Acute promyelocytic leukemia laboratory findings

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shyam Patel [2], Sogand Goudarzi, MD [3]; Grammar Reviewer: Natalie Harpenau, B.S.[4]


The laboratory abnormalities in acute promyelocytic leukemia can be broadly divided into abnormalities of the complete blood count and abnormalities of the coagulation system. The complete blood count usually shows anemia, thrombocytopenia, leukopenia, and elevated blast count. The coagulation profile usually shows elevated prothrombin time, elevated partial thromboplastin time, elevated thrombin time, elevated reptilase time, and low fibrinogen. This combination of coagulation parameters accounts for high hemorrhagic risk in patients with acute promyelocytic leukemia.

Laboratory Findings

Abnormalities of the complete blood count

  • Anemia:
  • Thrombocytopenia:
    • Thrombocytopenia refers to low platelet count. The platelet count is usually less than 150,000 cells per microliter. Low platelet count in patients with acute promyelocytic leukemia is typically due to two reasons.[4]
    • Firstly, leukemic cell infiltration in the bone marrow results in disruption of normal megakaryocyte production with decreased platelet production. Secondly, coagulopathy (disseminated intravascular coagulation) results in platelet consumption and therefore a low platelet count. This latter reason is unique to acute promyelocytic leukemia compared to other types of leukemia. The degree of thrombocytopenia also confers prognostic value in acute promyelocytic leukemia: platelet counts lower than 40,000 cells per microliter carries a worse prognosis than platelet counts greater than 40,000 cells per microliter.[5]
  • Leukopenia:
    • Leukopenia refers to white blood cell count below 4,000 cells per microliter. Leukopenia is common in patients with acute promyelocytic leukemia, unlike most other types of leukemia.[6]
    • In some cases, however, patients can have high white blood cell counts, which confers a worse prognosis. White blood cell count above 10,000 cells per microliter defines high-risk disease.[7]
  • Elevated blast count:
    • The white blood cell differential will typically show the presence of circulating blasts, which are the malignant cells in acute promyelocytic leukemia.[8]
    • An elevated peripheral blood blast count is a common initial finding in the disease, and this finding frequently serves as the trigger for additional workup. The presence of peripheral blood blasts must be evaluated further by performing a bone marrow biopsy.[9]

Abnormalities of coagulation parameters

  • Hypofibrinogenemia:
    • Hypofibrinogenemia, or a fibrinogen level below 100 mg/dl, is commonly found in patients with acute promyelocytic leukemia. Hypofibrinogenemia is a key component of disseminated intravascular coagulation, which is characterized by widespread clot formation and breakdown. Fibrinogen, also known as factor I of the coagulation cascade, is broken down in patients with acute promyelocytic leukemia, resulting in bleeding complications. Values of less than 100 mg/dl require treatment with cryoprecipitate, which restores fibrinogen levels towards normal range.[10]
  • Elevated prothrombin time (PT):
  • Elevated partial thromboplastin time (PTT):
  • Elevated thrombin time:
    • Thrombin time measures the conversion of fibrinogen to fibrin; therefore, a high thrombin time is seen in patients with coagulopathy from acute promyelocytic leukemia. Thrombin is also known as factor II of the coagulation cascade and is immediately upstream of fibrinogen.[10]
  • Elevated reptilase time:
    • Reptilase time also measures the conversion of fibrinogen to fibrin, but this test uses a different enzyme, known as reptilase, which is derived from snake venom. The unique feature of the reptilase time is that it can be used to differentiate high PTT caused by heparin effect. The reptilase time is not sensitive to heparin.[11]
    • Reptilase time is high in patients with coagulopathy from acute promyelocytic leukemia.[12]
  • Elevated D-dimer:
    • D-dimer measures simultaneous clot formation and breakdown. Elevated D-dimer is not specific to acute promyelocytic leukemia, as it can be found in patients with obstetric complications (eclampsia and amniotic fluid embolism) or sepsis from Neisseria meningitides. Elevated D-dimer is very sensitive for an underlying coagulopathy and is an excellent test for ruling out a hematologic condition, if the pre-test probability is low. D-dimer is elevated in the majority of cases of acute promyelocytic leukemia.[13]


