Acute myeloid leukemia laboratory tests

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2], Carlos A Lopez, M.D. [3], Shyam Patel [4]; Grammar Reviewer: Natalie Harpenau, B.S.[5]

Overview

The laboratory abnormalities in acute myeloid leukemia can be broadly divided into abnormalities of the complete blood count, abnormalities of serum chemistries, and abnormalities of the coagulation system. The complete blood count usually shows anemia, thrombocytopenia, leukopenia, and elevated blast count. The serum chemistries can show findings consistent with tumor lysis syndrome, which includes increased potassium, increased uric acid, increased phosphate, decreased calcium, and increased lactate dehydrogenase. In the acute promyelocytic leukemia subcategory of acute myeloid leukemia, 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 especially in patients with acute promyelocytic leukemia.

Laboratory Findings

Abnormalities of the complete blood count

  • Anemia: Anemia refers to decreased red blood cell production, which results in low hemoglobin content in the peripheral blood. Hemoglobin values are typically less than 10 g/dl in most patients with acute myeloid leukemia. The degree of anemia corresponds with the amount of bone marrow infiltration by leukemic cells. Patients with severe or advanced leukemia will usually have severe anemia. Severe anemia can result in profound fatigue, pallor, and shortness of breath.
  • 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 myeloid leukemia is typically due to two reasons. Firstly, leukemic cell infiltration in the bone marrow results in disruption of normal megakaryocyte production with decreased platelet production. Secondly, coagulopathy (disseminated intravascular coagulation) can result in platelet consumption and therefore a low platelet count.[1] This latter reason is unique to the acute promyelocytic leukemia category of acute myeloid 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.
  • Leukopenia: Leukopenia refers to white blood cell count below 4,000 cells per microliter. Hyperleukocytosis, or excessively elevated white blood cell count, is common in some types of acute myeloid leukemia. Leukopenia, or low white blood cell count, is more common in patients with acute promyelocytic leukemia, unlike most other types of leukemia. 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 in acute promyelocytic leukemia.
  • 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. Blasts are equivalent to stem cells, and the normal blast count in the bone marrow is less than 5%. 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.

Abnormalities of serum chemistries

  • Increased potassium: Increased potassium is a hallmark of tumor lysis syndrome, which occurs commonly in patients with acute myeloid leukemia with a high peripheral blood blast count.[2] Potassium is elevated because it is released from intracellular sources into the peripheral blood. Elevated potassium can contribute to arrhythmias. Treatment involves kayexalate, insulin, calcium, furosemide, sodium bicarbonate, and beta-adrenergic agonists.
  • Increased uric acid: Increased uric acid is a hallmark of tumor lysis syndrome, which occurs commonly in patients with acute myeloid leukemia with a high peripheral blood blast count.[2] Uric acid is elevated because it is released from intracellular sources into the peripheral blood. Elevated uric acid can contribute to gout and renal failure (urate nephropathy). Treatment involves allopurinol, rasburicase, or febuxostat.
  • Increased phosphorus: Increased phosphorus is a hallmark of tumor lysis syndrome, which occurs commonly in patients with acute myeloid leukemia with a high peripheral blood blast count.[2] Phosphorus is elevated because it is released from intracellular sources into the peripheral blood. Elevated phosphorus can contribute to other electrolyte abnormalities. Treatment involves sevelamer and calcium acetate.
  • Decreased calcium: Decreased phosphorus occurs sometimes in tumor lysis syndrome because elevated potassium binds to calcium, which lowers the serum calcium. Hypocalcemia can result in arrhythmias and tetany, or sustained muscle contractions with twitching. Treatment involves intravenous calcium gluconate.
  • Increased lactate dehydrogenase: Increased lactate dehydrogenase commonly occurs in tumor lysis syndrome, which occurs commonly in patients with acute myeloid leukemia with a high peripheral blood blast count.[2] This enzyme is elevated because it is released from intracellular sources into the peripheral blood. There is no harm from high levels of lactate dehydrogenase; it is simply a manifestation of underlying tumor lysis. There is no need for treatment of the high level of lactate dehydrogenase, but the underlying tumor lysis should be treated with allopurinol or rasburicase.

Abnormalities of coagulation parameters

  • Hypofibrinogenemia: Hypofibrinogenemia, or 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.[3]
  • Elevated prothrombin time (PT): High PT values, typically above 15 seconds, are common in patients with acute promyelocytic leukemia. This is due to disseminated intravascular coagulation, which results in consumption of coagulation factors of the intrinsic and extrinsic coagulation pathways. High PT reflects consumption of factors from the extrinsic pathway, such as factor VII.[3]
  • Elevated partial thromboplastin time (PTT): High PTT values, typically above 40 second, are common in patients with acute promyelocytic leukemia. This is due to disseminated intravascular coagulation, which results in consumption of coagulation factors of the intrinsic and extrinsic coagulation pathways. High PTT reflects consumption of factors from the intrinsic pathway, such as factors XII, XI, IX, and VIII.[3]
  • Elevated thrombin time: Thrombin time measures the conversion of fibrinogen to fibrin, and 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.[3]
  • 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. Reptilase time is high in patients with coagulopathy from acute promyelocytic leukemia.
  • 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 is the pre-test probability is low. D-dimer is elevated in the majority of cases of acute promyelocytic leukemia.[4]

References

  1. Asakura H (2014). "Classifying types of disseminated intravascular coagulation: clinical and animal models". J Intensive Care. 2 (1): 20. doi:10.1186/2052-0492-2-20. PMC 4267600. PMID 25520834.
  2. 2.0 2.1 2.2 2.3 Wilson FP, Berns JS (2014). "Tumor lysis syndrome: new challenges and recent advances". Adv Chronic Kidney Dis. 21 (1): 18–26. doi:10.1053/j.ackd.2013.07.001. PMC 4017246. PMID 24359983.
  3. 3.0 3.1 3.2 3.3 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.
  4. 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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