Acute myeloid leukemia overview: Difference between revisions
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==Medical Therapy== | ==Medical Therapy== | ||
The mainstay therapy from acute myeloid leukemia is [[chemotherapy]] and usually includes a combination of [[daunorubicin]], [[cytarabine]] and [[etoposide]] or [[mitoxantrone]] and anabolic [[steroids]]. Supportive care includes intravenous | The mainstay therapy from acute myeloid leukemia is [[chemotherapy]] and usually includes a combination of [[daunorubicin]], [[cytarabine]] and [[etoposide]] or [[mitoxantrone]] and anabolic [[steroids]]. Supportive care includes intravenous nutrition, antimicrobial therapy, and replacement of blood products. | ||
==References== | ==References== | ||
Revision as of 13:40, 4 September 2015
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Acute myeloid leukemia Microchapters |
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Acute myeloid leukemia overview On the Web |
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Risk calculators and risk factors for Acute myeloid leukemia overview |
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 myeloid leukemia may be classified according to the French-American-British (FAB) classification and World Health Organization (WHO).
Pathophysiology
Acute myeloid leukemia arises from myeloblasts, which are hematologic white cells that are normally involved in hematopoiesis. Genetic translocations involved in the pathogenesis of acute myeloid leukemia include translocations between chromosome 8 and 21 t(8;21) and translocations between chromosome 15 and 17 t(15;17). Inversions in the chromosomal translocations in chromosome 16 inv(16) are envolved in the pathogenesis of acute myeloid leukemia.
Differentiating Acute lymphoblastic leukemia from other Diseases
Acute myeloid leukemia must be differentiated from other diseases such as acute lymphoblastic leukemia, chronic myeloid leukemia, agranulocytosis, aplastic anemia and lymphoma.
Epidemiology and Demographics
In 2015, the incidence of acute myeloid leukemia was approximately 6.5 per 100,000 individuals with a case-fatality rate of approximately 50% in the United States. The incidence of acute myeloid leukemia increases with age; the median age at diagnosis is 63 years. Males are more commonly affected with acute myeloid leukemia than women. The male to female ratio is approximately 1.3 to 1.
Risk Factors
Common risk factors in the development of acute myeloid leukemia are myelodysplastic or myeloproliferative syndromes, aplastic anemia, myelofibrosis, paroxysmal nocturnal hemoglobinuria, polycythemia vera, chemical exposure and several congenital conditions such as Down syndrome, Bloom syndrome, Fanconi anemia, neurofibromatosis and congenital neutropenia.
Natural History, Complications, and Prognosis
Common complications of acute myeloid leukemia include infections, disseminated intravascular coagulation, pyoderma gangrenosum, hemorrhage and complications due to side effects of chemotherapy. Prognosis of acute myelogenous leukemia depends on cytogenetics. Cytogenetics that indicate a good prognosis include inversions in chromosome 16 inv(16), translocations between chromosome 8 and 21 t(8;21) and translocations between chromosome 15 and 17 t(15;17).
Diagnosis
History and Symptoms
Symptoms of acute myeloid leukemia include fever, fatigue, weight loss and loss of appetite.
Physical Examination
Common physical examination findings of acute myeloid leukemia include anemia, fever, pallor, Leukemia cutis, bruising, petechiae, ecchymosis and tachycardia.
Laboratory Findings
Laboratory findings consistent with the diagnosis of acute myeloid leukemia include leukocytosis, thrombocytopenia, anemia and leucopenia.
Chest X Ray
If a lung infection is suspected chest x-ray may be helpful in the diagnosis of acute myeloid leukemia.
CT
CT scan may be helpful in the diagnosis of acute myeloid leukemia.
Other Diagnostic Studies
Other diagnostic studies for acute myeloid leukemia include cytochemistry, flow cytometry, immunohistochemistry, PCR and biopsy.
Medical Therapy
The mainstay therapy from acute myeloid leukemia is chemotherapy and usually includes a combination of daunorubicin, cytarabine and etoposide or mitoxantrone and anabolic steroids. Supportive care includes intravenous nutrition, antimicrobial therapy, and replacement of blood products.
References
- ↑ Jemal A, Thomas A, Murray T, Thun M. Cancer statistics 2002. CA Cancer J Clin 52:23, 2002. PMID 11814064