{"id":5333,"date":"2021-05-15T23:53:42","date_gmt":"2021-05-15T21:53:42","guid":{"rendered":"https:\/\/meddists.com\/learn\/clinical\/hematology\/hematological-oncology\/acute-myeloid-leukemia-aml\/"},"modified":"2021-05-23T00:50:23","modified_gmt":"2021-05-22T22:50:23","slug":"acute-myeloid-leukemia-aml","status":"publish","type":"page","link":"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/hematology\/oncological-disorders\/acute-leukemias\/acute-myeloid-leukemia-aml\/","title":{"rendered":"Acute myeloid leukemia (AML)"},"content":{"rendered":"<span class=\"block-heading\" id=\"header_1\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Introduction<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_1\">\n\n\n<p class=\"wp-block-paragraph\">In healthy individuals, the number of precursor (-blast) cells in the bone marrow stays at a normal range (since cells maturate and new -blast cells are formed).<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li>In acute leukemias, precursor cells (-blasts) lose the ability to maturate, and these cells start proliferating and pile up in the bone marrow<\/li><li>This may affect hematopoiesis and cause&nbsp;<strong>cytopenia<\/strong>&nbsp;(cell number decrease in the blood) of other cell lineages (<strong>thrombocytopenia<\/strong>,&nbsp;<strong>anemia<\/strong>,&nbsp;<strong>leukopenia<\/strong>)<ul><li>The patient may present with symptoms that fit one of the cytopenia types (bleeding, hypoxia, or infections)<\/li><\/ul><\/li><li>Precursor cells usually reach the circulation<ul><li>They will seem polymorphic: larger, with and a big, pale nucleolus<\/li><li>This may result in an increased count of the specific cell lineage<\/li><\/ul><\/li><li>Acute leukemias have a sudden onset, they can arise on their own or as a progression of chronic leukemia<\/li><li>Progress quickly, but are curable<\/li><li>Mostly affect younger patients.<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_2\">\n<h3 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title1\">Acute myeloid leukemia<\/h3>\n<\/span><span class=\"block-content\" id=\"contents_2\">\n\n\n<p class=\"wp-block-paragraph\">Acute myeloid leukemia (AML) is a clonic proliferation of immature myeloid cells in the bone marrow.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Acute<\/strong> = sudden unsert, of precursor (blast) cells; <strong>myeloid<\/strong> = of the myeloid lineage (CD13, CD33, and MPO positive; TdT negative); <strong>leukemia<\/strong> = cancer of the blood and bone marrow.<\/li><li>Presents within<strong>&nbsp;weeks or months<\/strong>&nbsp;with symptoms related to the cytopenia<ul><li>Fatigue<\/li><li>Fever<\/li><li>Spontaneous bleeding<\/li><li>Opportunistic infections<\/li><\/ul><\/li><li>Appears mostly in adults (65yo), and is the most common acute leukemia<\/li><li>Most cases arise from inherited genetic mutations in 3 groups of genes:<ul><li>Proliferative: FLT3, JAK-2, C-KIT, ABL1<\/li><li>Inhibition of differentiation: RARA, NPM1<\/li><li>Epigenetic modulators: DNMT3A<\/li><\/ul><\/li><li>ASXL1 mutations typically appear in AML secondary to MDS<\/li><li>Features<ul><li><strong>Over 20%&nbsp;<\/strong>of cells in the bone-marrow are myeloblasts (normal is about 5%)<\/li><li>Bone marrow is usually hypercellular<\/li><li>Myeloblasts usually<strong>&nbsp;do not maturate<\/strong><\/li><\/ul><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_3\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Risk factors<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_3\">\n\n\n<ul class=\"wp-block-list\"><li>Trisomy 21 (Down syndrome)<\/li><li>Exposure to benzene, chemotherapy, ionizing radiation<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_4\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Classification<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_4\">\n\n\n<p class=\"wp-block-paragraph\">French-American-British classification with 7 classes (M0-M7) that has been replaced with 6 major groups defined by WHO.<\/p>\n\n\n\n<ul class=\"wp-block-list\"><li><strong>Class I \u2014 AML with recurrent genetic abnormalities<\/strong><ul><li>Include specific chromosomal translocations or gene mutations.<\/li><li>For example, t(15;17) in <strong>acute promyelocytic leukemia<\/strong>, in which RA receptors are disrupted, promyelocytes accumulate with a high number of Auer rods (risk for DIC); prophylaxis involves ATRA to help promyelocytes to maturate.<\/li><li>Good prognosis<\/li><\/ul><\/li><li><strong>Class II \u2014 AML with myelodysplasia-related changes<\/strong><ul><li>At least 50% of cells in two lineages show dysplasia<\/li><li>Worse prognosis than class I<\/li><\/ul><\/li><li><strong>Class III \u2014 Therapy-relayed AML (tAML)<\/strong><ul><li>Associated with chemotherapy (etoposide and alkylating agents)<\/li><li>MLL gene mutations<\/li><li>Poor prognosis<\/li><\/ul><\/li><li><strong>Class IV \u2014 Non-specific<\/strong><ul><li>No specific cytogenetic abnormalities.