Improvement of immune thrombocytopenia with imatinib therapy following chronic myeloid leukemia

• Published in: International journal of hematology Vol. 117; no. 4; pp. 613 - 617
• Main Authors: Nakamura, Yuichi, Itoh, Yoshihiro, Wakimoto, Naoki
• Format: Journal Article
• Language: English
• Published: Singapore Springer Nature Singapore 01.04.2023; Springer Nature B.V
• Subjects: Abnormalities; Adrenal Cortex Hormones - therapeutic use; Bone marrow; Case Report; Chronic Disease; Chronic myeloid leukemia; Cytogenetics; Hematology; Humans; Idiopathic thrombocytopenic purpura; Imatinib; Imatinib Mesylate - therapeutic use; Immune system; Immunology; Kinases; Leukemia; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - complications; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics; Male; Medicine; Medicine & Public Health; Middle Aged; Myeloid leukemia; Oncology; Prednisolone; Prednisolone - therapeutic use; Protein Kinase Inhibitors - therapeutic use; Protein-tyrosine kinase; Purpura, Thrombocytopenic, Idiopathic - complications; Purpura, Thrombocytopenic, Idiopathic - drug therapy; Steroids; Therapy; Thrombocytopenia; Thrombocytopenia - drug therapy; Tyrosine; Immunological off-target effects; Imatinib; Immune thrombocytopenia; Chronic myeloid leukemia; Tyrosine kinase inhibitor
• ISSN: 0925-5710; 1865-3774
• DOI: 10.1007/s12185-022-03492-9

Immune thrombocytopenia (ITP) and chronic myeloid leukemia (CML) are rarely observed concurrently. Here we report the case of a patient with ITP who developed CML that has been well controlled with tyrosine kinase inhibitor (TKI) therapy. A 55-year-old man was diagnosed with ITP. No cytogenetic abnormalities were found at the time of initial diagnosis. Four years later, he began corticosteroid therapy for progression of thrombocytopenia. At that time, the Philadelphia (Ph) chromosome was observed in 7 of 20 bone marrow (BM) cells, suggesting concurrent CML in the subclinical stage. Prednisolone resulted in a partial response. Seven months after starting prednisolone, he exhibited hematological features of CML with an increase in Ph-positive cells. TKI therapy with imatinib mesylate was started to treat CML and maintained at a daily dose of 400 mg. The patient achieved and sustained a major molecular response. His platelet count also increased, enabling discontinuation of corticosteroid therapy. TKIs have been reported to show various immunological off-target effects. In this case, off-target effects of TKI might have improved ITP by suppressing the autoimmune response. Alternatively, reconstitution of immune systems by Ph-negative cells or cancellation of immunoreaction against CML could have exerted favorable effects on ITP.