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| __NOTOC__ | | __NOTOC__ |
| {{DiseaseDisorder infobox |
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| Name = Acute myeloid leukemia |
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| ICD10 = {{ICD10|C|92|0|c|81}} |
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| ICD9 = {{ICD9|205.0}} |
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| ICDO = {{ICDO|9861|3}} |
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| Image = Auer_rods.PNG |
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| Caption = Bone marrow aspirate showing acute myeloid leukemia. Arrows indicate [[Auer rods]].|
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| OMIM = 602439 |
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| MedlinePlus = 000542 |
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| DiseasesDB = 203 |
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| }}
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| {{Acute myeloid leukemia}} | | {{Acute myeloid leukemia}} |
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| '''For patient information click [[Leukemia (patient information)|here]]''' | | '''For patient information click [[Leukemia (patient information)|here]]''' |
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| {{CMG}}; {{AE}} {{RT}} | | {{CMG}}; {{AE}} {{RT}} {{CLG}} {{shyam}}; {{GRR}} {{Nat}} |
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| ==Overview==
| | {{SK}} AML; acute granulocytic leukaemia; acute myeloblastic leukemia; acute myelogenous leukemia; acute nonlymphocytic leukemia; M7; megakaryocytic leukemia; Acute monocytic leukemia; AMoL; AML-M5 |
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| | ==[[Acute myeloid leukemia overview|Overview]]== |
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| ==History== | | ==[[Acute myeloid leukemia historical perspective|Historical Perspective]]== |
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| ==Signs and symptoms== | | ==[[Acute myeloid leukemia classification|Classification]]== |
| Most signs and symptoms of AML are due to an increased number of malignant white blood cells displacing or otherwise interfering with [[haematopoiesis|production of normal blood cells]] in the [[bone marrow]]. A lack of normal white blood cell production makes the patient susceptible to infections (while the leukemic cells themselves are derived from white blood cell precursors, they have no infection-fighting capacity).<ref name="symptoms">Hoffman, Ronald et al. (2005), pp. 1074–75.</ref> A lack of red blood cells ([[anemia]]) can cause fatigue, paleness, and shortness of breath. A lack of [[platelet]]s can lead to easy bruising or bleeding with minor trauma.
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| The early signs of AML are often non-specific, and may be similar to those of [[influenza]] or other common illnesses. Some generalized symptoms include [[fever]], [[Fatigue (physical)|fatigue]], [[weight loss]] or [[loss of appetite]], [[dyspnea|shortness of breath]] with exertion, [[anemia]], easy [[bruising]] or [[bleeding]], [[petechia]]e (flat, pin-head sized spots under the skin caused by bleeding), [[bone pain]] and [[joint pain]] and persistent or frequent [[infections]].<ref name = "symptoms"/>
| | ==[[Acute myeloid leukemia pathophysiology|Pathophysiology]]== |
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| [[Splenomegaly|Enlargement of the spleen]] may occur in AML, but it is typically mild and [[asymptomatic]]. [[lymphadenopathy|Lymph node swelling]] is rare in AML, in contrast to [[acute lymphoblastic leukemia]]. The skin is involved about 10% of the time in the form of [[chloroma|leukemia cutis]]. Rarely, [[Sweet syndrome|Sweet's syndrome]], a [[paraneoplastic syndrome|paraneoplastic]] inflammation of the skin, can occur with AML.<ref name = "symptoms"/> | | ==[[Acute myeloid leukemia causes|Causes]]== |
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| Some patients with AML may experience swelling of the gums because of infiltration of leukemic cells into the gum tissue. Rarely, the first sign of leukemia may be the development of a solid leukemic mass or tumor outside of the [[bone marrow]], called a [[chloroma]]. Occasionally, a person may show [[asymptomatic|no symptoms]], and the leukemia may be discovered incidentally during a routine blood test.<ref>
