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

Characteristic pulmonary findings in an autopsy case of a 46-year-old female who presented heavy dyspnea as her chief complaint after 3 months of busulfan therapy for chronic myeloid leukemia were reported. The pulmonary findings were classified into four types: I. alveolar proteinosis type, II. intra alveolar fibrosis type, III. interstitial fibrosis type, and IV. lipid pneumonia type with cholesterol granuloma. No other case with various findings like this case has been previously reported. It was considered that type I is the basic type, type II is a type that developed from type I, type III is a type with interstitial cell infiltration and fibrosis and type IV is a lipidrich variant of type I. A large lamellar body was first found in the granular material of type I. It is supposed that such a body consists of osmiophilic body which originated from type B alveolar epithelial cells and blood plasma.
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PMID:Varied pulmonary lesions with intraalveolar large lamellar bodies in an autopsy case with busulfan therapy. 26 57

An uncommon, but lethal, toxic side effect of busulfan (Myleran) therapy for chronic myelogenous leukemia is pulmonary fibrosis. A 16-month-old male infant treated for 11 months with busulfan for chronic myelogenous leukemia is, we believe, the first case of "busulfan lung" in the pediatric age group to be reported. Progressive roentgenographic changes in the lung of a diffuse intra-alveolar and interstitial pattern were noted. The patient died after a four-day episode of cough, fever, and progressive dyspnea. At autopsy, no evidence of infection or leukemic infiltrates were seen in the lungs. Characteristic histologic findings as a result of busulfan therapy were observed in the lung and pancreas.
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PMID:Busulfan lung. 26 39

In both animal models and human studies in leukemia, residual disease on day 8 following myelosuppressive therapy is in a proliferative phase and therefore may be sensitive to the S-phase specific drug cytarabine. Based on this concept, 17 patients with refractory or relapsed leukemia or lymphoma undergoing either autologous or allogeneic bone marrow transplantation (BMT) were treated on a Phase I protocol using high doses of busulfan (16 mg/kg, days -10, -9, -8, -7) and cyclophosphamide (120 mg/kg, days -6, -5) followed by escalating doses of a 48-h continuous infusion of cytarabine (starting dose 1000 mg/m2/48 h, days -3, -2). Ten patients received autologous transplants (two with Hodgkin's disease, seven with non-Hodgkin's lymphoma, one with chronic myelogenous leukemia (CML) in blast phase). Seven received allogeneic BMT (two with refractory acute myelocytic leukemia (AML), one with refractory acute lymphoblastic leukemia (ALL) undergoing a second BMT, one with Burkitt's-type leukemia, one with ALL in fifth relapse and two with CML in accelerated/blast phase). Two of these patients received a T cell-depleted haploidentical transplant. The maximum tolerated dose of cytarabine was 1500 mg/m2/48 h; a pulmonary syndrome including dyspnea, hypoxemia, and interstitial infiltrates which responded to aggressive diuresis was the dose limiting toxicity. Of the 10 patients who received cytarabine doses of 2000 or 2500 mg/m2/48 h, five patients developed adult respiratory distress syndrome (ARDS) with three patients requiring intubation; two recovered. Of the nine patients with lymphoma, seven responded with complete tumor clearance (CTC) with two patients tumor-free 13 and 15 months post-BMT, one remained refractory and one died too early to evaluate (TETE).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Phase I study of busulfan, cyclophosphamide, and timed sequential escalating doses of cytarabine followed by bone marrow transplantation. 154 48

Ten patients with severe hematologic malignancies (four with acute leukemia, three with multiple myeloma, one with prolymphocytic leukemia, one with malignant lymphoma and one with blastic crisis of chronic myelogenous leukemia) developed respiratory failure during the period between April 1986 and May 1990. Clinically, the patients manifested high-fever, dyspnea refractory to oxygen therapy, diffuse pulmonary rales and severe hypoxemia without evidence of cardiogenic pulmonary edema. Chest roentgenograms displayed diffuse alveolar infiltrates. Respiratory failure occurred as early as 48 hours and as late as 66 days after the administration of intensive anti-neoplastic chemotherapy. At that time leukocyte count was between 100/microliters and 54,900/microliters. Marked leukocytosis was observed in two patients with AML and PLL. Respiratory failure was preceded by sepsis in one patient with AML and by pneumonia in nine patients. DIC was diagnosed in four patients. All patients treated with high dose methyl prednisolone (mPSL) within 12 hours after the onset of respiratory failure. Only one patient required assisted ventilation. High dose mPSL had significant effect on seven of ten patients. But three patients died from progressive respiratory failure, sepsis, pneumonia and multi-organ failure.
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PMID:[Clinical investigation on acute respiratory failure in patients with severe hematologic malignancy]. 194 22

