Back To Search Results

Thrombocytopenia

Editor: Paras B. Khandhar Updated: 7/4/2023 12:21:41 AM

Introduction

A platelet count that falls below the lower limit of normal, i.e., 150000/microliter (for adults) is defined as thrombocytopenia. Platelets are blood cells that help in blood clotting and wound healing — risks associated with thrombocytopenia range from no risk at all to bleeding risks and thrombosis. The correlation of severity of thrombocytopenia and bleeding risk is uncertain. Spontaneous bleeding can occur with a platelet count under 10000/microliter and surgical bleeding with counts below 50000/microL. Thrombocytopenia is associated with risk of thrombosis in conditions like heparin-induced thrombocytopenia (HIT), antiphospholipid antibody syndrome (APS), disseminated intravascular coagulation (DIC), thrombotic microangiopathy (TMA), paroxysmal nocturnal hemoglobinuria (PNH).

Etiology

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

Etiology

Common causes of thrombocytopenia[1][2][3][4][5][6][7][8][9][10]:

  • Primary immune thrombocytopenia (primary ITP). An autoimmune condition where antibodies are produced against platelets resulting in platelet destruction.
  • Drug-induced immune thrombocytopenia:
    • Heparin-induced thrombocytopenia (HIT) - in this condition, anti-platelet antibodies activate platelets resulting in thrombosis (both arterial and venous)
    • Quinine
    • Sulfonamides, ampicillin, vancomycin, piperacillin
    • Acetaminophen, ibuprofen, naproxen
    • Cimetidine
    • Glycoprotein IIb/IIIa inhibitors
    • Other over the counter remedies, supplements, foods like African bean, sesame seeds, walnuts) and beverages (herbal teas and cranberry juice)
  • Drug-induced non-immune thrombocytopenia. Drugs like valproic acid, daptomycin, linezolid cause thrombocytopenia by dose-dependent suppression of platelet production.
  • Infections:
    • Viral: HIV, hepatitis C, Ebstein-Barr virus, parvovirus, mumps, varicella, rubella, Zika viral infections can cause thrombocytopenia.
    • Sepsis causes bone marrow suppression.
    • Helicobacter pylori
    • Leptospirosis, brucellosis, anaplasmosis, and other tick-borne infections are associated with thrombocytopenia.
    • Malaria, babesiosis intracellular parasite infections are associated with thrombocytopenia and hemolytic anemia
  • Hypersplenism due to chronic liver disease
  • Chronic alcohol abuse
  • Nutrient deficiencies (folate, vitamin B12, copper)
  • Autoimmune disorders like systemic lupus erythematosus, rheumatoid arthritis associated with secondary ITP
  • Pregnancy. Mild thrombocytopenia presents in gestational thrombocytopenia; moderate-severe thrombocytopenia can occur in preeclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome

Other causes[11]:

  • Myelodysplasia
  • Malignancy: cancer with chronic DIC, cancer with marrow suppression (leukemia, lymphoma, solid tumors)
  • Paroxysmal nocturnal hemoglobinuria (PNH)
  • Thrombotic microangiopathy (TMA)
    • Thrombotic thrombocytopenic purpura (TTP), a condition manifested by fever, renal failure, thrombocytopenia, microangiopathic hemolytic anemia with or without neurologic manifestations
    • A hemolytic uremic syndrome (HUS) caused by Shiga toxin-producing organism (E. coli and Shigella), seen in children.
    • Drug-induced TMA: quinine, specific chemotherapy agents
    • Antiphospholipid antibody syndrome
  • Aplastic anemia
  • Inherited thrombocytopenia. Often seen in children, rare in adults
    • Von Willebrand disease type 2
    • Alport syndrome
    • Wiskott-Aldrich syndrome
    • Fanconi syndrome.
    • Thrombocytopenia-absent radius syndrome
    • Bernard–Soulier syndrome
    • May-Hegglin anomaly

Epidemiology

Normal platelet count range varies by different ages, sexes, and ethnicity. Women, young individuals, and non-Hispanic blacks have slightly higher platelet counts.[12]

Pathophysiology

Decreased platelet production[13][14][13]:

  • Bone marrow failure presents in aplastic anemia, PNH
  • Bone marrow suppression is a feature with exposure to certain drugs, such as valproic acid, daptomycin, certain chemotherapy agents, and irradiation
  • Chronic alcohol abuse
  • Inherited thrombocytopenia)
  • Viral infection
  • Systemic conditions like nutrient deficiencies (folate, vitamin B12), sepsis, myelodysplastic syndrome impairs platelet production in the bone marrow - these conditions also associated with decreased production of other cell lines leading to anemia and leukopenia

Increased platelet destruction[15][16][17][18][14][19]:

In normal conditions, platelets get removed by monocytes/macrophages of the reticuloendothelial system. The life span of platelets is 8 to 10 days.

