Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Forty-four patients with Ph positive leukemia (36 developing blast crisis after chronic phase and eight presenting in acute leukemia) were classified into subgroups on the basis of reactivity of blasts with an anti-serum made against non-T,non-B acute lymphoid leukemia (ALL+), levels of terminal transferase enzyme (TdT+) and morphology. Positivity with anti-ALL serum was the most sensitive and reliable marker, and TdT was an important aid. The presence of "lymphoid" blasts in blast crisis of CML was related to the response to chemotherapy incorporating Vincristine and Prednisolone (VP). Patients with ALL+ blasts frequently (14 of 15 cases) responded to therapy while 21 of 25 patients who had no ALL+ blasts failed to respond. The clinical course of the ALL+ patients was variable: eight patients remitted with return to the appearances of the chronic phase; four patients demonstrated elimination of the Ph1 positive clone with hypoplasia and this was followed by normal (Ph1 negative) marrow regeneration in two. Subsequent relapse was of either the ALL+ "lymphoid" or the ALL-myeloid type. A regimen incorporating VP should be the treatment of choice in "lymphoid" blast crisis of CML.
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PMID:Relation of "lymphoid" phenotype and response to chemotherapy incorporating vincristine-prednisolone in the acute phase of Ph1 positive leukemia. 28 75

We present a patient with philadelphia chromosome (ph')-positive CML with extramedullary blast crisis in the lymph nodes before the bone marrow blast crisis. The morphological and cytochemical studies of lymph node touch preparation, and cytogenetic studies of lymph node tissue confirmed the extramedullary lymphoid blast transformation of CML, while the bone marrow continued to show the chronic phase of CML. When we changed our treatment to use Vincristine-Prednisolone therapy, the lymphadenopathy disappeared gradually. This case shows that the clinical and prognostic features of extramedullary disease can strongly affect disease acceleration in CML, and the therapy should be changed promptly. Besides, cytogenetic study of extramedullary tumor tissue in CML can be useful for accurate diagnosis.
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PMID:Lymph node blast crisis of chronic myelogenous leukemia. One case report. 237 82

After 4 years of chronic phase, a 22-year-old female with Ph1 (+) chronic myelogenous leukemia developed myelomonocytic crisis. On admission, her Hb was 9.9 g/dl, Plt 4.1 x 10(4)/microliters, WBC 138,000/microliters with 16.5% blasts. Bone marrow contained 38% blasts. She received a combination chemotherapy of mithramycin and hydroxyurea, as reported by Koller et al. Dose of mithramycin was reduced to 20 micrograms/kg. Following 1st and 2nd infusions of mithramycin, severe nasal bleeding was seen. Prednisolone 10 mg/day was given from the 3rd dose of mithramycin with apparent hemostatic effects. Calcium gluconate 3 g/day was administered concomitantly. Her disease responded promptly to this treatment and hematological remission was achieved.
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PMID:[Myeloid crisis of chronic myelogenous leukemia showing dramatic response to mithramycin and hydroxyurea combination]. 253 8

Imatinib mesylate is a drug that has been approved for treatment of chronic myeloid leukemia, Philadelphia-positive acute lymphoblastic leukemia, and advanced gastrointestinal stromal tumors. Several cases of hepatotoxicity, including fatal liver failure, have been reported with the long-term use of imatinib mesylate. Generally hepatotoxicity resolves after discontinuation of imatinib. Despite discontinuation of imatinib, hepatotoxicity can be progressive. Steroid may be useful in these patients and should be started early. We report a 53-year-old woman with advanced gastrointestinal stromal tumors who developed hepatotoxicity while receiving imatinib and subsequently acute liver failure. Ten weeks after commencing imatinib treatment, hepatotoxicity was determined. Imatinib was immediately ceased. Subsequently, a week later hepatic encephalopathy, jaundice, and coagulopathy occurred. Prednisolone was commenced. Liver biopsy was performed five weeks after the determining of hepatotoxicity. Biopsy showed sinusoidal congestion, necrosis of hepatocytes, inflammation, and hepatocyte drop out around the hepatic venule consistent with drug toxicity. Her liver function tests normalized with a nine-week prednisolone treatment. The patient was discharged. Her liver enzymes remained in normal range following visits. In cases of imatinib-induced acute hepatitis, the administration of prednisolone may be useful in the resolution of the acute episode and allow the reintroduction of a drug without risking recurrence of hepatitis.
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PMID:Imatinib mesylate-induced acute liver failure in a patient with gastrointestinal stromal tumors. 1966 40

