[Chemotherapy for a child with relapsed acute myeloid leukemia complicated with persistent hepatitis C virus infection]

Rinsho Ketsueki. 2017;58(6):619-623. doi: 10.11406/rinketsu.58.619.
[Article in Japanese]

Abstract

An 8-year-old Mongolian female was diagnosed with acute myeloid leukemia (AML) and treated at a hospital in Mongolia according to the BFM-AML2004 SR protocol. Although complete remission (CR) was achieved, chemotherapy was interrupted because of shortage of drugs. The patient moved to Japan 7 months after diagnosis. Screening for viral infection revealed the presence of hepatitis C virus (HCV) antibody and RNA. At 11 months after initial diagnosis, the patient experienced bone marrow relapse and a RUNX1-RUNX1T1 fusion transcript was detected. Considering the inadequate intensity of initial treatment and the persistent HCV infection, chemotherapy was preferred and initiated over hematopoietic cell transplantation. After the first course of induction therapy, a second CR was confirmed and the chimeric transcript disappeared. The viral load mildly increased during myelosuppression and transient elevation of liver enzymes was observed along with hematological recovery. HCV infection remained stable, without progression to reactivation of hepatitis C. Given the high risk of second relapse and liver fibrosis and sclerosis following chronic HCV infection, treatment against HCV may be indicated during second remission.

Keywords: Acute myeloid leukemia; Chemotherapy; Hepatitis C; Transfusion.

Publication types

  • Case Reports

MeSH terms

  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Child
  • Core Binding Factor Alpha 2 Subunit / genetics
  • Female
  • Hepatitis C / complications*
  • Humans
  • Leukemia, Myeloid, Acute / complications*
  • Leukemia, Myeloid, Acute / drug therapy*
  • Leukemia, Myeloid, Acute / genetics
  • Oncogene Proteins, Fusion / genetics
  • RUNX1 Translocation Partner 1 Protein
  • Recurrence
  • Remission Induction

Substances

  • AML1-ETO fusion protein, human
  • Core Binding Factor Alpha 2 Subunit
  • Oncogene Proteins, Fusion
  • RUNX1 Translocation Partner 1 Protein