In immune-mediated thrombocytopenia, anti-platelet autoantibodies bind to platelets and megakaryocytes, resulting in increased platelet destruction by the reticuloendothelial system and decreased platelet production.

Anti-platelets antibodies are present in primary ITP, drug-induced ITP, lymphoproliferative disorders, autoimmune conditions like SLE and in chronic infections like HEP C, HIV, and Helicobacter pylori.

Non-immune mediated increased platelet destruction occurs in mechanical valve replacement patients, preeclampsia/HELLP syndrome, DIC, and thrombotic microangiopathy. In conditions like DIC and thrombotic microangiopathy, increased platelet consumption within thrombi takes place. 

Dilutional thrombocytopenia[20][21]:

Dilutional thrombocytopenia presents in massive fluid resuscitation and massive blood transfusion.

Redistribution of platelets[22]:

In normal individuals, one-third of platelet mass is in the spleen. In conditions that cause splenomegaly and increases spleen congestion (cirrhosis) results in increased platelet mass in spleen and a decrease in circulating platelets.

Histopathology

Review of peripheral blood smear. Analysis of platelet size and morphology helps in identifying conditions that are associated with platelet destruction and increased platelet consumption.

  • Clumping of platelets occurs when EDTA is used as anticoagulant causing pseudothrombocytopenia.[23]
  • Adhesion of platelets to polymorphonuclear cells is known as “platelet satellitism” can be identified by review of a peripheral blood smear.[24]

  • Giant platelets present in inherited conditions like Bernard-Soulier syndrome.

A review of WBC and RBC morphology may suggest a specific condition.

  • Schistocytes are a feature in thrombotic microangiopathic conditions.
  • Teardrop cells, nucleated RBCs, leukoerythroblastic findings suggest bone marrow infiltrative process.
  • Immature WBCs suggest leukemia.
  • Megaloblastic process characterized by hypersegmented neutrophils seen in nutritional deficiencies.

History and Physical

History. Obtaining a thorough history helps to identify the etiology of thrombocytopenia. Patients with platelets greater than 50000/mL, rarely have symptoms. Patients with platelets under 20000/mL most likely have spontaneous bleeding.

  • Ask the patient about the prior blood count testing and baseline platelet count. The recent drop in platelet count is concerning.
  • Ask for the history of bleeding (petechiae, hemorrhagic bleeding, gingival bleeding, epistaxis)
  • Ask for any potential exposure and symptoms of infections (viral, bacterial, rickettsial). Assess risk factors for HIV infection. Ask about travel to an area endemic for malaria [25] [26], dengue virus, and Ebola.
  • Obtain a diet history to detect any nutritional deficiencies.
  • Ask about other conditions like SLE, RA, bariatric surgery, and blood transfusion.
  • Review the medication list. Ask whether the patient is taking over the counter medications, quinine-containing beverages, and herbal teas.
  • In the hospitalized patient, look for exposure to heparin products.
  • Check for a family history of thrombocytopenia or bleeding disorders.
  • In pregnant patients ask for headache, visual symptoms, abdominal pain, flu-like symptoms; these patients may have preeclampsia/HELLP syndrome.

Physical Examination includes examining the skin and other sites of bleeding and examination of liver, spleen, and lymph nodes. Bleeding caused by thrombocytopenia characteristically demonstrates petechiae, nonpalpable purpura, and ecchymosis. Dry purpura refers to purpura in the skin; wet purpura refers to purpura in the mucosa. Examine for hepatomegaly and splenomegaly which occur in lymphoma, chronic liver disease, and other hematologic conditions. Enlarged lymph nodes are present in infections, autoimmune disorders, lymphoma, and other malignancies.

