Because of the prospect of hypogammaglobulinaemia after rituximab, IgG amounts were monitored following the rituximab treatment was completed regular

Because of the prospect of hypogammaglobulinaemia after rituximab, IgG amounts were monitored following the rituximab treatment was completed regular. disorder in youth, is certainly classically an isolated serious thrombocytopenia reported in usually healthy school-age children, often following a viral illness. ITP has been associated with haematological malignancies like chronic lymphocytic leukaemia, Hodgkins lymphoma and non-Hodgkins lymphoma.1 However, the presence of ITP in children with acute lymphoblastic leukaemia (ALL) is rare and not well?described in the literature.2?Cytomegalovirus (CMV) can be associated with ITP in the general population. Immunosuppressed patients, such as those receiving chemotherapy, are at increased risk for clinically significant CMV infections. This case report describes the presentation and treatment of ITP associated with CMV infection in a 13-year-old male patient with pre-B ALL receiving maintenance chemotherapy for isolated central nervous system (CNS) relapse. Case presentation A 13-year-old male patient with a diagnosis of pre-B ALL presented to the oncology service during maintenance chemotherapy for evaluation of the new onset of gross haematuria and petechiae. The patient was initially diagnosed with ALL at 10 years of age. He received high-risk chemotherapy for pre-B ALL, but suffered an isolated CNS relapse at age 12 during maintenance chemotherapy. He went into remission with reinduction chemotherapy and at ENX-1 the time of presentation with petechiae he was undergoing maintenance chemotherapy on Childrens Oncology Group protocol AALL1331, low-risk arm. He had been randomly assigned to the arm that did not receive blinatumomab, which is a bispecific T?cell engager that targets the CD19 surface antigen on B lymphocytes. On evaluation for the new onset CP-466722 of petechiae, the patient had a platelet count of 3109/L. His physical examination was unremarkable to the evaluation of thrombocytopenia. In particular, he CP-466722 had petechiae and small bruises, but no deep vein thromboses, lymphadenopathy, hepatomegaly or splenomegaly. The platelet count remained refractory to CP-466722 multiple platelet transfusions and decreased to a nadir of 1109/L during the hospitalisation. Investigations An indirect anti-platelet antibody screen was obtained and was negative for antibodies against glycoprotein?(GP) IIB/IIIA, GP IA/IIA, GP IB/IX and human leucocyte antigen?class I. Direct platelet antibody testing via flow cytometry was unable to be performed due to the patients severe thrombocytopenia. A bone marrow aspirate was obtained and was normocellular, negative for malignant cells and positive for megakaryocytes. Differential diagnosis ITP Myelosuppression due to chemotherapy Myelosuppression due to viral infection Bone marrow relapse of pre-B ALL Secondary haematologic malignancy Microangiopathic consumption of platelets Hypersplenism Treatment The evaluation of the bone marrow described above supported a peripheral consumption of platelets, such as ITP, rather than insufficient platelet production as the cause of the thrombocytopenia. Splenic sequestration was ruled out due to his normal splenic size. The patients platelet count improved slightly with two courses of intravenous immunoglobulin (IVIG) and steroids, further supporting the diagnosis of ITP; however, this response was not long?lasting. The first dose of IVIG (750?mg/kg) was given with no significant change in the platelet count, which rose from 3109/L to 9109/L 2?days later, but fell back to 1109/L 2?days afterwards. A second dose of IVIG (830?mg/kg) with methylprednisolone (5?mg/kg) was given 4?days after the first dose, and the platelet count rose from 1109/L to 37109/L 2?days later, but fell back to 10109/L 2?days afterwards. During his hospitalisation, the patient was found to have a positive qualitative CMV DNA PCR raising the suspicion of CMV-associated ITP. However, his viral load was low (7767 copies/mL) so its significance was unclear. He completed a treatment course of valganciclovir with a subsequent undetectable CMV count. Five days after the second dose of IVIG, the patients platelet count was stable at 10109/L, he was without signs of active bleeding and he was discharged home. He restarted maintenance chemotherapy dexamethasone pulse (3?mg/m2 twice a day for 5 days) with vincristine 1?day after discharge, but the platelet count was still 10109/L. A third dose of IVIG (800?mg/kg).

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