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Case Reports
. 2025 Jan 16;29(3):50.
doi: 10.3892/etm.2025.12800. eCollection 2025 Mar.

Successful treatment of a chronic myeloid leukemia patient with extreme thrombocytosis by a combination of imatinib and interferon‑α: A case report

Affiliations
Case Reports

Successful treatment of a chronic myeloid leukemia patient with extreme thrombocytosis by a combination of imatinib and interferon‑α: A case report

Meng-Xiao Jia et al. Exp Ther Med. .

Abstract

Chronic myeloid leukemia with extreme thrombocytosis (CML-T), defined by a platelet count >1,000x109/l is a rare leukemia subtype. The present case report described a 66-year-old female CML-T patient presenting with a platelet count of 3,798x109/l, but a consistently normal spleen size. Following treatment with imatinib combined with interferon-α, the patient achieved hematological remission within 2 months, with a platelet count reduction to 311x109/l and complete cytogenetic remission after 10 months. The patient experienced myocardial infarction and liver injury during treatment, which was managed with supportive care. The present case suggested that imatinib combined with interferon-α may be a safe and effective treatment option for patients with CML-T and extreme thrombocytosis and suboptimal response to imatinib monotherapy.

Keywords: chronic myeloid leukemia with thrombocytosis; imatinib; interferon-α; thrombocytosis.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Peripheral blood and bone marrow smears. (A) Bone marrow aspirate before treatment: Hypercellular bone marrow with prominent granulocytic hyperplasia. Blasts and various stages of granulocytic maturation are observed. Eosinophils and basophils are readily identifiable. Megakaryocytes are significantly increased, with a predominance of small megakaryocytes. Platelets are seen in aggregates and sheets. (B) Peripheral blood smear before treatment: Leukocytosis is evident. Blasts and various stages of granulocytic maturation are observed. Eosinophils and basophils are readily identifiable. Platelet clumping is frequently observed. (C) Bone marrow aspirate after treatment: Cellular bone marrow with normal myeloid-to-erythroid ratios. Myelocytes and later stages of granulocytic maturation are observed. Megakaryocytes appear normal and platelets are dispersed with occasional small clusters. (D) Peripheral blood smear after treatment: White blood cell count is normal. Mature granulocytes, lymphocytes and monocytes are observed. Platelets are dispersed with occasional small clusters. (Magnification, x1,000, Wright-Giemsa stain).
Figure 2
Figure 2
Bone marrow biopsy. (A) The bone marrow is markedly cellular with an increased myeloid-to-erythroid ratio. Myeloid cells are present at various stages of maturation, with a slight increase in immature forms. Eosinophils are readily observed. Erythroid precursors are predominantly late erythroblasts (magnification, x40; H&E stain). (B) Megakaryocytes are significantly increased, predominantly small megakaryocytes with fewer nuclear lobes. Scattered lymphocytes and plasma cells are observed (magnification, x400; H&E stain). H&E, hematoxylin and eosin.
Figure 3
Figure 3
Cytogenetic analysis. (A) Pre-treatment karyotype showing the typical Ph+ translocation t(9;22) (q34.1;q11.2), with red arrows indicating chromosomes 9 and 22 involved in the translocation. (B) Post-treatment karyotype, no Philadelphia chromosome detected, achieving complete cytogenetic response, with red arrows indicating the normal chromosomes 9 and 22.
Figure 4
Figure 4
BCR-ABL1 fusion gene transcript level (IS%) trend. The patient received 7 BCR-ABL1 fusion gene transcript level tests, with an initial value of 70.78%. The transcript level gradually decreased with treatment, reaching 0.14% in June 2024, approaching the MMR criteria (IS% ≤0.1%). MMR, major molecular response; IS, International Scale.
Figure 5
Figure 5
Changes of white blood cell and platelet count during the treatment. (A) Platelet count gradually decreased following imatinib therapy (blue arrow indicates the start of imatinib monotherapy), with plateletpheresis (red arrows indicate the time points of plateletpheresis) performed on days 2, 4, 7, 9, 12, 15 and 20. The addition of interferon-α (green arrow indicates the start of combined imatinib and interferon-α therapy) on day 11 further accelerated the decline. By day 30, platelet count had significantly decreased but remained elevated. (B) White blood cell count, initially elevated, rapidly decreased after imatinib therapy and remained within the normal range throughout treatment.
Figure 6
Figure 6
Clinical timeline. The patient received 10 days of imatinib monotherapy, followed by 20 days combined with daily IFN-α (QD) until symptom resolution and discharge. After discharge, treatment continued with imatinib combined with twice-weekly IFN-α (BIW) for one month, achieving a CHR. IFN-α was then discontinued and imatinib monotherapy was continued for 8 months, resulting in a CCyR. The final BCR-ABL1 level reached 0.14%, approaching MMR and the patient remains under follow-up. CHR, complete hematological response; CCyR, complete cytogenetic response; MMR, major molecular response; SD, stable disease.

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