Evaluation

Evaluation of patients with isolated thrombocytopenia includes obtaining a CBC, peripheral blood smear, HIV, and HCV tests.

  • Repeat CBC to confirm that thrombocytopenia is real.
  • Anemia and thrombocytopenia occur with infections, DIC, sepsis, thrombotic microangiopathy, autoimmune disorders like Felty syndrome.  
  • Leucocytosis and thrombocytopenia can present in infection, malignancy, chronic inflammatory conditions.
  • Pancytopenia occurs in myelodysplastic syndromes.
  • In patients with symptoms or signs of autoimmune disorders like SLE, antiphospholipid antibody syndrome (APS), obtain anti-nuclear antibodies and antiphospholipid antibodies, respectively.
  • In patients with thrombosis, one should consider heparin-induced thrombocytopenia (obtain platelet factor 4 antibodies), APS (check antiphospholipid antibodies ), DIC and PNH (check PT,aPTT, fibrinogen, LDH)
  • Check liver enzymes and coagulation tests in patients with liver disease.
  • Bone marrow biopsy is indicated in conditions when the cause of thrombocytopenia is unclear, and when a hematologic disorder is suspected.
    • A normal number or rise in megakaryocytes in bone marrow is a presenting feature in conditions with increased platelet destruction.
    • The decrease in megakaryocytes, along with an overall reduction in other cells, is seen in aplastic anemia.
    • In SLE, severe reduction or absence of megakaryocytes is seen due to an autoantibody directed against the thrombopoietin receptor.
    • Megaloblastic changes in RBC and granulocytes occur in vitamin B12, folate, and copper deficiency. In myelodysplasia, cells are dysplastic.

Treatment / Management

In asymptomatic, mild thrombocytopenia patients, repeat CBC and routine monitoring is the recommended process.

Thrombocytopenic emergencies that require immediate action includes conditions of suspected HIT, TTP, HUS, drug-induced ITP, pregnancy with severe thrombocytopenia, bleeding with severe thrombocytopenia, urgently needed an invasive procedure in the presence of severe thrombocytopenia, leukopenia, and aplastic anemia.

In patients with bleeding and severe thrombocytopenia, treatment includes platelet transfusion.  

Management includes identifying the underlying cause and treating it.

Primary immune thrombocytopenia:

This condition is a diagnosis of exclusion. First line treatment includes glucocorticoids and intravenous immune globulins; these agents inhibit autoantibody production and platelet degradation. Second line treatment includes rituximab, immunosuppressive drugs, and splenectomy. Third line agents are thrombopoietin receptor agonists, which stimulate platelet production.[27]

Drug-induced thrombocytopenia:

  • Withholding the causative drug usually results in improvement of platelet counts in cases of drug-induced thrombocytopenia.
  • The mainstay of treatment in HIT is to withdraw all heparin products and to initiate anti-thrombin and anti-Xa activity anticoagulant agents. Dicoumarol agents added once platelet count reaches normal.[28][29][30]
  • (A1)

TTP gets treated with plasma exchange.[31](A1)

In patients with secondary ITP managing the underlying condition is recommended, like, in SLE, SLE treatment is with immunosuppressive agents, and in patients with H. pylori-associated thrombocytopenia, eradication of H.pylori increases platelet count.[32][33](B3)

Differential Diagnosis

Psuedothrombocytopenia: Invitro platelet clumping results from ethylenediaminetetracetic acid (EDTA) dependent agglutinins, inadequately anticoagulated specimen, glycoprotein IIb/IIIa inhibitors. Giant platelets are counted as white blood cells rather than platelets by an automated counter.

Prognosis

A prospective study, it was found that patients with mild thrombocytopenia (100000 to 150000/microliter) have a 10-year probability of developing autoimmune disorders of 12 %.[34]

Complications

Severe thrombocytopenia is associated with severe internal bleeding. Bleeding in the brain is fatal.

In heparin-induced thrombosis (HIT), arterial and venous thrombosis is seen leading to deep venous thrombosis, pulmonary embolism, cerebrovascular accident, and myocardial infarction.[35]

Antiphospholipid antibody syndrome associated with arterial and venous thrombosis, and abortions.[36][37]

In TTP microvascular thrombosis involving various organ systems predominantly central nervous system, whereas in HUS kidneys are affected.

