CD19-positive acute myeloblastic leukemia developed 12 years after the onset of hypereosinophilic syndrome

• HANDA Tomoyuki

  Department of Hematology, Dokkyo University School of Medicine

• YAMAMOTO Katsuya

  Department of Hematology, Dokkyo University School of Medicine

• TADOKORO Jiro

  Department of Hematology, Dokkyo University School of Medicine

• KIKKAWA Yasuko

  Department of Hematology, Dokkyo University School of Medicine

• TSURUMI Shigeharu

  Department of Hematology, Dokkyo University School of Medicine

• NAKAMURA Yuichi

  Department of Hematology, Dokkyo University School of Medicine

• SAITO Kenji

  Department of Hematology, Dokkyo University School of Medicine

• UZUKA Yoshiro

  Sendai Blood Disease Center

• SAITO Yoshiko

  Third Department of Internal Medicine, Tohoku University School of Medicine

• FURUSAWA Shinpei

  Department of Hematology, Dokkyo University School of Medicine

Bibliographic Information

Other Title

• Hypereosinophilic syndromeの診断から12年後に発症したCD19陽性acute myeloblastic leukemia
• 症例 Hypereosinophilic syndromeの診断から12年後に発症したCDI9陽性acute myeloblastic leukemia
• ショウレイ Hypereosinophilic syndrome ノ シンダン カラ 12ネンゴ ニ ハッショウ シタ CDI9 ヨウセイ acute myeloblastic leukemia

Abstract

We report a rare case of hypereosinophilic syndrome (HES) that developed to acute myeloblastic leukemia (AML). The patient, a 34-year-old man, presented with eosinophilia of unknown origin (white blood cells 38,200/μl with 74% eosinophils) and pericardial effusion, and was diagnosed as having HES with a normal karyotype. He received four cycles of combination chemotherapy including cyclophosphamide, cytosine arabinoside and vindesine, and thereafter remained in remission. After 12 years, he was referred to our hospital because of fever and malaise. On admission, CBC showed white blood cells 3,000/μl with 70% myeloblasts and 3% eosinophils. The bone marrow was hypercellular with 95% blasts, which were negative for myeloperoxidase (MPO) staining. Immunophenotype analysis revealed that the cells were positive for CD13, CD19, CD34, HLA-DR and cytoplasmic MPO. CD19-positive AML was diagnosed. Cytogenetic analysis showed 46, XY, t(6;21)(q13;q22), add(7)(q11) in 19 of 20 metaphase spreads. Rearrangement of the AML1 gene at 21q22 and fusion of the BCR/ABL gene could not be detected by fluorescence in situ hybridization analysis. The patient received combination chemotherapy and achieved a complete remission. Chromosome aberrations involving 7q as well as 21q22 suggested that the initial chemotherapy for HES might have been implicated in the pathogenesis of acute leukemia in this case.

Journal

• Rinsho Ketsueki

  Rinsho Ketsueki 41 (9), 723-728, 2000

  The Japanese Society of Hematology

Keywords

• Hypereosinophilic syndrome
• Acute myeloblastic leukemia
• AML1 gene
• t(6;21)(q13;q22)

Details

• CRID: 1390282680009194112
• NII Article ID: 10008038210
• NII Book ID: AN00252940
• DOI: 10.11406/rinketsu.41.723
• COI: 1:STN:280:DC%2BD3crhtlOisA%3D%3D
• ISSN: 18820824
• ISSN: 04851439
• NDL BIB ID: 6295471
• PubMed: 11070933
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I6295471
• Web Site: https://search.jamas.or.jp/link/ui/2001101632
• Text Lang: ja
• Data Source:
  • JaLC
  • NDL
  • PubMed
  • CiNii Articles
• Abstract License Flag: Disallowed