetiology and pathogenesis of thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome: the role of von Willebrand factor-cleaving protease". Best Pract Res Clin Haematol. 14 (2): 437–54. PMID 11686108.
- ↑ Tsai H (2003). "Advances in the pathogenesis, diagnosis, and treatment of thrombotic thrombocytopenic purpura". J Am Soc Nephrol. 14 (4): 1072–81. PMID 12660343.
- ↑ Bussel J, Kuter D, George J, McMillan R, Aledort L, Conklin G, Lichtin A, Lyons R, Nieva J, Wasser J, Wiznitzer I, Kelly R, Chen C, Nichol J (2006). "AMG 531, a thrombopoiesis-stimulating protein, for chronic ITP". N Engl J Med. 355 (16): 1672–81. PMID 17050891.
- ↑ Broudy V, Lin N (2004). "AMG531 stimulates megakaryopoiesis in vitro by binding to Mpl". Cytokine. 25 (2): 52–60. PMID 14693160.