| | ==[[Acute myeloid leukemia differential diagnosis|Differentiating Acute Myeloid Leukemia from Other Diseases]]== |
| {{cite book |last = Abeloff |first = Martin ''et al.'' |title= Clinical Oncology |year= 2004 |publisher= Elsevier Churchill Livingstone |location= St. Louis, Mo. |edition = 3rd. edition |pages = p. 2834 |id= ISBN 0-443-06629-9}}</ref>
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| ==Causes== | | ==[[Acute myeloid leukemia epidemiology and demographics|Epidemiology and Demographics]]== |
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| ==Epidemiology== | | ==[[Acute myeloid leukemia risk factors|Risk Factors]]== |
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| ==Pathophysiology== | | ==[[Acute myeloid leukemia screening|Screening]]== |
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| | ==[[Acute myeloid leukemia natural history|Natural History, Complications and Prognosis]]== |
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| ==Diagnosis== | | ==Diagnosis== |
| The first clue to a diagnosis of AML is typically an abnormal result on a [[complete blood count]]. While an excess of abnormal white blood cells ([[leukocytosis]]) is a common finding, and leukemic blasts are sometimes seen, AML can also present with isolated decreases in [[platelet]]s, [[red blood cell]]s, or even with a ''low'' white blood cell count ([[leukopenia]]).<ref>Abeloff, Martin et al. (2004), p. 2834.</ref> While a presumptive diagnosis of AML can be made via examination of the peripheral blood smear when there are circulating leukemic blasts, a definitive diagnosis usually requires an adequate bone marrow aspiration and biopsy
| | [[Acute myeloid leukemia diagnostic study of choice|Diagnostic Study of Choice]] | [[Acute myeloid leukemia history and symptoms|History and Symptoms]] | [[Acute myeloid leukemia physical examination|Physical Examination]] | [[Acute myeloid leukemia laboratory tests|Laboratory Findings]] | [[Acute myeloid leukemia electrocardiogram|Electrocardigram]] | [[Acute myeloid leukemia chest x ray|Chest X Ray]] | [[Acute myeloid leukemia echocardiograph and ultrasound|Echocardiograph and Ultrasound]] | [[Acute myeloid leukemia CT|CT]] | [[Acute myeloid leukemia mri|MRI]] | [[Acute myeloid leukemia other imaging findings|Other Imaging Findings]] | [[Acute myeloid leukemia other diagnostic studies|Other Diagnostic Studies]] |
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| A [[bone marrow examination]] is often performed to identify the type of abnormal blood cells; however, if there are many leukemic cells circulating in the peripheral blood, a bone marrow [[biopsy]] may not be necessary. Marrow or blood is examined via [[light microscopy]] as well as [[flow cytometry]] to diagnose the presence of leukemia, to differentiate AML from other types of leukemia (e.g. [[acute lymphoblastic leukemia]]), and to classify the subtype of disease (see below). A sample of marrow or blood is typically also tested for [[chromosomal translocation]]s by routine [[cytogenetics]] or [[fluorescent in situ hybridization]].
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| The diagnosis and classification of AML can be challenging, and should be performed by a qualified [[hematopathologist]] or [[hematologist]]. In straightforward cases, the presence of certain morphologic features (such as [[Auer rods]]) or specific flow cytometry results can distinguish AML from other leukemias; however, in the absence of such features, diagnosis may be more difficult.<ref>Abeloff, Martin et al. (2004), p. 2835.</ref>
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| According to the widely used [[WHO]] criteria, the diagnosis of AML is established by demonstrating involvement of more than 20% of the blood and/or bone marrow by leukemic [[myeloblast]]s.<ref>{{cite journal | author = Harris N, Jaffe E, Diebold J, Flandrin G, Muller-Hermelink H, Vardiman J, Lister T, Bloomfield C | title = The World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues. Report of the Clinical Advisory Committee meeting, Airlie House, Virginia, November, 1997 | journal = Ann Oncol | volume = 10 | issue = 12 | pages = 1419–32 | year = 1999 | pmid = 10643532}}</ref> AML must be carefully differentiated from "pre-leukemic" conditions such as [[myelodysplastic syndrome|myelodysplastic]] or [[myeloproliferative syndrome|myeloproliferative]] syndromes, which are treated differently.