Consultations

Newly- diagnosed patients with thrombocytopenia are referred to a hematologist to confirm the diagnosis. In patients with unexplained thrombocytopenia, consulting hematologist is the recommendation. Immediate consultation is necessary for conditions like TTP, HUS, HIT, aplastic anemia, leukemia, and other bone marrow failure conditions.

Pregnant patients with HELLP/preeclampsia require an obstetrician consultation.

Deterrence and Patient Education

Educate patients about activity restrictions. Patients with a platelet count over 50000/mL should be cautious while participating in contact sports. Restriction from contact sports and other potentially traumatic activities is recommended in patients with platelets count under 10000/ mL.[34][38]

Educate patients that certain over the counter medications like aspirin, Non-steroidal anti-inflammatory drugs, and ginkgo biloba interfere with platelet function. Educate patients about quinine-containing beverages and herbal teas, causing the low platelet count.

Enhancing Healthcare Team Outcomes

Due to the complexity of this condition, management of emergent thrombocytopenic conditions requires an interprofessional team of health care professionals, including specialty-trained nursing, pharmacists, physicians, and specialists working together collaboratively to achieve optimal patient outcomes.

References


[1]

Kam T, Alexander M. Drug-induced immune thrombocytopenia. Journal of pharmacy practice. 2014 Oct:27(5):430-9. doi: 10.1177/0897190014546099. Epub 2014 Aug 17     [PubMed PMID: 25134884]


[2]

LAVY R. THROMBOCYTOPENIC PURPURA DUE TO LUPINUS TERMIS BEAN. The Journal of allergy. 1964 Sep-Oct:35():386-9     [PubMed PMID: 14216353]


[3]

Arnold J, Ouwehand WH, Smith GA, Cohen H. A young woman with petechiae. Lancet (London, England). 1998 Aug 22:352(9128):618     [PubMed PMID: 9746024]

Level 3 (low-level) evidence

[4]

Achterbergh R, Vermeer HJ, Curtis BR, Porcelijn L, Aster RH, Deenik W, Daemen-Gubbels C. Thrombocytopenia in a nutshell. Lancet (London, England). 2012 Feb 25:379(9817):776. doi: 10.1016/S0140-6736(11)61643-7. Epub     [PubMed PMID: 22364760]

Level 3 (low-level) evidence

[5]

Azuno Y, Yaga K, Sasayama T, Kimoto K. Thrombocytopenia induced by Jui, a traditional Chinese herbal medicine. Lancet (London, England). 1999 Jul 24:354(9175):304-5     [PubMed PMID: 10440313]

Level 3 (low-level) evidence

[6]

Ohmori T, Nishii K, Hagihara A, Takeda M, Sekido K. Acute thrombocytopenia induced by jui, a traditional herbal medicine. Journal of thrombosis and haemostasis : JTH. 2004 Aug:2(8):1479-80     [PubMed PMID: 15304064]

Level 3 (low-level) evidence

[7]

Davies JK, Ahktar N, Ranasinge E. A juicy problem. Lancet (London, England). 2001 Dec 22-29:358(9299):2126     [PubMed PMID: 11784628]

Level 3 (low-level) evidence

[8]

George JN, Raskob GE, Shah SR, Rizvi MA, Hamilton SA, Osborne S, Vondracek T. Drug-induced thrombocytopenia: a systematic review of published case reports. Annals of internal medicine. 1998 Dec 1:129(11):886-90     [PubMed PMID: 9867731]

Level 1 (high-level) evidence

[9]

Scaradavou A. HIV-related thrombocytopenia. Blood reviews. 2002 Mar:16(1):73-6     [PubMed PMID: 11914001]


[10]

Karimi O, Goorhuis A, Schinkel J, Codrington J, Vreden SGS, Vermaat JS, Stijnis C, Grobusch MP. Thrombocytopenia and subcutaneous bleedings in a patient with Zika virus infection. Lancet (London, England). 2016 Mar 5:387(10022):939-940. doi: 10.1016/S0140-6736(16)00502-X. Epub 2016 Feb 20     [PubMed PMID: 26906627]


[11]

