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==Laboratory Findings==
The diagnosis of ITP is a diagnosis of exclusion. First, one has to make sure that there are no other blood abnormalities except for low platelet count and no physical signs except for signs of bleeding. Then, the secondary causes (usually 5-10% of suspected ITP cases) should be excluded. Secondary causes could be [[leukemia]], medications (e.g. [[quinine]], [[heparin]]), [[lupus erythematosus]], [[cirrhosis]], [[HIV]], [[hepatitis]] C, congenital causes, [[antiphospholipid syndrome]], [[von Willebrand factor]] deficiency and others.


Despite the destruction of platelets by splenic macrophages, the spleen is normally not enlarged. In fact, an enlarged spleen should lead a clinician to investigate other possible causes for the thrombocytopenia.
==Overview==


Bleeding time is prolonged in ITP patients; however, the use of bleeding time in diagnosis is discouraged by the American Society of Hematology practice guidelines<ref name="pmid9036806">{{cite journal |author= |title=Diagnosis and treatment of idiopathic thrombocytopenic purpura: recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel |journal=Ann. Intern. Med. |volume=126 |issue=4 |pages=319-26 |year=1997 |pmid=9036806 |doi=}}</ref> as useless. For example the [[BMJ]] review of the basics of hematology states: "The bleeding time  may or may not be prolonged in congenital or acquired platelet dysfunction, and therefore a normal bleeding time does not exclude these conditions."<ref name="pmid9081003">{{cite journal |author=Liesner RJ, Machin SJ |title=ABC of clinical haematology. Platelet disorders |journal=BMJ |volume=314 |issue=7083 |pages=809-12 |year=1997 |pmid=9081003 |doi=}}</ref>
==Laboratory Findings==
 
* The diagnosis of ITP is a diagnosis of exclusion.
Platelet-associated [[antibody]] (IgG), which was the standard test of past years, is not now considered mandatory to diagnose ITP. Test for platelet antibody are not helpful as both their [[sensitivity]] and [[specificity]] are limited.  The blood analysis for the antiplatelet antibodies is a matter of clinician's preference, as there is a disagreement whether the 80% specificity of this test is sufficient. In conditions associated with bone marrow failure (aplastic anemia) thrombopoietin (TPO)levels are high whereas in ITP thrombopoietin levels are low. Thus TPO could distinguish between decreased platelets due to bone marrow failure or increased due to their destruction.  The bone marrow in ITP contains normal or high numbers of megakaryocytes but they may be small or immature (& may have been damaged by antibodies).
* Check  there are no other blood abnormalities except for decrease platelet count and no physical signs except for signs of bleeding.
* Then the  secondary causes ( 5-10% of  ITP cases).
* Secondary causes could be [[leukemia]], medications (e.g. [[quinine]], [[heparin]]), [[lupus erythematosus]], [[cirrhosis]], [[HIV]], [[hepatitis]] C, congenital causes, [[antiphospholipid syndrome]], [[von Willebrand factor]] deficiency and others.
* Despite the destruction of platelets by splenic macrophages, the spleen is normally not enlarged. In fact, an enlarged spleen should lead  to investigate other possible causes for the thrombocytopenia.
* Bleeding time is prolonged in ITP patients; however, the use of bleeding time in diagnosis is not recommended by the American Society of Hematology practice guidelines<ref name="pmid9036806">{{cite journal |author= |title=Diagnosis and treatment of idiopathic thrombocytopenic purpura: recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel |journal=Ann. Intern. Med. |volume=126 |issue=4 |pages=319-26 |year=1997 |pmid=9036806 |doi=}}</ref> .
* The bleeding time  may or may not be prolonged in congenital or acquired platelet dysfunction, and therefore a normal bleeding time does not exclude these conditions."<ref name="pmid9081003">{{cite journal |author=Liesner RJ, Machin SJ |title=ABC of clinical haematology. Platelet disorders |journal=BMJ |volume=314 |issue=7083 |pages=809-12 |year=1997 |pmid=9081003 |doi=}}</ref>
* Platelet-associated [[antibody]] (IgG), which was the standard test in past , is now not considered mandatory to diagnose ITP. Test for platelet antibody are not helpful as both their [[sensitivity]] and [[specificity]] are limited.  The blood analysis for the antiplatelet antibodies is prefered , as there is a disagreement whether the 80% specificity of this test is sufficient. In conditions associated with bone marrow failure ([[aplastic anemia]]) [[thrombopoietin]] (TPO) levels are high whereas in ITP thrombopoietin levels are low. Thus TPO could distinguish between decreased platelets due to bone marrow failure or increased due to their destruction.  The bone marrow in ITP contains normal or high numbers of megakaryocytes but they may be small or immature (& may have been damaged by antibodies).<ref name="pmid27040023">{{cite journal |vauthors=Ostertag EM, Bdeir K, Kacir S, Thiboutot M, Gulendran G, Yunk L, Hayes VM, Motto DG, Poncz M, Zheng XL, Cines DB, Siegel DL |title=ADAMTS13 autoantibodies cloned from patients with acquired thrombotic thrombocytopenic purpura: 2. Pathogenicity in an animal model |journal=Transfusion |volume=56 |issue=7 |pages=1775–85 |date=July 2016 |pmid=27040023 |pmc=4938757 |doi=10.1111/trf.13583 |url=}}</ref>