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| Because [[acute promyelocytic leukemia]] (APL) has the highest curability and requires a unique form of treatment, it is important to quickly establish or exclude the diagnosis of this subtype of leukemia. [[Fluorescent in situ hybridization]] performed on blood or bone marrow is often used for this purpose, as it readily identifies the [[chromosomal translocation]] (t[15;17]) that characterizes APL.<ref>{{cite journal | author = Grimwade D, Howe K, Langabeer S, Davies L, Oliver F, Walker H, Swirsky D, Wheatley K, Goldstone A, Burnett A, Solomon E | title = Establishing the presence of the t(15;17) in suspected acute promyelocytic leukaemia: cytogenetic, molecular and PML immunofluorescence assessment of patients entered into the M.R.C. ATRA trial. M.R.C. Adult Leukaemia Working Party. | journal = Br J Haematol | volume = 94 | issue = 3 | pages = 557-73 | year = 1996 | pmid = 8790159}}</ref>
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| ===Pathology===
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML.jpg|AML - Auer Rods, DIC<ref>http://picasaweb.google.com/mcmumbi/USMLEIIImages</ref>
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| Image:AML (with Auer Rods).jpg|AML (with Auer Rods)<ref>http://picasaweb.google.com/mcmumbi/USMLEIIImages</ref>
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| </gallery>
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| </div>
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| (Images shown below are courtesy of Melih Aktan MD., Istanbul Medical Faculty - Turkey, and Kyoto University - Japan)
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M0 0001.jpg|AML-M0
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| Image:AML-M1 0002.jpg|AML-M1
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M1 peroxidase 0001.jpg|AML-M1 peroxidase
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| Image:AML-M1 0005.jpg|AML-M1
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M1 0004.jpg|AML-M1
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| Image:AML-M1 0003.jpg|AML-M1
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M2 0002.jpg|AML-M2
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| Image:AML-M2 0001.jpg|AML-M2
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| </gallery>
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| </div>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M2 0004.jpg|AML-M2
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| Image:AML-M2 0003.jpg|AML-M2
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M3 0006.jpg|AML-M3
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| Image:AML-M3 0004.jpg|AML-M3
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M3 0002.jpg|AML-M3
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| Image:AML-M3 0001.jpg|AML-M3
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| </gallery>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M3 Auer bodies 0005.jpg|AML-M3 Auer bodies
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| Image:AML-M3 Auer bodies 0003.jpg|AML-M3 Auer bodies
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M3 variation 0007.jpg|AML-M3 variation
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| Image:AML-M4 0001.jpg|AML-M4
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M5a 0003.jpg|AML-M5a
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| Image:AML-M5a 0001.jpg|AML-M5a
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M5a alpha naphtyle acetat 0002.jpg|AML-M5a (alpha naphtyle acetat)
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| Image:AML-M5b 0001.jpg|AML-M5b
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| </gallery>
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| </div>
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| <div align="left">
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| <gallery heights="175" widths="175">
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| Image:AML-M5b 0002.jpg|AML-M5b
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| Image:AML-M7 0001.jpg|AML-M7
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| Image:AML-M7 CD41 0001.jpg|AML-M7
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| </gallery>
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| </div>
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| ==Classification==
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| ==Prognosis==
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| ==Treatment== | | ==Treatment== |
| Treatment of AML consists primarily of [[chemotherapy]], and is divided into two phases: ''induction'' and ''postremission'' (or ''consolidation'') therapy. The goal of ''induction'' therapy is to achieve a complete remission by reducing the amount of leukemic cells to an undetectable level; the goal of ''consolidation'' therapy is to eliminate any residual undetectable disease and achieve a cure.
| | [[Acute myeloid leukemia medical therapy|Medical Therapy]] | [[Acute myeloid leukemia surgery|Surgery]] | [[Acute myeloid leukemia primary prevention|Primary Prevention]] | [[Acute myeloid leukemia secondary prevention|Secondary Prevention]] | [[Acute myeloid leukemia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Acute myeloid leukemia future or investigational therapies|Future or Investigational Therapies]] |
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| In addition, specific treatment plans may be used, depending on the type of leukemia that has been diagnosed. Whatever the plan, it is important for the patient to understand the treatment that is being given and the decision-making process behind the choice.
