Effective treatment of autoimmune thrombocytopenia with rituximab in CLL patient undergoing therapy with acalabrutinib

affecting the skin and mucosa and active epistaxis.She had been complaining of severe night sweats and loss of weight (10 kg during the last four months).Her medical history included hypertension for five years and no other diseases or autoimmune disorders.On examination, thrombocytopenia (7G/L), mild anemia (8.7 g/dL) and leukocytosis (125G/L) were observed.An indirect Coombs test was negative.Whole body CT scans demonstrated splenomegaly (20 cm) and generalized lymphadenopathy up to 4 cm in diameter.Bone marrow aspirate showed 82% infiltration of mature lymphoid cells and numerous megakaryocytes with inhibited proplatelet formation.Immunophenotyping by flow cytometry from peripheral blood samples revealed the typical immunophenotype of chronic lymphocytic leukemia (CD19+, CD20+, CD23+, CD5+, CD200+, lambda+).Cytogenetic examination by FISH did not reveal any aberrations.Molecular tests showed unmutated IGHV gene and no TP53 gene mutation.The patient was diagnosed with high-risk CLL according to the Rai staging system, with secondary ITP.Due to epistaxis, the patient first received a platelet transfusion to stop the bleeding and then began a fourday pulse with dexamethasone at a daily dose of 40 mg.Therapy with acalabrutinib was also initiated.Dosing of BTKi was according to the standard administration schedule (i.e. 100 mg twice per day) [6].After the steroid pulse, platelet counts were still below 10G/l.An infusion of 1g/kg bw intravenous immunoglobulin (IVIg) for two consecutive days was ordered, and the platelet count increased to 57G/l.After the first three months of therapy with acalabrutinib, the general symptoms eased with a significant reduction in lymph node and spleen size.In addition, white blood