<\/li><\/ul><\/li><li><strong>Class V \u2014 Myeloid sarcoma<\/strong><ul><li>Rare, resembling a solid tumor composed of myeloid blast cells.<\/li><\/ul><\/li><li><strong>Class VI \u2014 Myeloid proliferation related to Down syndrome<\/strong><\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_5\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Clinical manifestation<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_5\">\n\n\n<ul class=\"wp-block-list\"><li>Thrombocytopenia, anemia, and sometimes neutropenia result in bleeding, anemia, and infections<\/li><li>DIC in acute promyelocytic leukemia<\/li><li>Gum hypertrophy due to leukemic infiltration<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_6\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Diagnosis<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_6\">\n\n\n<ul class=\"wp-block-list\"><li>Blood count (showing anemia and thrombocytopenia with increased white cell count)<\/li><li>Blood smear (showing blast cells)<\/li><li>Bone marrow sampling (hypercellular with many blast cells) with immunohistological staining<\/li><li>Flow cytometry (identifying the blast cells)<\/li><li>Cytogenic analysis (karyotyping, FISH)<\/li><li>Molecular genetic analysis (to detect FLT3, NPM1)<\/li><\/ul>\n\n\n<\/span><span class=\"block-heading\" id=\"header_7\">\n<h4 class=\"wp-block-heading\" class=\"wp-block-heading\" class=\"title_collection title2\">Treatment<\/h4>\n<\/span><span class=\"block-content\" id=\"contents_7\">\n\n\n<ul class=\"wp-block-list\"><li>Supportive treatment<ul><li>Insertion of a venous cannula<\/li><li>Administration of blood products<\/li><li>Prevention of tumor lysis syndrome (elevated potassium, phosphate, and uric acid) using allopurinol, fluids, diuretics<\/li><\/ul><\/li><li>Treatment protocol<ul><li>Induction: Cytarabine + anthracyclin<ul><li>This is sometimes called a\u00a0<strong>7 + 3 regimen<\/strong>, because it consists of getting cytarabine continuously for 7 days, along with short infusions of an anthracycline on each of the first 3 days.<\/li><li>In FLT3 mutations, <strong>midostaurin\u00a0<\/strong>can be added.<\/li><li>Anti-CD33 mAbs: <strong>gemtuzumab ozogamicin<\/strong><\/li><\/ul><\/li><\/ul><ul><li>Postinduction (consolidation): Several cycles of high-dose cytarabine (HD-ara-C); in young patients, stem cell transplantation<\/li><\/ul><\/li><li>Treatment protocol for acute promyelocytic leukemia<ul><li>Induction: ATRA + anthracyclin or arsenic trioxide<\/li><li>Posinduction: Anthracyclin + intermittent ATRA<\/li><li>Maintenance: thioguanine + methotrexate + ATRA<\/li><li><strong>ATRA syndrome <\/strong>can occur after the differentiation of the promyelocytes.<\/li><\/ul><\/li><li>&lt;5% blast cells without Auer rods = complete remission; the majority of patients will relapse<\/li><\/ul>\n<\/span><div id=\"the_titles\" style=\"display:none;\"><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Introduction<\/h3><h3 class=\"wp-block-heading\" class=\"wp-block-heading\">Acute myeloid leukemia<\/h3><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Risk factors<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Classification<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Clinical manifestation<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Diagnosis<\/h4><h4 class=\"wp-block-heading\" class=\"wp-block-heading\">Treatment<\/h4><\/div>","protected":false},"excerpt":{"rendered":"<p>Introduction In healthy individuals, the number of precursor (-blast) cells in the bone marrow stays at a normal range (since cells maturate and new -blast cells are formed). In acute leukemias, precursor cells (-blasts) lose the ability to maturate, and these cells start proliferating and pile up in the bone marrow This may affect hematopoiesis [&hellip;]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":5472,"menu_order":0,"comment_status":"closed","ping_status":"closed","template":"","meta":{"footnotes":""},"class_list":["post-5333","page","type-page","status-publish","hentry"],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v27.9 - https:\/\/yoast.com\/product\/yoast-seo-wordpress\/ -->\n<title>Acute myeloid leukemia (AML) &#8211; Meddists<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/meddists.com\/learn\/clinical\/internal-medicine\/hematology\/oncological-disorders\/acute-leukemias\/acute-myeloid-leukemia-aml\/\" \/>\n<meta name=\"twitter:label1\" content=\"Est. reading time\" \/>\n\t<meta name=\"twitter:data1\" content=\"3 minutes\" \/>\n<script type=\"application\/ld+json\" class=\"yoast-schema-graph\">{\"@context\":\"https:\\\/\\\/schema.org\",\"@graph\":[{\"@type\":\"WebPage\",\"@id\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/hematology\\\/oncological-disorders\\\/acute-leukemias\\\/acute-myeloid-leukemia-aml\\\/\",\"url\":\"https:\\\/\\\/meddists.com\\\/learn\\\/clinical\\\/internal-medicine\\\/hematology\\\/oncological-disorders\\\/acute-leukemias\\\/acute-myeloid-leukemia-aml\\\/\",\"name\":\"Acute myeloid leukemia (AML) &#8211; 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