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| ===Acute Myelogenous Leukemia (AML)===
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| It is most common for adults; more men than women are affected.
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| Many different chemotherapeutic plans are available for the treatment of AML. Overall, the strategy is to control bone marrow and systemic (whole-body) disease while offering specific treatment for the central nervous system (CNS), if involved. In general, most oncologists rely on combinations of drugs for the initial, induction phase of chemotherapy. Such combination chemotherapy usually offers the benefits of early remission (lessening of the disease) and a lower risk of disease resistance. Consolidation or "maintenance" treatments may be given to prevent disease recurrence once remission has been achieved. Consolidation treatment often entails a repetition of induction chemotherapy or the intensification chemotherapy with added drugs. By contrast, maintenance treatment involves drug doses that are lower than those administered during the induction phase.
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| ====Initial treatment of AML====
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| Initial treatment of AML usually begins with induction chemotherapy using a combination of drugs such as [[daunorubicin]] ([[DNR]]), [[cytarabine]] ([[ara-C]]), [[idarubicin]], [[thioguanine]], [[etoposide]], or [[mitoxantrone]], anabolic [[steroids]].
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| ====Follow-up treatment====
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| Follow-up therapy for such patients may involve:
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| * supportive care, such as intravenous nutrition and treatment with oral antibiotics (e.g., ofloxacin, rifampin), especially in patients who have prolonged granulocytopenia; that is too few mature granulocytes (neutrophils), the bacteria-destroying white blood cells that contain small particles, or granules (< 100 granulocytes per cubic millimeter for 2 weeks)
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| * injection with colony-stimulating factors such as granulocyte colony-stimulating factor (G-CSF), which may help to shorten the period of granulocytopenia that results from induction therapy
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| * transfusions with red blood cells and platelets
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| Patients with newly diagnosed disease also may be considered for stem cell transplantation (SCT), either from the bone marrow or other sources. Allogeneic bone marrow transplant (alloBMT) is reserved primarily for patients under 55 years of age who have a compatible family donor. Approximately half of newly diagnosed AML patients are in this age group, with 75% achieving a complete remission (CR) after induction and consolidation therapy. Allogeneic bone marrow transplant is available for about 15% of all patients with AML. Unfortunately, it is estimated that only 7% of all AML patients will be cured using this procedure.
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| People who receive stem cell transplantation (SCT, alloBMT) require protective isolation in the hospital, including filtered air, sterile food, and sterilization of the microorganisms in the gut, until their total white blood cell (WBC) count is above 500.
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| Treatment of central nervous system leukemia, if present, may involve injection of chemotherapeutic drugs (e.g., cytarabine or ara-C, methotrexate) into the areas around the brain and spinal cord.
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| ===Induction===
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| As of 2006, all FAB subtypes except M3 are usually given induction chemotherapy with [[cytarabine]] (ara-C) and an [[anthracycline]] (such as [[daunorubicin]] or [[idarubicin]]).<ref name="treatment">Abeloff, Martin et al. (2004), pp. 2835–39.</ref> Other alternatives, including high-dose ara-C alone, may also be used.<ref>Weick JK, Kopecky KJ, Appelbaum FR, et al: A randomized investigation of high-dose versus standard-dose cytosine arabinoside with daunorubicin in patients with previously untreated acute myeloid leukemia: A Southwest Oncology Group Study. ''Blood'' 1996;88:2841–2851. PMID 8874180</ref><ref>Bishop JF, Matthews JP, Young GA, et al: A randomized study of high-dose cytarabine in induction in acute myeloid leukemia. ''Blood'' 1996;87:1710–1717. PMID 8634416 </ref> Because of the toxic effects of therapy, including [[myelosuppression]] and an increased risk of infection, induction chemotherapy may not offered to the very elderly. Induction chemotherapy usually requires a hospitalization of about 1 month to receive the chemotherapy and recover from its side effects.
