View source for Acute myeloid leukemia laboratory tests

__NOTOC__
{{Acute myeloid leukemia}}

{{CMG}}; {{AE}} {{RT}} {{CLG}} {{shyam}}

==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.<ref name="pmid25520834">{{cite journal| author=Asakura H| title=Classifying types of disseminated intravascular coagulation: clinical and animal models. | journal=J Intensive Care | year= 2014 | volume= 2 | issue= 1 | pages= 20 | pmid=25520834 | doi=10.1186/2052-0492-2-20 | pmc=4267600 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25520834  }} </ref> 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.<ref name="pmid24359983">{{cite journal| author=Wilson FP, Berns JS| title=Tumor lysis syndrome: new challenges and recent advances. | journal=Adv Chronic Kidney Dis | year= 2014 | volume= 21 | issue= 1 | pages= 18-26 | pmid=24359983 | doi=10.1053/j.ackd.2013.07.001 | pmc=4017246 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24359983  }} </ref> 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.<ref name="pmid24359983">{{cite journal| author=Wilson FP, Berns JS| title=Tumor lysis syndrome: new challenges and recent advances. | journal=Adv Chronic Kidney Dis | year= 2014 | volume= 21 | issue= 1 | pages= 18-26 | pmid=24359983 | doi=10.1053/j.ackd.2013.07.001 | pmc=4017246 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24359983  }} </ref> 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.<ref name="pmid24359983">{{cite journal| author=Wilson FP, Berns JS| title=Tumor lysis syndrome: new challenges and recent advances. | journal=Adv Chronic Kidney Dis | year= 2014 | volume= 21 | issue= 1 | pages= 18-26 | pmid=24359983 | doi=10.1053/j.ackd.2013.07.001 | pmc=4017246 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24359983  }} </ref> 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.<ref name="pmid24359983">{{cite journal| author=Wilson FP, Berns JS| title=Tumor lysis syndrome: new challenges and recent advances. | journal=Adv Chronic Kidney Dis | year= 2014 | volume= 21 | issue= 1 | pages= 18-26 | pmid=24359983 | doi=10.1053/j.ackd.2013.07.001 | pmc=4017246 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24359983  }} </ref> 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.<ref name="pmid16504043">{{cite journal| author=Franchini M, Lippi G, Manzato F| title=Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation. | journal=Thromb J | year= 2006 | volume= 4 | issue=  | pages= 4 | pmid=16504043 | doi=10.1186/1477-9560-4-4 | pmc=1402263 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16504043  }} </ref>
*'''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.<ref name="pmid16504043">{{cite journal| author=Franchini M, Lippi G, Manzato F| title=Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation. | journal=Thromb J | year= 2006 | volume= 4 | issue=  | pages= 4 | pmid=16504043 | doi=10.1186/1477-9560-4-4 | pmc=1402263 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16504043  }} </ref>
*'''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.<ref name="pmid16504043">{{cite journal| author=Franchini M, Lippi G, Manzato F| title=Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation. | journal=Thromb J | year= 2006 | volume= 4 | issue=  | pages= 4 | pmid=16504043 | doi=10.1186/1477-9560-4-4 | pmc=1402263 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16504043  }} </ref>
*'''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]].<ref name="pmid16504043">{{cite journal| author=Franchini M, Lippi G, Manzato F| title=Recent acquisitions in the pathophysiology, diagnosis and treatment of disseminated intravascular coagulation. | journal=Thromb J | year= 2006 | volume= 4 | issue=  | pages= 4 | pmid=16504043 | doi=10.1186/1477-9560-4-4 | pmc=1402263 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16504043  }} </ref>
*'''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.<ref name="pmid23049403">{{cite journal| author=Bassi SC, Rego EM| title=Molecular basis for the diagnosis and treatment of acute promyelocytic leukemia. | journal=Rev Bras Hematol Hemoter | year= 2012 | volume= 34 | issue= 2 | pages= 134-9 | pmid=23049403 | doi=10.5581/1516-8484.20120033 | pmc=3459394 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23049403  }} </ref>

{| align="center"
!
|- valign="top"
|
|
|}

==References==
{{reflist|2}}

{{Hematology}}
{{Hematological malignancy histology}}
[[Category:Hematology]]
[[Category:Types of cancer]]
[[Category:Leukemia]]


{{WikiDoc Help Menu}}
{{WikiDoc Sources}}
 [[Category:Up-To-Date]]
[[Category:Oncology]]
[[Category:Medicine]]
[[Category:Hematology]]
[[Category:Immunology]]