ASH Image Bank (2001); doi:10.1182/ashimagebank-2001-100177
Copyright © 2001 by the American Society of Hematology.
Idiopathic Thrombocytopenic Purpura
John Lazarchick, M.D.
Medical University of South Carolina
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Figure 1. Large ecchymotic area over the thigh following minor trauma. The platelet count at the time was 7000/uL.
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Figure 2. Peripheral smear in a patient with ITP showing an almost total absence of platelets. A large, young platelet is seen in the center of the smear.
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Figure 3. Peripheral smear showing a macrothrombocyte which can be seen in any disorder causing shortened platelet survival, including ITP.
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Figure 4. Peripheral smear in a patient with acute ITP showing several reactive lymphocytes. These cells can also be seen following cytomegalovirus (CMV) and Epstein-Barr virus (EBV) infections.
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Figure 5. Bone marrow aspirate showing megakaryocytic hyperplasia with clustering of the megakaryocytes around a spicule.
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Figure 6. Bone marrow showing an immature megakaryocyte with cytoplasmic budding. Young megakaryocytes are seen in increased numbers in ITP.
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Figure 7. Bone marrow aspirate showing an increased number of small lymphocytes with scant cytoplasm and smooth chromatin. These are normal precursor B cells and can lead to an erroneous diagnosis of acute lymphoblastic leukemia if not recognized.
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Figure 8. Marrow aspirate showing the normal precursor B cells (hematogones) which are often found to be increased in children with ITP. These Cells are CD 19 and 20+, TdT positive and often CD34 positive.
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Clinical Summary
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A 43-year-old white woman, previously in good health, presented to her physician with complaint about the recent onset of easy bruisability. She noted spontaneous epistaxis and complained of large bruises on her legs. She was on no medications except for occasional Tylenol.
Except for scattered petechiae on her upper extremities and ecchymoses in various stages of resolution on her lower extremities, her examination was unremarkable.
Lab: Hemoglobin (Hgb) 12.1 g/dl, white blood cells (WBC) 5200 with normal differential, platelets 11,000/uL. Mean platelet volume was increased at 15.7. ANA, single stranded DNA were negative. Thyroid studies were unremarkable. Hepatitis B and C serologies were negative. Platelet antibody assay was positive with specificity to epitope on platelet glycoprotein IIb/IIIa.
A diagnosis of idiopathic thrombocytopenic purpura (ITP) was made and the patient was started on corticosteroids. Her platelet count at followup 3 weeks later was 125,000/uL. Her steroid dosage is being tapered.
Sex
Female
Age
43
Ethnicity
White
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Diagnosis
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Secondary immune-mediated thrombocyopenias, Disseminated intravascular coagulation, Thrombotic thrombocytopenic purpura/Hemolytic-uremic syndrome,Viral infection with associated thrombocytopenia
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Discussion
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Autoimmune thrombocytopenic purpura is the generic term used to classify immune-mediated thrombocytopenic disorders. Primary or idiopathic thrombocytopenic purpura (ITP) is used when no underlying disease is present. When the thrombocytopenia is associated with a disease process that has an immune component it is considered as secondary. Examples of the latter include systemic lupus erythematosus, and lymphoproliferative disorders, most commonly chronic lymphocytic leukemia. Similar immune-mediated thrombo- cytopenia can be seen with a variety of drugs. Characteristic laboratory findings of autoimmune thrombocytopenic purpura include: large platelets on examination of the peripheral smear, an elevated mean platelet volume (MPV), increased beta-thromboglobulin, bone marrow aspirate and biopsy showing megakaryoctic hyperplasia with increased young forms present, and a positive platelet anti-body assay. These antibodies are directed at epitopes on platelet glycoproteins IIb/IIIa or Ib/IX complex. The prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen concentration are normal. The onset in children is acute with mucocutaneous bleeding being prominent -petechiae, purpura, epistaxis, gastrointestinal. Platelet counts are often less than 10,000/uL. Spontaneous remissions are common in children with 80% to 90% of the cases showing normalization of the platelet count within one to two months. For those cases in which the thrombocytopenia persists beyond six months, splenectomy is a consideration. If performed, prophylactic immunization with pneumococcal vaccine is indicated. Other therapeutic options include corticosteroids, IVIg, anti-Rh(D), and vincristine. In adults the onset is more typically insidious and rarely resolves spontaneously. Treatment options are similar to those listed above for children. Platelet transfusions should only be considered if bleeding is severe or has occurred in a critical area (e.g. intracranial bleed). In addition to the hemorrhagic diathesis due to quantitative platelet deficiency, a qualitative platelet defect can be demonstrated in a small percentage of both adults and children with this disorder. Platelet aggregation studies often show diminished in vitro aggregation and release patterns to one or more agonists used to elicit the aggregation response (ADP, epinephrin, arachadonic acid, and collagen).
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Differential Diagnosis
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Secondary immune-mediated thrombocyopenias, Disseminated intravascular coagulation, Thrombotic thrombocytopenic purpura/Hemolytic-uremic syndrome, Viral infection with associated thrombocytopenia
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| Related ASH-SAP Chapter: |
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Chapter 15: Hemostasis and Thrombosis
Copyright © 2001 by the American Society of Hematology.
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