|
|
| Line 6: |
Line 6: |
| ==Overview== | | ==Overview== |
| ==Treatment== | | ==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 [[thrombotic thrombocytopenic purpura|TTP]] was revolutionized in the 1980s with the application of [[plasmapheresis]]. According to the Furlan-Tsai hypothesis
| |
| <ref>{{cite journal |author=Furlan M, Lämmle B |title=Aetiology and pathogenesis of thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome: the role of von Willebrand factor-cleaving protease |journal=Best Pract Res Clin Haematol |volume=14 |issue=2 |pages=437-54 |year=2001 |pmid=11686108}}</ref>
| |
| <ref>{{cite journal |author=Tsai H |title=Advances in the pathogenesis, diagnosis, and treatment of thrombotic thrombocytopenic purpura |journal=J Am Soc Nephrol |volume=14 |issue=4 |pages=1072-81 |year=2003 |pmid=12660343}}</ref>
| |
| , this treatment theoretically works by removing [[antibodies]] directed against the [[von Willebrand factor]] cleaving [[protease]], [[ADAMTS13|ADAMTS-13]]. The [[plasmapheresis]] procedure also adds active [[ADAMTS13|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 [[thrombotic thrombocytopenic purpura|TTP]], and these antibodies alone are not sufficient to explain the how [[plasmapheresis]] treats [[thrombotic thrombocytopenic purpura|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:
| |
| *[[Prednisone]] and other [[corticosteroids]]
| |
| *[[Intravenous gamma globulin]]
| |
| *[[Splenectomy]]
| |
| *[[Danazol]]
| |
| *[[Rituximab]]
| |
|
| |
| 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.
| |
| <ref>{{cite journal |author=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 |title=AMG 531, a thrombopoiesis-stimulating protein, for chronic ITP |journal=N Engl J Med |volume=355 |issue=16 |pages=1672-81 |year=2006 |pmid=17050891}}</ref>
| |
| 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.
| |
| <ref>{{cite journal |author=Broudy V, Lin N |title=AMG531 stimulates megakaryopoiesis in vitro by binding to Mpl |journal=Cytokine |volume=25 |issue=2 |pages=52-60 |year=2004 |pmid=14693160}}</ref>
| |
|
| |
| ===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===
| |
| {{MedCondContrAbs
| |
|
| |
| |MedCond = Thrombocytopenia|Abciximab|Ticlopidine|Enoxaparin|Fondaparinux|Heparin|Methotrexate}}
| |
|
| |
| {{MedCondContrAbs
| |
|
| |
| |MedCond = History of thrombocytopenia following prior exposure to|Tirofiban}}
| |
|
| |
| ==References== | | ==References== |
| {{reflist|2}} | | {{reflist|2}} |