Medication Summary
The chemotherapeutic regimen chosen depends on the subtype of leukemia. B-cell leukemia can be treated with rituximab containing chemotherapy regimen. An extensive discussion of specific chemotherapeutic protocols can be found in Medscape Drugs & Diseases articles on the individual type of leukemia. The listing below includes some of the common chemotherapeutic drugs used to treat acute leukemia.
Antineoplastic agents
Class Summary
These agents inhibit cell proliferation.
Daunorubicin hydrochloride (Cerubidine)
Daunorubicin hydrochloride inhibits DNA and RNA synthesis by intercalating between DNA base pairs. Daunorubicin is rapidly and widely distributed in the tissues (distribution half-life is 2 min) following IV infusion. It is metabolized extensively by the liver.
Idarubicin hydrochloride (Idamycin)
Idarubicin inhibits cell proliferation by inhibiting DNA and RNA polymerase.
Cytarabine (Cytosar-U)
Cytarabine is converted intracellularly to active compound cytarabine-5'-triphosphate, which inhibits DNA polymerase.
Tretinoin (Vesanoid)
Tretinoin is an all-trans -retinoic acid derived from naturally occurring all-trans -retinol (vitamin A-1). Oral tretinoin is more than 95% bound to plasma proteins and is metabolized by cytochrome P450 enzymes in liver.
Arsenic trioxide (Trisenox)
Arsenic trioxide is used to treat patients with APL whose conditions have relapsed or are refractory to retinoid or anthracycline chemotherapy. It may cause DNA fragmentation and damage or degrade fusion protein PML-RAR alpha in APL.
Etoposide (VePesid, Toposar)
Etoposide is administered as combination salvage chemotherapy in patients with relapsed AML. It inhibits topoisomerase II and causes DNA strand breakage, causing cell proliferation to arrest in the late S or early G2 portion of the cell cycle.
Methotrexate (Folex PFS, Rheumatrex)
Methotrexate is an antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction in malignant cells. It is administered as combination salvage therapy for relapse.
Growth factors
Class Summary
These agents are indicated in patients receiving chemotherapy with signs of infection and neutropenia.
Sargramostim (Leukine)
Sargramostim is a GM-CSF that stimulates division and maturation of earlier myeloid and macrophage precursor cells.
Uricosuric agents
Class Summary
These agents increase the renal clearance of uric acid by inhibiting the renal tubular reabsorption of uric acid.
Allopurinol (Zyloprim)
Allopurinol inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. It reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines.
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Involvement of the face in a patient with acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.
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Red-brown papules can be seen in leukemia cutis. They are confluent in this patient. Courtesy of Nevena Damjanov, MD, and Elizabeth Prechtel.
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Papules and nodules on the face of an African American patient with acute myelogenous leukemia (AML). Courtesy of Mona Mofid, MD.
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A patient with typical plum-colored lesions seen in leukemia cutis. This patient had acute myelogenous leukemia. Courtesy of Grant Anhalt, MD.
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This photograph shows linear areas, which are more violaceous in color, likely due to trauma to the area, such as excoriation, which results in hemorrhage into the skin. Frequent hemorrhage into the skin can make any inflammatory skin lesion appear more violaceous in patients with leukemia. Courtesy of Nevena Damjanov, MD, and Elizabeth Prechtel.
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Low-power view of leukemia cutis acute myeloblastic leukemia (AML-M1). Note the perivascular and periadnexal infiltrate with relative epidermal sparing. Courtesy of Kim Hiatt, MD.
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This is a higher power view of leukemia cutis acute myeloblastic leukemia (AML-M1). This photo illustrates a perivascular infiltrate of leukemic cells. The nuclei are round to oval with little cytoplasm. Courtesy of Kim Hiatt, MD.
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Leukemia cutis of acute monocytic leukemia. Perivascular and periadnexal infiltration is also present, but the cell morphology is distinct. Many of the nuclei are folded or indented. The cytoplasm of the leukemic cells is gray-blue and more abundant than in the M1 subtype. Courtesy of Kim Hiatt, MD.
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Low-power view of acute promyelocytic leukemia cutis with a perivascular and periadnexal but also interstitial infiltrate, with epidermal sparing but significant upper dermal edema, which could be confused with Sweet syndrome at a low-power view. Courtesy of Kim Hiatt, MD.
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Acute promyelocytic leukemia cutis at high power. The round-to-indented nuclei with prominent cytoplasmic granules are evident. Courtesy of Kim Hiatt, MD.
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Photo illustrates leukocyte esterase staining of the cytoplasm of the leukemic cells in acute promyelocytic leukemia. Courtesy of Kim Hiatt, MD.
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Leukemia cutis at low power demonstrating a Grenz zone and intercalation of leukemic cells between collagen bundles. Courtesy of Keliegh Culpepper, MD.
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Infiltration of leukemic cells between collagen bundles.
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Infiltration of dermoepidermal junction by clonal T cells in Sézary syndrome.
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Diffuse macules and papules on the scalp of a patient with chronic myelogenous leukemia.
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Gingival infiltration in a patient with acute myelogenous leukemia.
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Diffuse truncal eruption of infiltrated papules and plaques in chronic lymphocytic leukemia.
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Close-up photo of diffuse truncal eruption of infiltrated papules and plaques in chronic lymphocytic leukemia.