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| Induction chemotherapy is known as "7 and 3" because the [[cytarabine]] is given as a continuous IV infusion for seven consecutive days, while the [[anthracycline]] is given for three consecutive days as an IV push. Up to 70% of patients will achieve a remission with this protocol.<ref>{{cite journal |author=Bishop J |title=The treatment of adult acute myeloid leukemia |journal=Semin Oncol |volume=24 |issue=1 |pages=57–69 |year=1997 |pmid=9045305}}</ref>
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| The M3 subtype of AML, also known as [[acute promyelocytic leukemia]], is almost universally treated with the drug [[ATRA]] (all-''trans''-retinoic acid) in addition to induction chemotherapy.<ref>Huang ME, Ye YC, Chen SR, et al: Use of all-trans retinoic acid in the treatment of acute promyelocytic leukemia. ''Blood'' 1988;72:567–572. PMID 3165295</ref><ref>Tallman MS, Anderson JW, Schiffer CA, et al: All-trans-retinoic acid in acute promyelocytic leukemia. ''N Engl J Med'' 1997;337:1021–1028. PMID 9321529</ref><ref>Fenaux P, Chastang C, Chevret S, et al: A randomized comparison of all transretinoic acid (ATRA) followed by chemotherapy and ATRA plus chemotherapy and the role of maintenance therapy in newly diagnosed acute promyelocytic leukemia. The European APL Group. ''Blood'' 1999;94:1192–1200. PMID 10438706</ref> Care must be taken to prevent disseminated intravascular coagulation ([[Disseminated intravascular coagulation|DIC]]), complicating the treatment of [[Acute promyelocytic leukemia|APL]] when the promyelocytes release the contents of their granules into the peripheral circulation. [[APL]] is eminently curable with well-documented treatment protocols.
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| The goal of the induction phase is to reach a ''complete remission''. Complete remission does not mean that the disease has been cured; rather, it signifies that no disease can be detected with available diagnostic methods (i.e., <5% leukemic cells remain in the [[bone marrow]]).<ref name="treatment"/> Complete remission is obtained in about 50%–75% of newly diagnosed adults, although this may vary based on the prognostic factors described above.<ref>{{cite journal | author = Estey E | title = Treatment of acute myelogenous leukemia | journal = Oncology (Williston Park) | volume = 16 | issue = 3 | pages = 343–52, 355–6; discussion 357, 362, 365–6 | year = 2002 | pmid = 15046392}}</ref>
| | ==Case Studies== |
| | [[Acute myeloid leukemia case study one|Case #1]] |
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| The durability of remission depends on the prognostic features of the original leukemia. In general, all remissions will fail without consolidation (post-remission) chemotherapy, and consolidation has become an important component of treatment.<ref>{{cite journal |author=Cassileth P, Harrington D, Hines J, Oken M, Mazza J, McGlave P, Bennett J, O'Connell M |title=Maintenance chemotherapy prolongs remission duration in adult acute nonlymphocytic leukemia |journal=J Clin Oncol |volume=6 |issue=4 |pages=583–7 |year=1988 |pmid=3282032}}</ref>
| | ==Related Chapters== |
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| ===Consolidation===
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| Even after complete remission is achieved, leukemic cells likely remain in numbers too small to be detected with current diagnostic techniques. If no further ''postremission'' or consolidation therapy is given, almost all patients will eventually relapse.<ref>Cassileth PA, Hines JD, Oken MM, et al: Maintenance chemotherapy prolongs remission duration in adult acute nonlymphocytic leukemia. ''J Clin Oncol'' 1988;6(4):583–587. PMID 3282032</ref> Therefore, more therapy is necessary to eliminate non-detectable disease and prevent relapse — that is, to achieve a cure.