Clare NM, Montiel MM, Lifschitz MD, Bannayan GA. Alport's syndrome associated with macrothrombopathic thrombocytopenia. American journal of clinical pathology. 1979 Jul:72(1):111-7     [PubMed PMID: 453097]

Level 3 (low-level) evidence

[12]

Segal JB, Moliterno AR. Platelet counts differ by sex, ethnicity, and age in the United States. Annals of epidemiology. 2006 Feb:16(2):123-30     [PubMed PMID: 16246584]

Level 2 (mid-level) evidence

[13]

Veneri D, Franchini M, Randon F, Nichele I, Pizzolo G, Ambrosetti A. Thrombocytopenias: a clinical point of view. Blood transfusion = Trasfusione del sangue. 2009 Apr:7(2):75-85. doi: 10.2450/2008.0012-08. Epub     [PubMed PMID: 19503627]


[14]

Franchini M, Veneri D, Lippi G. Thrombocytopenia and infections. Expert review of hematology. 2017 Jan:10(1):99-106. doi: 10.1080/17474086.2017.1271319. Epub 2016 Dec 20     [PubMed PMID: 27936979]


[15]

Mason KD, Carpinelli MR, Fletcher JI, Collinge JE, Hilton AA, Ellis S, Kelly PN, Ekert PG, Metcalf D, Roberts AW, Huang DC, Kile BT. Programmed anuclear cell death delimits platelet life span. Cell. 2007 Mar 23:128(6):1173-86     [PubMed PMID: 17382885]

Level 3 (low-level) evidence

[16]

Dowling MR, Josefsson EC, Henley KJ, Hodgkin PD, Kile BT. Platelet senescence is regulated by an internal timer, not damage inflicted by hits. Blood. 2010 Sep 9:116(10):1776-8. doi: 10.1182/blood-2009-12-259663. Epub 2010 Jun 7     [PubMed PMID: 20530288]

Level 3 (low-level) evidence

[17]

Stasi R. Immune thrombocytopenia: pathophysiologic and clinical update. Seminars in thrombosis and hemostasis. 2012 Jul:38(5):454-62. doi: 10.1055/s-0032-1305780. Epub 2012 Mar 5     [PubMed PMID: 22753097]


[18]

Budman DR, Steinberg AD. Hematologic aspects of systemic lupus erythematosus. Current concepts. Annals of internal medicine. 1977 Feb:86(2):220-9     [PubMed PMID: 835948]


[19]

Kuwana M. Helicobacter pylori-associated immune thrombocytopenia: clinical features and pathogenic mechanisms. World journal of gastroenterology. 2014 Jan 21:20(3):714-23. doi: 10.3748/wjg.v20.i3.714. Epub     [PubMed PMID: 24574745]

Level 3 (low-level) evidence

[20]

Leslie SD, Toy PT. Laboratory hemostatic abnormalities in massively transfused patients given red blood cells and crystalloid. American journal of clinical pathology. 1991 Dec:96(6):770-3     [PubMed PMID: 1746495]

Level 2 (mid-level) evidence

[21]

Counts RB, Haisch C, Simon TL, Maxwell NG, Heimbach DM, Carrico CJ. Hemostasis in massively transfused trauma patients. Annals of surgery. 1979 Jul:190(1):91-9     [PubMed PMID: 464685]


[22]

Aster RH. Pooling of platelets in the spleen: role in the pathogenesis of "hypersplenic" thrombocytopenia. The Journal of clinical investigation. 1966 May:45(5):645-57     [PubMed PMID: 5327481]


[23]

Mant MJ, Doery JC, Gauldie J, Sims H. Pseudothrombocytopenia due to platelet aggregation and degranulation in blood collected in EDTA. Scandinavian journal of haematology. 1975 Oct:15(3):161-70     [PubMed PMID: 812172]

Level 3 (low-level) evidence

[24]

Peters M, Heyderman RS, Klein NJ. Platelet satellitism. The New England journal of medicine. 1998 Jul 9:339(2):131-2     [PubMed PMID: 9669908]

Level 3 (low-level) evidence

[25]

Ladhani S, Khatri P, El-Bashir H, Shingadia D. Imported malaria is a major cause of thrombocytopenia in children presenting to the emergency department in east London. British journal of haematology. 2005 Jun:129(5):707-9     [PubMed PMID: 15916695]