  1. Brodsky RA, Jones RJ (October 2004). "Riddle: what do aplastic anemia, acute promyelocytic leukemia, and chronic myeloid leukemia have in common?". Leukemia. 18 (10): 1740–2. doi:10.1038/sj.leu.2403487. PMID 15356647.
  2. Lee HJ, Park HJ, Kim HW, Park SG (December 2013). "Comparison of laboratory characteristics between acute promyelocytic leukemia and other subtypes of acute myeloid leukemia with disseminated intravascular coagulation". Blood Res. 48 (4): 250–3. doi:10.5045/br.2013.48.4.250. PMC 3894382. PMID 24466548.
  3. Jillella AP, Arellano ML, Heffner LT, Gaddh M, Langston AA, Khoury HJ, Mangoankar A, Kota VK (September 2017). "Managing acute promyelocytic leukemia in patients belonging to the Jehovah's Witness congregation". Hematol Rep. 9 (3): 7083. doi:10.4081/hr.2017.7083. PMC 5641824. PMID 29071052.
  4. Qian, Xu; Wen-jun, Liu (2013). "Platelet Changes in Acute Leukemia". Cell Biochemistry and Biophysics. 67 (3): 1473–1479. doi:10.1007/s12013-013-9648-y. ISSN 1085-9195.
  5. Qian, Xu; Wen-jun, Liu (2013). "Platelet Changes in Acute Leukemia". Cell Biochemistry and Biophysics. 67 (3): 1473–1479. doi:10.1007/s12013-013-9648-y. ISSN 1085-9195.
  6. McDonnell, Megan H.; Smith, Elton T.; Lipford, Edward H.; Gerber, Jonathan M.; Grunwald, Michael R. (2017). "Microgranular acute promyelocytic leukemia presenting with leukopenia and an unusual immunophenotype". Hematology/Oncology and Stem Cell Therapy. 10 (1): 35–38. doi:10.1016/j.hemonc.2015.12.004. ISSN 1658-3876.
  7. Kelaidi, Charicleia; Ades, Lionel; Fenaux, Pierre (2011). "TREATMENT OF ACUTE PROMYELOCYTIC LEUKEMIA WITH HIGH WHITE CELL BLOOD COUNTS". Mediterranean Journal of Hematology and Infectious Diseases. 3 (1): e2011038. doi:10.4084/mjhid.2011.038. ISSN 2035-3006.
  8. Chabot-Richards, D. S.; George, T. I. (2014). "Leukocytosis". International Journal of Laboratory Hematology. 36 (3): 279–288. doi:10.1111/ijlh.12212. ISSN 1751-5521.
  9. Percival, Mary-Elizabeth; Lai, Catherine; Estey, Elihu; Hourigan, Christopher S. (2017). "Bone marrow evaluation for diagnosis and monitoring of acute myeloid leukemia". Blood Reviews. 31 (4): 185–192. doi:10.1016/j.blre.2017.01.003. ISSN 0268-960X.
  10. 10.0 10.1 10.2 10.3 Franchini M, Lippi G, Manzato F (2006). "Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation". Thromb J. 4: 4. doi:10.1186/1477-9560-4-4. PMC 1402263. PMID 16504043.
  11. Karapetian, Hratsch (2013). "Reptilase Time (RT)". 992: 273–277. doi:10.1007/978-1-62703-339-8_20. ISSN 1064-3745.
  12. Wheeler, Arthur P.; Rice, Todd W. (2010). "Coagulopathy in Critically III Patients". Chest. 137 (1): 185–194. doi:10.1378/chest.08-2535. ISSN 0012-3692.
  13. Bassi SC, Rego EM (2012). "Molecular basis for the diagnosis and treatment of acute promyelocytic leukemia". Rev Bras Hematol Hemoter. 34 (2): 134–9. doi:10.5581/1516-8484.20120033. PMC 3459394. PMID 23049403.

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