Therapy Related Acute Lymphoblastic Leukemia ( tALL ) : Case Report and Literature Review (original) (raw)
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Indian Journal of Hematology and Blood Transfusion, 2011
A young adult diagnosed as T-acute lymphoblastic leukemia presented with unusual complications during chemotherapy. He was diagnosed to have tubercular splenic abscess and had neurologic complaints like vincristine-induced peripheral neuropathy and focal neurologic deficit complicating the course of chemotherapy. Cases of hepatosplenic tuberculosis presenting as abscesses during prolonged neutropenia in patients with acute leukemia during or after chemotherapy are rare but reported. Vincristine induced neuropathy is reported to be higher in Indian children possibly due to co-existent malnutrition. The focal lesions in the brain were intriguing as regards to the symptomatology and exact etiology especially with the limitation of imaging in such patients. This case highlights the difficulty in the course of chemotherapy due to the rare complications encountered.
Opsta medicina
Introduction. Acute lymphoblastic leukemia (ALL) is a heterogeneous disease distinguished by clonal replication and piling of immature lymphoid cells in the bone marrow and lymph organs. The etiology is unknown but radiation and some chemical exposure, as well as genetics, might play a role. The disease onset is abrupt. Clinical presentation is characterized by a variety of general symptoms: fatigue, malaise, night sweats, weight loss, fever. The diagnosis is based on a patient's history, physical examination, blood tests, bone marrow biopsy, cytogenetic, and immunohistochemical tests. Core treatments are poly-chemotherapy, radiation therapy, hematopoietic stem cell transplantation. Case report. We presented a 20-year-old patient. On his first visit, he complained of neck pain. He was treated by a physiotherapist. After he finished with physical therapy we noticed pancytopenia in his lab work. His general practitioner (GP) referred him to a hematologist where further medical exa...
Large cell lymphoma complicating acute lymphoblastic leukemia
Blood, 1984
Non-Hodgkin's lymphoma (NHL) is a very rare complication of acute lymphoblastic leukemia (ALL). We present the pathologic, clinical, immunologic, and ultrastructural features of the third reported example of NHL following successfully treated ALL. This white girl developed ALL with predominantly L1 cells at 3.5 yr of age. The lymphoblasts were terminal deoxynucleotidyl transferase (TdT) positive and were non-B, non-T cells. She achieved a complete remission with standard induction therapy and has remained in continuous complete remission. Four and one-third years after the onset of ALL, she developed multifocal, pleomorphic large cell lymphoma of the small bowel, which resulted in episodes of intussusception and obstruction. These pleomorphic and frequently multinucleated lymphoma cells lacked TdT, common ALL antigen, and all tested markers of B cell, T cell, and histiocyte differentiation. Following three small bowel resections, systemic multiagent chemotherapy, and abdominal i...
Case Report on Acute Lymphoblastic Leukemia B-Cell
Journal of Pharmaceutical Research International, 2021
Introduction: B-Cell lymphoblastic leukaemia of blood cancer that influences B-Lymphocytes, which are white blood cells that create within the delicate marrow of your bones (marrow) [1]. When healthy blood cells start to alter and expand out of control, this is called leukaemia. ALL is a tumour of immature lymphocytes. Lymphocytes are white blood cells that help the immune system function. Acute lymphoid leukaemia (ALL) is also known as acute lymphoblastic leukaemia. ALL is most visits in youthful children and people over the age of 50, but it can influence anybody at any age [2].
Therapy-related leukemia and myelodysplasia: susceptibility and incidence
Haematologica, 2007
Therapy-related myelodysplastic syndrome/acute myeloid leukemia (t-MDS/AML) is an increasingly recognized treatment complication in patients treated with radiotherapy or chemotherapy for previous hematologic malignancies or solid tumors. Distinct clinical entities have been described according to the primary treatment, corresponding to defined genetic lesions. Chromosome 7 and/or 5 losses or deletions are typical of alkylating agent-induced AML, while development of t-AML with balanced translocations involving chromosome bands 11q23 and 21q22 has been related to previous therapy with drugs targeting DNA-topoisomerase II. In addition, anti-metabolites, and in particular the immunosuppressant azathioprine, have been shown to induce defective DNA-mismatch repair. This could promote survival of misrepaired cells giving rise to the leukemic clone. Individual predisposing factors, including polymorphisms in detoxification and DNA repair enzymes have been identified. Their combination may significantly increase the risk of t-MDS/AML. Among patients with hematologic malignancies, long-term survivors of Hodgkin's lymphoma are exposed to an increased risk of t-MDS/AML, particularly when receiving MOPP-based, and escalated BEACOPP regimens, and when alkylators are combined with radiotherapy. Patients with Hodgkin's and non-Hodgkin's lymphoma are at highest risk when total body irradiation followed by autologous stem cell transplantation is used as rescue or consolidation therapy. The addition of granulocyte-colony-stimulating factor and radiotherapy plays a significant role in t-AML following treatment of children with acute lymphoblastic leukemia. In non-hematologic malignancies, treatment for breast cancer and germcell tumors has been associated with a 1-5% lifetime risk of both lymphoid as well as myeloid leukemia. In all cases the risk of t-MDS/AML drops sharply by 10 years after treatment.