acute myeloid leukaemia

(redirected from acute myelocytic leukaemia)

acute myeloid leukaemia

A rapidly progressing form of leukaemia characterised by the proliferation of immature WBCs (blasts in peripheral circulation).
 
Epidemiology
Primarily in adults or infants under age 1; 2,000 new cases are diagnosed/year, UK.
 
Clinical findings
Fatigue, weight-loss, fever, weakness, pallor, bone and joint pain, bleeding gums, nosebleeds, bruising, lymphadenopathy.
 
Complications
Bleeding, increased infections.
 
Management
Chemotherapy, bone marrow transplantation.

FAB classification, acute leukaemias
Acute myeloid leukaemia (AML) 
M0—Myeloblasts with minimal differentiation.
M1—Myeloblasts without maturation.
M2—Myeloblasts with maturation (best AML prognosis).
M3—Hypergranular promyelocytic leukaemia (faggot cells).
M3V—Variant, microgranular promyelocytic leukaemia.
M4—Myelomonocytic leukocytes.
M5—Monocytic, subtype: 
  a. Poorly differentiated monocytic leukaemia. 
  b. Well-differentiated monocytic leukaemia.
M6—Erythroleukaemia/DiGuglielmo syndrome.
M7—Megakaryocytic leukaemia—pleomorphic undifferentiated cells with cytoplasmic blebs; myelofibrosis or increased marrow reticulin; positive for platelet peroxidase antifactor VIII. 

WHO classification
AML with recurrent cytogenetic abnormalities.
AML with multi-lineage dysplasia (as a precursor to myelodysplastic syndrome).
AML related to therapy.
AML NOS.

AML variants
AML with recurrent cytogenetic abnormalities.
AML with t(8;21)(q22;q22).
AML with inv(16)(p13q22).
AML with t(15;17)(q22;q12).
AML with 11q23 (MLL) abnormalities.
AML with multilineage dysplasia.
AML (and MDS), therapy-related:
• Alkylating agent related;
• Topoisomerase-II inhibitor related.
AML, not otherwise categorised.

acute myeloid leukaemia

A form of LEUKAEMIA in which the cells present in abnormal numbers are derived from primitive precursors, in the bone marrow, of the white blood cells. The median age of presentation is 70. Genetic defects and age-related factors are thought to be the principal determinants of lack of success of chemotherapy in elderly patients.
References in periodicals archive ?
Unique genetic alterations in combinations or in isolation account for a small fraction of MDS suggesting the epigenetic hypermethylation as a possible leading cause for MDS and its transformation to acute myelocytic leukaemia (AML).
In myelodysplastic transformation to acute myelocytic leukaemia (AML), the neoplastic event occurs at the level of a committed myeloid stem cells in most patients (5-7).
0 RA, refractory anaemia; RARS, refractory anaemia ringed sideroblast; RAEB, refractory anaemia excess blast; RAEB-t, refractory anaemia excess blast in transformation; AML, acute myelocytic leukaemia

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