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Pediatric Acute Lymphoblastic Leukemia Medication

  • Author: Vikramjit S Kanwar, MBBS, MBA, MRCP(UK), FAAP; Chief Editor: Jennifer Reikes Willert, MD  more...
 
Updated: Dec 04, 2014
 

Medication Summary

Drugs commonly used during remission induction therapy include dexamethasone or prednisone, vincristine, asparaginase, and daunorubicin. Consolidation therapy often includes methotrexate (MTX) and 6-mercaptopurine (6-MP) or cyclophosphamide and cytarabine. Drugs used for intensification include cytarabine, cyclophosphamide, etoposide, dexamethasone, asparaginase, doxorubicin, MTX, 6-MP, and vincristine. Continuation therapy is based on oral 6-MP and MTX with pulses of vincristine and glucocorticoid (prednisone or dexamethasone). Intrathecal chemotherapy includes primarily MTX, which may also be combined with hydrocortisone and cytarabine (“triple-intrathecal therapy”). Imatinib is also approved for children newly diagnosed with Ph+ ALL.[35, 14]

It is important to note that corticosteroids can adversely suppress the function of the hypothalamic-pituitary-adrenal (HPA) axis and such suppression can have adverse effects on a patient's ability to respond to different stresses, such as severe infection. A Cochrane Database review of 7 studies showed adrenal insufficiency occurred in nearly all ALL patients in the first days after cessation of glucocorticoid therapy. Although the majority of patients recovered within a few weeks, a small number of patients had adrenal insufficiency lasting up to 34 weeks.[35]

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Antineoplastic Agents

Class Summary

Cancer chemotherapy is based on an understanding of tumor cell growth and how drugs affect this growth. After cells divide, they enter a period of growth (ie, phase G1), followed by DNA synthesis (ie, phase S). The next phase is a premitotic phase (ie, G2), then finally a mitotic cell division (ie, phase M).

Cell-division rates vary for different tumors. Most common cancers grow slowly compared with normal tissues, and the rate may be decreased in large tumors. This difference allows normal cells to recover from chemotherapy more quickly than malignant ones and is the rationale behind current cyclic dosage schedules.

Antineoplastic agents interfere with cell reproduction. Some agents act at specific phases of the cell cycle, whereas others (ie, alkylating agents, anthracyclines, cisplatin) are not phase-specific. Cellular apoptosis (ie, programmed cell death) is another potential mechanism of many antineoplastic agents.

Vincristine (Vincasar PFS)

 

Vincristine is a chemotherapeutic agent derived from the periwinkle plant. This agent acts by inhibiting microtubule formation in mitotic spindles, causing metaphase arrest.

Asparaginase (Elspar)

 

Extracts of Escherichia coli or Erwinia L-asparaginase impair asparagine synthesis. Asparaginase is lethal to lymphoblasts that cannot synthesize the essential amino acid asparagine.

Asparaginase Erwinia chrysanthemi (Erwinaze)

 

Catalyzes deamidation of asparagine to aspartic acid and ammonia, thereby reducing circulating levels of asparagine. Lack of asparagine synthetase activity results in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine. Indicated as part of a multiagent chemotherapeutic regimen for patients with acute lymphoblastic leukemia (ALL) who have developed hypersensitivity to E coli –derived asparaginase. It is estimated that 15-20% of patients with ALL develop a hypersensitivity to E coli –derived asparaginase, which extrapolates to approximately 450-600 children in the United States annually.

Daunorubicin (Cerubidine)

 

Daunorubicin is an anthracycline that intercalates with DNA and interferes with DNA synthesis.

Methotrexate (Trexall)

 

Methotrexate is a folate analogue that competitively inhibits dihydrofolate reductase, thus inhibiting DNA, RNA, and protein synthesis.

Mercaptopurine (Purinethol)

 

Mercaptopurine is a synthetic purine analogue that kills cells by incorporating into DNA as a false base.

Cytarabine

 

Cytarabine is a synthetic analogue of nucleoside deoxycytidine. This agent undergoes phosphorylation to arabinofuranosyl-cytarabine-triphosphate (ara-CTP), a competitive inhibitor of DNA polymerase.

Etoposide (Toposar)

 

Etoposide inhibits topoisomerase II and breaks DNA strands, causing cell proliferation to arrest in the late S or early G2 portion of the cell cycle.

Cyclophosphamide

 

Cyclophosphamide is chemically related to the nitrogen mustards. When this drug is used as an alkylating agent, the mechanism of action of its active metabolites may involve cross-linking of DNA, which may interfere with the growth of normal and neoplastic cells.

Nelarabine (Arranon)

 

Nelarabine is a prodrug of 9-beta-D-arabinofuranosylguanine (ara-G). This agent is converted to the active arabinofuranosyl-guanine-5'-triphosphate (ara-GTP), a T-cell–selective nucleoside analogue. Leukemic blast cells accumulate ara-GTP, which allows for incorporation into DNA, leading to inhibition of DNA synthesis and cell death.

Nelarabine was approved by the US Food and Drug Administration [FDA] as an orphan drug to treat T-cell lymphoblastic lymphoma (a type of non-Hodgkin lymphoma [NHL]) that does not respond or that relapses with at least 2 chemotherapy regimens.

