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Role of autoimmune hemolytic anemia as an initial indicator for chronic myeloid leukemia: A case report
Xiang Li1, Sisi Cai1, Zhaodong Zhong1
1Institution of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan.
Insights
Autoimmune hemolytic anemia may precede chronic myeloid leukemia progression. Splenectomy and tyrosine kinase inhibitors may increase infection risk, leading to poor outcomes in CML patients with chromosomal abnormalities.
Area of Science:
- Hematology
- Oncology
- Genetics
Background:
- A patient with chronic myeloid leukemia (CML) in the chronic phase was diagnosed with autoimmune hemolytic anemia (AIHA) one year prior.
- The study aimed to investigate if AIHA represented a progression of CML and identify factors contributing to a poor prognosis despite achieving molecular complete remission (MCR).
Observation:
- The patient with AIHA underwent splenectomy due to poor response to immune inhibitors, with spleen biopsy revealing reactive hyperplasia.
- Diagnosis of CML was confirmed by BCR-ABL (P210) gene over-expression in bone marrow.
- Despite MCR, the patient exhibited persistently high peripheral white blood cell counts post-splenectomy.
Findings:
- Spleen biopsy confirmed 22q11/9q34 translocation; no BCR-ABL kinase domain mutations, WT1, or EVI1 gene expression were detected.
- Bone marrow gene array analysis revealed chromosomal abnormalities: gain (14q32.33), and uniparental disomy (UPD) of Xp11.22-p11.1 and Xp11.1-q13.1.
- The patient died from severe infection two years after CML diagnosis.
Implications:
- AIHA may represent an early clinical manifestation of CML progression.
- Splenectomy and prolonged tyrosine kinase inhibitor therapy might have increased susceptibility to infection, contributing to the fatal outcome.
- The gain of chromosome 14q32.33 is a potential factor associated with the patient's poor prognosis in CML.
Introduction:
We report here the case of a patient with chronic myeloid leukemia (CML) in the chronic phase who was diagnosed 1 year after receiving a diagnosis of autoimmune hemolytic anemia (AIHA). The objective was to assess if the CML patient progressed from AIHA and explore the underlying factors of the poor outcome after the achievement of molecular complete remission (MCR).
Patient Concerns:
A patient with AIHA underwent splenectomy because of poor response to immune inhibitors. The spleen biopsy showed reactive hyperplasia.
Diagnosis:
The patient was diagnosed with CML because of over-expression of the BCR-ABL (P210) gene in the bone marrow (BM), 1 year after receiving the diagnosis of AIHA.
Interventions:
The splenectomy was performed as the patient was unresponsive to the standard treatments consisting of immunoglobulin and dexamethasone. The removed spleen was sent for pathological examination. After she was diagnosed with CML, she received imatinib treatment.
Outcomes:
The spleen biopsy confirmed the translocation of 22q11/9q34. No BCR-ABL kinase domain mutation was detected and there was no expression of the WT1 or EVI1 genes. After splenectomy, the number of peripheral white blood cells was consistently higher than normal during the total therapy time for CML even though she showed MCR. Two years after CML was diagnosed, the patient died from severe infection. The BM gene array analysis displayed 3 types of chromosomal abnormalities: gain (14q32.33), uniparental disomy (UPD) Xp11.22-p11.1), and UPD Xp11.1-q13.1.
Lessons:
AIHA may be a clinical phase of CML progression in this patient. Both splenectomy and prolonged oral tyrosine kinase inhibitors may have contributed to the high risk of infection and her subsequent death. In addition, the gain of chromosome 14q32.33 may be related to her poor outcome.
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