Level 3 (low-level) evidence

[26]

Patel U, Gandhi G, Friedman S, Niranjan S. Thrombocytopenia in malaria. Journal of the National Medical Association. 2004 Sep:96(9):1212-4     [PubMed PMID: 15481750]

Level 2 (mid-level) evidence

[27]

Blickstein D. [TREATMENT OF IMMUNE THROMBOCYTOPENIC PURPURA IN ADULTS: UPDATE]. Harefuah. 2019 Mar:158(3):196-199     [PubMed PMID: 30916510]


[28]

Bakchoul T, Marini I. Drug-associated thrombocytopenia. Hematology. American Society of Hematology. Education Program. 2018 Nov 30:2018(1):576-583. doi: 10.1182/asheducation-2018.1.576. Epub     [PubMed PMID: 30504360]


[29]

Lewis BE, Wallis DE, Berkowitz SD, Matthai WH, Fareed J, Walenga JM, Bartholomew J, Sham R, Lerner RG, Zeigler ZR, Rustagi PK, Jang IK, Rifkin SD, Moran J, Hursting MJ, Kelton JG, ARG-911 Study Investigators. Argatroban anticoagulant therapy in patients with heparin-induced thrombocytopenia. Circulation. 2001 Apr 10:103(14):1838-43     [PubMed PMID: 11294800]

Level 1 (high-level) evidence

[30]

Alving BM. How I treat heparin-induced thrombocytopenia and thrombosis. Blood. 2003 Jan 1:101(1):31-7     [PubMed PMID: 12393689]


[31]

Rock GA,Shumak KH,Buskard NA,Blanchette VS,Kelton JG,Nair RC,Spasoff RA, Comparison of plasma exchange with plasma infusion in the treatment of thrombotic thrombocytopenic purpura. Canadian Apheresis Study Group. The New England journal of medicine. 1991 Aug 8     [PubMed PMID: 2062330]

Level 1 (high-level) evidence

[32]

Veneri D, Franchini M, Gottardi M, D'Adda M, Ambrosetti A, Krampera M, Zanetti F, Pizzolo G. Efficacy of Helicobacter pylori eradication in raising platelet count in adult patients with idiopathic thrombocytopenic purpura. Haematologica. 2002 Nov:87(11):1177-9     [PubMed PMID: 12414347]


[33]

Kado R, McCune WJ. Treatment of primary and secondary immune thrombocytopenia. Current opinion in rheumatology. 2019 May:31(3):213-222. doi: 10.1097/BOR.0000000000000599. Epub     [PubMed PMID: 30920453]

Level 3 (low-level) evidence

[34]

Stasi R, Amadori S, Osborn J, Newland AC, Provan D. Long-term outcome of otherwise healthy individuals with incidentally discovered borderline thrombocytopenia. PLoS medicine. 2006 Mar:3(3):e24     [PubMed PMID: 16401142]


[35]

Franchini M. Heparin-induced thrombocytopenia: an update. Thrombosis journal. 2005 Oct 4:3():14     [PubMed PMID: 16202170]


[36]

Finazzi G, Brancaccio V, Moia M, Ciaverella N, Mazzucconi MG, Schinco PC, Ruggeri M, Pogliani EM, Gamba G, Rossi E, Baudo F, Manotti C, D'Angelo A, Palareti G, De Stefano V, Berrettini M, Barbui T. Natural history and risk factors for thrombosis in 360 patients with antiphospholipid antibodies: a four-year prospective study from the Italian Registry. The American journal of medicine. 1996 May:100(5):530-6     [PubMed PMID: 8644765]

Level 2 (mid-level) evidence

[37]

Lockshin MD, Druzin ML, Goei S, Qamar T, Magid MS, Jovanovic L, Ferenc M. Antibody to cardiolipin as a predictor of fetal distress or death in pregnant patients with systemic lupus erythematosus. The New England journal of medicine. 1985 Jul 18:313(3):152-6     [PubMed PMID: 3925336]


[38]

Lacey JV,Penner JA, Management of idiopathic thrombocytopenic purpura in the adult. Seminars in thrombosis and hemostasis. 1977 Jan     [PubMed PMID: 322290]