==References==
==References==
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[[Category:Disease]]
 
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Blood disorders]]
[[Category:Hematology]]
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[[Category:Dermatology]]
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[[Category:Needs overview]]

Latest revision as of 22:17, 30 July 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Laboratory Findings

  • The diagnosis of ITP is a diagnosis of exclusion.
  • Check there are no other blood abnormalities except for decrease platelet count and no physical signs except for signs of bleeding.
  • Then the secondary causes ( 5-10% of ITP cases).
  • Secondary causes could be leukemia, medications (e.g. quinine, heparin), lupus erythematosus, cirrhosis, HIV, hepatitis C, congenital causes, antiphospholipid syndrome, von Willebrand factor deficiency and others.
  • Despite the destruction of platelets by splenic macrophages, the spleen is normally not enlarged. In fact, an enlarged spleen should lead to investigate other possible causes for the thrombocytopenia.
  • Bleeding time is prolonged in ITP patients; however, the use of bleeding time in diagnosis is not recommended by the American Society of Hematology practice guidelines[1] .
  • The bleeding time may or may not be prolonged in congenital or acquired platelet dysfunction, and therefore a normal bleeding time does not exclude these conditions."[2]
  • Platelet-associated antibody (IgG), which was the standard test in past , is now not considered mandatory to diagnose ITP. Test for platelet antibody are not helpful as both their sensitivity and specificity are limited. The blood analysis for the antiplatelet antibodies is prefered , as there is a disagreement whether the 80% specificity of this test is sufficient. In conditions associated with bone marrow failure (aplastic anemia) thrombopoietin (TPO) levels are high whereas in ITP thrombopoietin levels are low. Thus TPO could distinguish between decreased platelets due to bone marrow failure or increased due to their destruction. The bone marrow in ITP contains normal or high numbers of megakaryocytes but they may be small or immature (& may have been damaged by antibodies).[3]

References

  1. "Diagnosis and treatment of idiopathic thrombocytopenic purpura: recommendations of the American Society of Hematology. The American Society of Hematology ITP Practice Guideline Panel". Ann. Intern. Med. 126 (4): 319–26. 1997. PMID 9036806.
  2. Liesner RJ, Machin SJ (1997). "ABC of clinical haematology. Platelet disorders". BMJ. 314 (7083): 809–12. PMID 9081003.
  3. Ostertag EM, Bdeir K, Kacir S, Thiboutot M, Gulendran G, Yunk L, Hayes VM, Motto DG, Poncz M, Zheng XL, Cines DB, Siegel DL (July 2016). "ADAMTS13 autoantibodies cloned from patients with acquired thrombotic thrombocytopenic purpura: 2. Pathogenicity in an animal model". Transfusion. 56 (7): 1775–85. doi:10.1111/trf.13583. PMC 4938757. PMID 27040023.

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