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| The specific type of postremission therapy is individualized based on a patient's prognostic factors (see above) and general health. For good-prognosis leukemias (i.e. inv(16), t(8;21), and t(15;17)), patients will typically undergo an additional 3–5 courses of intensive chemotherapy, known as ''consolidation'' chemotherapy.<ref>Mayer RJ, Davis RB, Schiffer CA, et al: Intensive post-remission chemotherapy in adults with acute myeloid leukemia. ''N Engl J Med'' 1994;331:896–903. PMID 8078551</ref><ref name="nccn">O'Donnell MR, Appelbaum FR, Baer MR, et al: NCCN practice guidelines for acute myelogenous leukemia. ''Oncology NCCN Proc'' 2000;14:53–61. PMID 11195419</ref> For patients at high risk of relapse (e.g. those with high-risk cytogenetics, underlying MDS, or therapy-related AML), [[bone marrow transplant|allogeneic stem cell transplantation]] is usually recommended if the patient is able to tolerate a transplant and has a suitable donor. The best postremission therapy for intermediate-risk AML (normal cytogenetics or cytogenetic changes not falling into good-risk or high-risk groups) is less clear and depends on the specific situation, including the age and overall health of the patient, the patient's personal values, and whether a suitable stem cell donor is available.<ref name="nccn"/>
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| If, however, the AML patient has resistant disease (about 15%) or relapses (about 70%), second remissions sometimes are achieved by treating them with:
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| * conventional induction chemotherapy
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| * high-dose ara-C (HDAC), with/without other drugs
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| * etoposide or other single chemotherapeutic agents
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| Elderly AML patients have special treatment concerns. They may be less able to tolerate the septicemia (blood poisoning) associated with granulocytopenia, and they often have higher rates of myelodysplastic ('preleukemia') syndrome (MDS). Individuals who are over age 75 or who have significant medical conditions can be treated effectively with low-dose ara-C. High-dose post-induction chemotherapy is unlikely to be tolerated by elderly patients.
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| Until recently, the treatment plans and responses of children with AML did not differ much from those of adults. Yet new, more intensive induction and consolidation treatments have resulted in higher remission rates and prolonged survivals. Many induction trials have produced good results using combinations of cytarabine (ara-C) plus an anthracycline (e.g., daunorubicin, doxorubicin). In children under 3 years of age, the anthracycline used for induction should be chosen with care, since doxorubicin produces more toxicity and related deaths than daunorubicin.
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| Consolidation therapy is complex, but it should include at least two courses of high-dose ara-C (HDAC). Children who have hyperleukocytosis (too many white blood cells), especially monocytic M5 leukemia, have a poor prognosis.
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| ===Relapsed AML===
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| Despite aggressive therapy, however, only 20%–30% of patients enjoy long-term disease-free survival. For patients with relapsed AML, the only proven potentially curative therapy is a [[stem cell transplant]], if one has not already been performed.<ref name="relapse">Abeloff, Martin et al. (2004), pp. 2840–41.</ref><ref>Appelbaum FR: Who should be transplanted for AML? editorial. ''Leukemia'' 2001;15:680–682. PMID 11368380</ref><ref>Appelbaum FR: Hematopoietic cell transplantation beyond first remission keynote Address. ''Leukemia'' 2002;16:157–159. PMID 11840278</ref> In 2000, [[Mylotarg]] (gemtuzumab zogamicin) was approved in the United States for patients aged more than 60 years with relapsed AML who are not candidates for high-dose chemotherapy.<ref>Sievers EL, Larson RA, Stadmauer EA, et al: Efficacy and safety of gemtuzumab ozogamicin in patients with CD33-positive acute myeloid leukemia in first relapse. ''J Clin Oncol'' 2001;19:3244–3254. PMID 11432892</ref>
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| Patients with relapsed AML who are not candidates for stem cell transplantion, or who have relapsed after a stem cell transplant, should be strongly considered for enrollment in a [[clinical trial]], as conventional treatment options are limited. Agents under investigation include cytotoxic drugs such as [[clofarabine]] as well as [[targeted therapy|targeted therapies]] such as [[farnesyltransferase inhibitor|farnesyl transferase inhibitors]], decitabine, and inhibitors of MDR1 (multidrug-resistance protein). Since treatment options for relapsed AML are so limited, another option which may be offered is [[palliative care]].
