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[Giant platelet-like cell fragments produced from abnormal promyelocytes in acute myelogenous leukemia]
1Section of Internal Medicine, Kobe Kyodo Hospital.
Abstract:
A 38-year old man was transmitted to our hospital because of his pneumonia and disconsciousness. Laboratory data showed leukocytosis (32,500/microliter), mild anemia, and decreased platelet count (6.7 x 10(4)/microliter). The bone marrow aspiration revealed the presence of 40% blastoid cells and cytogenetic study showed abnormal karyotype, 45, X, -Y, t(8; 21) (q22; q22), indicating acute myeloid leukemia (AML, M2). Furthermore, on the microscopic observation, cell fragments resembling giant platelets were observed which were positive for myeloperoxidase, and several fragments connected with abnormal promyelocytes through thin cytoplasm. These results suggested these cell fragments may be produced from abnormal promyelocytes in this case.
Insights
This case study details a 38-year-old man diagnosed with acute myeloid leukemia (AML M2). The patient presented with pneumonia and altered consciousness, revealing abnormal promyelocytes and giant platelet-like fragments in bone marrow analysis.
Area of Science:
- Hematology
- Oncology
- Cytogenetics
Background:
- A 38-year-old male presented with pneumonia and altered consciousness.
- Initial laboratory findings included leukocytosis, mild anemia, and thrombocytopenia.
Observation:
- Bone marrow aspiration revealed 40% blastoid cells.
- Cytogenetic analysis identified an abnormal karyotype: 45, X, -Y, t(8; 21) (q22; q22).
- Microscopic examination showed myeloperoxidase-positive cell fragments resembling giant platelets, connected to abnormal promyelocytes.
Findings:
- The patient was diagnosed with acute myeloid leukemia (AML, M2).
- The observed cell fragments are suggested to originate from abnormal promyelocytes.
Implications:
- This case highlights a rare presentation of AML M2.
- Understanding the origin of these unique cell fragments may offer insights into leukemic cell differentiation and morphology.