Diagnosis

Laboratory tests and other studies used in the workup for ALL include the following:

Complete blood count with differential

Coagulation studies
Peripheral blood smear
Chemistry profile, including lactic dehydrogenase, uric acid, liver function studies, and
BUN/creatinine
Appropriate cultures (in particular, blood cultures) in patients with fever or other signs of
infection
Chest x-ray
Computed tomography
Multiple-gated acquisition scanning
Electrocardiography
Bone marrow aspiration and biopsy (definitive for confirming leukemia)
Immunohistochemistry
Flow cytometry
Cytogenetics
Polymerase chain reaction
Gene expression profiling

Management
Treatment of ALL may include the following:

Induction chemotherapy (eg, standard 4- or 5-drug regimen, ALL-2, or hyper-CVAD)

Consolidation chemotherapy
Maintenance chemotherapy
Intrathecal chemotherapy for central nervous system (CNS) prophylaxis
Supportive care (eg, blood products, antibiotics, growth factors)

Pathophysiology
The malignant cells of acute lymphoblastic leukemia (ALL) are lymphoid precursor cells (ie,
lymphoblasts) that are arrested in an early stage of development. This arrest is caused by an
abnormal expression of genes, often as a result of chromosomal translocations. The lymphoblasts
replace the normal marrow elements, resulting in a marked decrease in the production of normal
blood cells. Consequently,anemia, thrombocytopenia, and neutropenia occur to varying degrees.
The lymphoblasts also proliferate in organs other than the marrow, particularly the liver, spleen,
and lymph nodes.

Etiology
Less is known about the etiology of acute lymphoblastic leukemia (ALL) in adults compared
with acute myelogenous leukemia (AML). Most adults with ALL have no identifiable risk
factors.

Although most leukemias occurring after exposure to radiation are AML rather than ALL, an
increased prevalence of ALL was noted in survivors of the Hiroshima atomic bomb but not in
those who survived the Nagasaki atomic bomb.

Rare patients have an antecedent hematologic disorder (AHD) such as myelodysplastic

syndrome (MDS) that evolves to ALL. However, most patients with MDS that evolves to acute
leukemia develop AML rather than ALL. Similarly, a small number of patients receiving
lenalidomide as maintenance therapy for multiple myeloma have developed secondary ALL. [ 1]

Increasingly, cases of ALL with abnormalities of chromosome band 11q23 following treatment
with topoisomerase II inhibitors for another malignancy have been described. However, most
patients who develop secondary acute leukemia after chemotherapy for another cancer develop
AML rather than ALL.