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| For relapsed acute promyelocytic leukemia (APL), [[arsenic trioxide]] has been tested in trials and approved by the [[Food and Drug Administration]]. Like ATRA, arsenic trioxide does not work with other subtypes of AML.<ref>Soignet SL, Frankel SR, Douer D, et al: United States multicenter study of arsenic trioxide in relapsed acute promyelocytic leukemia. ''J Clin Oncol'' 2001;19:3852–3860. PMID 11559723</ref>
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| ==See also==
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| * [[Chloroma]] | | * [[Chloroma]] |
| * [[Chronic myelogenous leukemia]] | | * [[Chronic myelogenous leukemia]] |
| * [[Acute lymphoblastic leukemia]] | | * [[Acute lymphoblastic leukemia]] |
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| ==Further reading==
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| * {{cite book |author = Martin Abeloff |coauthors= James Armitage, John Niederhuber, Michael Kastan, W. Gillies McKenna |title= Clinical Oncology |year= 2004 |publisher= Elsevier Churchill Livingstone |location= St. Louis, Mo. |edition = 3rd. edition |id= ISBN 0-443-06629-9}}
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| * {{cite book |author = Ronald Hoffman |coauthors= Edward Benz, Jr., Sanford Shattil, Bruce Furie, Harvey Cohen, Leslie Silberstein, Philip McGlave |title= Hematology: Basic Principles and Practice |year= 2005 |publisher= Elsevier Churchill Livingstone |location= St. Louis, Mo. |edition = 4th. edition |id= ISBN 0-443-06629-9}}
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| ==References==
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| {{reflist|2}}
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| ==External links== | | ==External links== |
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| * [http://www.kanbilim.com/dahiliyeatlasi.htm Atlas of Hematology]
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| * [http://www.cancer.org/docroot/CRI/CRI_2_1x.asp?rnav=criov&dt=82 American Cancer Society page on Acute Myeloid Leukemia]
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| * [http://leukemia.acor.org/ Association of Cancer Online Resource (ACOR) Leukemia Links]
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| * [http://www.leukemia-lymphoma.org/all_page?item_id=8459 Leukemia & Lymphoma Society page on Acute Myeloid Leukemia]
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| * [http://www.cchs.net/health/health-info/docs/1400/1403.asp?index=6211 Childhood Acute Myeloid Leukemia]
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| * [http://www.marrow.org National Marrow Donor Program]
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| * [http://www.bmtinfonet.org/ Blood & Marrow Transplant Information Network]
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| * [http://www.cancer.gov/cancer_information/doc.aspx?viewid=4d3f920e-87d6-4b6a-a2fe-74c6efa53398&version=1 National Cancer Institute (NCI) PDQ statement on AML for health professionals] | | * [http://www.cancer.gov/cancer_information/doc.aspx?viewid=4d3f920e-87d6-4b6a-a2fe-74c6efa53398&version=1 National Cancer Institute (NCI) PDQ statement on AML for health professionals] |
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| {{Hematological malignancy histology}} | | {{Hematological malignancy histology}} |
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| [[ar:ابيضاض الدم النقوي الحاد]]
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| [[de:Akute myeloische Leukämie]]
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| [[es:Leucemia mieloide aguda]]
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| [[he:לוקמיה מיאלואידית חריפה]]
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| [[ja:急性骨髄性白血病]]
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| [[pl:Ostra białaczka szpikowa]]
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| [[pt:Leucemia mielóide aguda]]
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| [[sr:Акутна мијелоцитна леукемија]]
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| [[sv:Akut myeloisk leukemi]]
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| [[zh:急性骨髓性白血病]]
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| {{WikiDoc Help Menu}} | | {{WikiDoc Help Menu}} |
| {{WikiDoc Sources}} | | {{WikiDoc Sources}} |
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| [[Category:Disease]] | | [[Category:Disease]] |
| [[Category:Hematology]] | | [[Category:Hematology]] |
| [[Category:Types of cancer]] | | [[Category:Types of cancer]] |
| [[Category:Oncology]] | | [[Category:Oncology]] |
| [[Category:Overview complete]] | | [[Category:Leukemia]] |
| | [[Category:Up-To-Date]] |
| | [[Category:Oncology]] |
| | [[Category:Medicine]] |
| | [[Category:Hematology]] |
| | [[Category:Immunology]] |