Evolution to acute myeloblastic leukemia from chronic neutrophilic leukemia with dysplastic features in granulocytic lineage.
We experienced the case of an 82-year-old man with chronic neutrophilic leukemia (CNL) with dysplastic features in the granulocytic lineage which subsequently progressed to acute myeloblastic leukemia (AML) with myelofibrosis. The patient had hepatosplenomegaly, but there was no evident cause of neutrophilic leukocytosis. The cytogenetic study showed that he had a normal karyotype. Concentrations of the serum granulocyte colony-stimulating factor (G-CSF) were not detectable. Two years after the diagnosis of CNL, blastic transformation to AML occurred with myelofibrosis and significant morphological abnormalities in neutrophils. The blasts were positive for myeloperoxidase, CD33, CD34, and HLA-DR, and the presence of dysplasia within the granulocytic lineage suggested that he had an abnormality at the level of the granulocyte-committed progenitors. Heterogeneous origins of CNL might lead to various clinicopathological features in each case.
Third Department of Internal Medicine, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo, 060-8648, Japan. shuota@med.hokudai.ac.jp
S
S
Ota
J
J
Tanaka
S
S
Kobayashi
Y
Y
Tsuda
A
A
Mori
S
S
Noto
Y
Y
Yamamoto
S
S
Hashino
M
M
Musashi
M
M
Imamura
M
M
Asaka
D000368:Aged; D000369:Aged, 80 and over; D019070:Cell Lineage; D006098:Granulocytes / Q000473:pathology*; D006801:Humans; D016130:Immunophenotyping; D015470:Leukemia, Myeloid, Acute / Q000150:complications / Q000209:etiology / Q000473:pathology*; D015467:Leukemia, Neutrophilic, Chronic / Q000473:pathology*; D008213:Lymphocyte Activation; D008297:Male; D055728:Primary Myelofibrosis / Q000209:etiology