Clofarabine (Clolar)

 

Clofarabine is a purine nucleoside antimetabolite that inhibits DNA synthesis and is indicated for relapsed or refractory acute lymphoblastic leukemia in pediatric patients. Pools of cellular deoxynucleotide triphosphate are decreased by inhibiting ribonucleotide reductase and terminating DNA chain elongation and repair. This agent also disrupts mitochondrial membrane integrity.

Imatinib (Gleevec)

 

Imatinib is a selective BCR-ABL tyrosine kinase inhibitor. It is approved for children newly diagnosed with Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL).

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Corticosteroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body’s immune response to diverse stimuli. These agents are significantly toxic to lymphoblasts, and two thirds of patients with pediatric ALL who receive steroid therapy alone go into remission.

Prednisone

 

Prednisone is a corticosteroid and an important chemotherapeutic agent in the treatment of acute lymphoblastic leukemia (ALL). This agent is used in induction therapy and is also given as intermittent pulses during continuation therapy.

Dexamethasone (Baycadron, Maxidex, Ozurdex)

 

Dexamethasone is another corticosteroid that acts as an important chemotherapeutic agent in the treatment of ALL. Like prednisone, this agent is used in induction and reinduction therapy and is also given as intermittent pulses during continuation therapy.

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Antimicrobials

Class Summary

Prophylactic antimicrobial drugs are given to prevent infection in patients receiving chemotherapy.

Sulfamethoxazole and trimethoprim (Septra, Bactrim)

 

Sulfamethoxazole and trimethoprim inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. All immunocompromised patients can be given cotrimoxazole to prevent Pneumocystis carinii pneumonia (PCP).

Pentamidine

 

Immunocompromised patients who do not tolerate cotrimoxazole due to myelosuppression may receive IV pentamidine to prevent Pneumocystis carinii pneumonia (PCP).

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Antifungals

Class Summary

These agents may change the permeability of the fungal cell, resulting in a fungicidal effect.

Fluconazole

 

Fluconazole may be used in patients at high risk (eg, infant ALL) to prevent fungal infections. It is a synthetic triazole that inhibits fungal cell growth by inhibiting CYP-dependent synthesis of ergosterol, a vital component of fungal cell membranes.

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Contributor Information and Disclosures
Author

Vikramjit S Kanwar, MBBS, MBA, MRCP(UK), FAAP Professor of Pediatrics, Albany Medical College; Chief, Division of Pediatric Hematology-Oncology, John and Anna Landis Endowed Chair for Pediatric Hematology-Oncology, Medical Director, Melodies Center for Childhood Cancer and Blood Disorders, Albany Medical Center

Vikramjit S Kanwar, MBBS, MBA, MRCP(UK), FAAP is a member of the following medical societies: American Academy of Pediatrics, American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, International Society of Pediatric Oncology

Disclosure: Nothing to disclose.

Coauthor(s)

Noriko Satake, MD Assistant Professor, Department of Pediatric Hematology/Oncology, University of California, Davis, School of Medicine, UC Davis Medical Center

Disclosure: Nothing to disclose.

Janet M Yoon, MD Assistant Clinical Professor, Department of Pediatric Hematology/Oncology, University of California, Davis, School of Medicine, UC Davis Medical Center

Janet M Yoon, MD is a member of the following medical societies: American Society of Pediatric Hematology/Oncology, Children's Oncology Group

Disclosure: Nothing to disclose.

Chief Editor

Jennifer Reikes Willert, MD Associate Clinical Professor, Department of Pediatrics, Division of Pediatric Hematology/Oncology, Section of Stem Cell Transplantation, Stanford University Medical Center, Lucile Packard Children's Hospital

Jennifer Reikes Willert, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Hematology, American Society for Blood and Marrow Transplantation, Children's Oncology Group, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.

Acknowledgements

Timothy P Cripe, MD, PhD Professor of Pediatrics, Division of Hematology/Oncology, Cincinnati Children's Hospital Medical Center; Clinical Director, Musculoskeletal Tumor Program, Co-Medical Director, Office for Clinical and Translational Research, Cincinnati Children's Hospital Medical Center; Director of Pilot and Collaborative Clinical and Translational Studies Core, Center for Clinical and Translational Science and Training, University of Cincinnati College of Medicine

Timothy P Cripe, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American Pediatric Society, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Stephan A Grupp, MD, PhD Director, Stem Cell Biology Program, Department of Pediatrics, Division of Oncology, Children's Hospital of Philadelphia; Associate Professor of Pediatrics, University of Pennsylvania School of Medicine

Stephan A Grupp, MD, PhD is a member of the following medical societies: American Association for Cancer Research, American Society for Blood and Marrow Transplantation, American Society of Hematology, American Society of Pediatric Hematology/Oncology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Bone marrow aspirate from a child with B-precursor acute lymphoblastic leukemia. The marrow is replaced primarily with small, immature lymphoblasts that show open chromatin, scant cytoplasm, and a high nuclear-cytoplasmic ratio.
Bone marrow aspirate from a child with T-cell acute lymphoblastic leukemia. The marrow is replaced with lymphoblasts of various sizes. No myeloid or erythroid precursors are seen. Megakaryocytes are absent.
Bone marrow aspirate from a child with B-cell acute lymphoblastic leukemia. The lymphoblasts are large and have basophilic cytoplasm with prominent vacuoles.
 
 
 
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