Chapter 35
Drug-Induced Mitochondrial Cardiomyopathy and Cardiovascular Risks in Children
Neha Bansal,
Mariana Gerschenson,
Tracie L. Miller,
Stephen E. Sallan,
Jason Czachor,
Hiedy Razoky,
Ashley Hill,
Miriam Mestre,
Steven E. Lipshultz,
Neha Bansal
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorMariana Gerschenson
John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI, USA
Search for more papers by this authorTracie L. Miller
Miller School of Medicine, University of Miami, Miami, FL, USA
Search for more papers by this authorStephen E. Sallan
Dana Farber Cancer Institute, Department of Pediatric Oncology, Harvard Medical School, Boston, MA, USA
Department of Medicine, Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA, USA
Search for more papers by this authorJason Czachor
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorHiedy Razoky
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorAshley Hill
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorMiriam Mestre
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorSteven E. Lipshultz
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorNeha Bansal,
Mariana Gerschenson,
Tracie L. Miller,
Stephen E. Sallan,
Jason Czachor,
Hiedy Razoky,
Ashley Hill,
Miriam Mestre,
Steven E. Lipshultz,
Neha Bansal
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorMariana Gerschenson
John A. Burns School of Medicine, University of Hawaii at Manoa, Honolulu, HI, USA
Search for more papers by this authorTracie L. Miller
Miller School of Medicine, University of Miami, Miami, FL, USA
Search for more papers by this authorStephen E. Sallan
Dana Farber Cancer Institute, Department of Pediatric Oncology, Harvard Medical School, Boston, MA, USA
Department of Medicine, Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA, USA
Search for more papers by this authorJason Czachor
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorHiedy Razoky
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorAshley Hill
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorMiriam Mestre
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorSteven E. Lipshultz
Wayne State University School of Medicine, Children's Hospital of Michigan, Detroit, MI, USA
Search for more papers by this authorBook Editor(s):Yvonne Will PhD, ATS Fellow,
James A. Dykens,
Yvonne Will PhD, ATS Fellow
Pfizer Drug Safety R&D, Groton, CT, USA
Search for more papers by this authorFirst published: 23 February 2018
Summary
This chapter describes the mechanisms and the short- and long-term consequences of human immunodeficiency virus (HIV) medications and cancer chemotherapies that are associated with mitochondrial dysfunction and its cardiac consequences in children. Adults and children with HIV are living longer because of advances in antiretroviral therapy (ART). Mitochondrial dysfunction secondary to ART is drug and organ specific. This specificity was first described in 1988, in HIV patients treated with high doses of the nucleoside reverse transcriptase inhibitor (NRTI), zidovudine. One of the major successes of pediatric oncology is that children with childhood cancers are living substantially longer and healthier lives because of advances in chemotherapeutic agents. Chemotherapeutic medications are designed to interfere with rapidly dividing neoplastic cells. However, in the process, they can adversely affect normal cell division, especially in tissues with rapid turnover.
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