We describe a rare case of sudden blast crisis of chronic myeloid leukemia that occurred after a 13-year durable remission, following allogeneic bone marrow transplantation and donor lymphocyte infusion. A 55-year-old Japanese man was diagnosed with chronic-phase chronic myeloid leukemia 24 years previously. He underwent allogeneic bone marrow transplantation 2 years after diagnosis. Although the disease recurred 6 years after transplantation, the patient achieved remission again by a donor lymphocyte infusion. Despite a 13-year durable remission, the disease later relapsed into a sudden blast crisis. Prednisolone and vincristine combined with imatinib mesylate effectively achieved a major molecular response. However, the disease relapsed repeatedly with central nervous system infiltration. Dasatinib and intrathecal methotrexate, cytarabine, and dexamethasone administration via the Ommaya reservoir controlled disease progression. Nevertheless, the disease became refractory to treatment with the emergence of a T315I Bcr-Abl gene mutation. The patient eventually died 43 months post crisis.
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PMID:[Sudden blast crisis of chronic myeloid leukemia after a 13-year durable remission following allogeneic bone marrow transplantation and donor lymphocyte infusion]. 2474 12

Lipoid pneumonia is an uncommon noninfectious inflammatory lung disease characterized by lipid deposition in the alveoli, and its etiology and treatment have not been elucidated. We report the case of a 32-year-old woman who developed lipoid pneumonia 9 months after allogeneic hematopoietic stem cell transplant for chronic myelogenous leukemia in lymphoid blast crisis. She complained of progressive cough and dyspnea shortly after discontinuation of immunosuppressive therapy given for graft-vs-host disease. Computed tomography demonstrated diffuse ground-glass opacities in the lungs, and pulmonary function test revealed restrictive impairment. Bronchoalveolar lavage fluid showed milky appearance, and transbronchial lung biopsy specimen revealed foamy macrophages infiltrating the alveoli. Based on these findings, she was diagnosed as having lipoid pneumonia. Prednisolone (1 mg/kg/d) promptly improved the symptoms, pulmonary shadows, and pulmonary function. The findings and clinical course of this case suggest that lipoid pneumonia should be recognized as one of the pulmonary complications of allogeneic hematopoietic stem cell transplantation.
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PMID:Successful Steroid Therapy for Lipoid Pneumonia Developing After Allogeneic Hematopoietic Stem Cell Transplant: A Case Report. 3057 23

Introduction: Nilotinib is a BCR-ABL tyrosine kinase inhibitor approved for chronic myeloid leukemia. We present a case of severe immune-mediated liver injury by nilotinib treatment. Case report: A 59-year-old woman was referred to the liver clinic because of elevated liver enzyme levels. One year prior, she was diagnosed as having chronic myeloid leukemia and treated with nilotinib therapy. The level of aspartate aminotransferase and alanine aminotransferase were 578 IU/L and 499 IU/L, respectively. Percutaneous needle liver biopsy showed extensive centrilobular infiltration of immune cells and destruction of the lobular architecture with minimal inflammation in the portal triad. Immunohistochemical staining showed that many CD8+ T cells and CD56+ cells infiltrated the site of inflammation. Multicolor fluorescence-activated cell-sorting analysis revealed that a considerable number of intrahepatic CD8+ T cells showed an activated phenotype compared with the healthy control. She was diagnosed with nilotinib-induced, immune-mediated liver injury. Prednisolone treatment (30 mg daily) was started and caused rapid normalization of liver enzyme levels. Conclusion: Nilotinib can cause immune-mediated liver injury. The use of corticosteroid can be treatment option in immune-mediated liver injury.
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PMID:Nilotinib-Induced Immune-Mediated Liver Injury: Corticosteroid as a Possible Therapeutic Option. 3275 45