Acute myeloid leukemia overview
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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]
Overview
Acute myeloid leukemia (AML), also known as acute myelogenous leukemia, is a cancer of the myeloid line of white blood cells, characterized by the rapid proliferation of abnormal cells which accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults, and its incidence increases with age. Although AML is a relatively rare disease, accounting for approximately 1.2% of cancer deaths in the United States,[1] its incidence is expected to increase as the population ages.
The symptoms of AML are caused by replacement of normal bone marrow with leukemic cells, resulting in a drop in red blood cells, platelets, and normal white blood cells. These symptoms include fatigue, shortness of breath, easy bruising and bleeding, and increased risk of infection. Although several risk factors for AML have been identified, the specific cause of AML remains unclear. As an acute leukemia, AML progresses rapidly and is typically fatal within weeks or months if left untreated.
Acute myeloid leukemia is a potentially curable disease; but only a minority of patients are cured with current therapy. AML is treated initially with chemotherapy aimed at inducing a remission; some patients may go on to receive a hematopoietic stem cell transplant.
Areas of active research in acute myeloid leukemia include further elucidation of the cause of AML, identification of better prognostic indicators, development of new methods of detecting residual disease after treatment, and the development of new drugs and targeted therapies.
Historical Perspective
Leukemia was first described in 1827 by a french physician named Alfred-Armand-Louis-Marie Velpeau. In 1900 the myeloblast was first identified in the pathogenesis of acute myeloid leukemia.
Classification
Acute lymphoblastic leukemia may be classified according to the French-American-British (FAB) classification and World Health Organization (WHO). The French-American-British (FAB) classification is divided into 3 groups: ALL-L1: small uniform cells, ALL-L2: large varied cells, ALL-L3: large varied cells with vacuoles (bubble-like features). World Health Organization (WHO) classification is divided into 3 groups: B lymphoblastic leukemia/lymphoma, B lymphoblastic leukemia/lymphoma (Not organ specific), B lymphoblastic leukemia/lymphoma with recurrent genetic abnormalities.
Pathophysiology
Generally cancer is caused by damage to DNA that leads to uncontrolled cellular growth causing the development of acute lymphoblastic leukemia. Genetic mutations involved in the pathogenesis of acute lymphoblastic leukemia are related with chromosomal translocations. Genes involved in the pathogenesis of acute limphoblastic leukemia include t(9;22)(q34;q11.2) BCR-ABL1, t(v;11q23);, t(12;21)(p13;q22) TEL-AML1, t(5;14)(q31;q32)IL3-IGH and t(1;19)(q23;p13.3) TCF3-PBX1.
Differentiating Acute lymphoblastic leukemia from other Diseases
Acute lymphoblastic leukemia must be differentiated from other diseases such as acute myelogenous leukemia, hairy cell leukemia and malignant lymphoma.
Epidemiology and Demographics
In 2011, the incidence of acute lymphocytic leukemia was estimated to be 1.77 cases per 100,000 individuals and the prevalence of 17.4 per 100,000 individuals in the United States. In 2015 according with the National cancer institute the incidence of acute lymphocytic leukemia is 1.9 per 100,000 individuals and the case fatality rate of 2.3 per 100,000 individuals in the United States. Males are more commonly affected with acute lymphoblastic leukemia than females.
Risk Factors
Common risk factors in the development of acute lymphoblastic leukemia are down syndrome, ataxia telangiectasia, bloom syndrome, X-linked agammaglobulinemia, fanconi's anemia and severe combined immunodeficiency.
Screening
According to the National cancer institute screening for acute lymphoblastic leukemia is not recommended.
Natural History, Complications, and Prognosis
Prognosis has improved from a 0% to 20-75% survival rate largely due to the continuous development of clinical trials and improvements in bone marrow transplantation (BMT) and stem cell transplantation (SCT) technology. The prognosis for acute Lymphoblastic leukemia differs between individuals depending on a wide variety of factors such as gender, ethnicity, age, blood cell count, dissemination and genetic involvement.
Diagnosis
History and Symptoms
Symptoms of acute lymphoblastic leukemia include generalised weakness and fatigue, frequent or unexplained fever and infections, weight loss and/or loss of appetite, excessive bruising, bleeding from wounds, nosebleeds, petechiae, bone pain, joint pains and dyspnea.
Physical Examination
Common physical examination findings of acute lymphoblastic leukemia include lymphadenopathy, hepatomegaly, stridor, splenomegaly, pallor, petechiae, bruising, papilledema, nuchar rigidity, craneal nerve palsy and in males testicular enlargement.
Laboratory Findings
Laboratory findings consistent with the diagnosis of acute lymphoblastic leukemia include eosinophilia, lymphocytosis, red cell production reduced, thrombocytopenia. Chemistry panels with altered levels of uric acid, creatinine, blood urea nitrogen, potassium, phosphate, calcium, bilirubin, hepatic transaminases and ferritin. A spinal tap will tell if the spinal column and brain has been invaded.
Chest X Ray
On Chest x ray acute lymphoblastic leukemia is characterized by swollen lymph nodes.
X Ray
On x ray, acute lymphoblastic leukemia is characterized by periosteal reaction.
CT
Acute lymphoblastic leukemia CT scanning findings can show invasion of other organs commonly the lung, liver, spleen, lymph nodes, brain, kidneys and reproductive organs.
Other Diagnostic Studies
Other diagnostic studies about acute lymphoblastic leukemia can be made made by cytogenetics, Bone marrow biopsy, flow cytometry, RT-PCR and FISH.
Medical Therapy
Chemotherapy is indicated for acute lymphocytic leukemia and can be divided in several phases: Induction chemotherapy, consolidation therapy, CNS prophylaxis and maintenance treatments with chemotherapeutic drugs such as prednisone plus vincristine plus cyclophosphamide plus doxorubicin or methotrexate plus 6-MP. Radiation therapy is used on painful bony areas in severe disease or as part of the preparations for a bone marrow transplant (total body irradiation).
References
- ↑ Jemal A, Thomas A, Murray T, Thun M. Cancer statistics 2002. CA Cancer J Clin 52:23, 2002. PMID 11814064