A 61-year-old male was diagnosed as chronic myelocytic leukemia (CML) in 1985 and had been treated with busulfan for 4 years and 5 months (total 3,572 mg). Since he had complained dyspnea with abnormal lung shadow on a chest x-ray film in May 31, 1989, he was treated with 3 mg/day of dexamethasone under a diagnosis of busulfan lung. Dyspnea and lung shadow was remarkably improved after the treatment. On July 11, he was admitted our hospital with high fever, hypoxemia and diffuse interstitial shadow on a chest x-p. Although intensive treatment with 10 mg/day of dexamethasone and various antibiotics were done, he died in Aug 6. An autopsy revealed the intra-alveolar fibrosis, dense hyaline deposits in alveoli associated with atypical type II epithelial cells in the lung. Seven cases of busulfan lung have been reported in the Japanese literature. The clinical and pathological aspects of these cases, including our case, were discussed.
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PMID:[Busulfan lung exacerbated during steroid therapy: a review of Japanese literature]. 228 77

Twenty-five patients with disseminated cancer (nine with renal cell carcinoma, five with melanoma, three with Hodgkin's lymphoma and chronic myelocytic leukemia [CML], two with soft tissue sarcoma, one each with large-cell lymphoma, breast cancer, and colon cancer), 13 males and 12 females, aged 25 to 68, were treated with recombinant human interleukin-2 (rIL2) by continuous infusion and adoptive transfer of autologous lymphocytes activated in vitro with IL2. Patients underwent leukapheresis on days 1, 8, 15, and 22 of the treatment. Cells, bulk activated for 20 hours in serum-free culture medium with 1,000 U IL2/mL in transfusion transfer packs as culture vessels, were transfused the following day. The infusion of IL2 by continuous infusion for six days started immediately after each adoptive transfer for 4 weekly courses. The dose of IL2 was escalated weekly in each patient; starting doses of IL2 were also escalated in subsequent cohorts of patients until maximally tolerated doses were reached. Nine patients had objective tumor regressions (three with renal cell cancer, two with Hodgkin's lymphoma, and one each with melanoma, sarcoma, breast, and colon cancer). Six responses were partial, two were minor, and one was mixed. Responding patients were maintained with IL2 by continuous infusion for six days every 6 to 8 weeks, without adoptive cell transfer. The median duration of responses was 16 weeks (3 to 60 + weeks). Tumor regression was related to the dose of IL2 (greater than or equal to 3.4 x 10(6) U/m2/d for six days) and to the in vivo lymphoproliferative effects of the lymphokine, but not to the total number of cells adoptively transferred. Side effects of treatment were transient and quickly reversible. Renal, hepatic dysfunction, and dyspnea were directly related to the dose of IL2 and to lymphocytosis. Other toxicities were mild hypotension with mild fluid retention, oral mucositis, anemia, thrombocytopenia, fever, and fatigue.
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PMID:Recombinant interleukin-2 by continuous infusion and adoptive transfer of recombinant interleukin-2-activated cells in patients with advanced cancer. 266 33

A 38-year-old woman with megakaryoblastic chronic myelocytic leukemia (CML) crisis developed recurrent episodes of severe hypercalcemia, manifested by nausea and vomiting and later by dyspnea and hypoxia. The levels of serum parathyroid hormone and serum and urine cyclic AMP were normal. Autopsy revealed widespread metastatic calcifications in various organs, including the lungs. The case suggests that hypercalcemia complicating blast crisis of CML is not related to blast cell phenotype, can cause severe pulmonary malfunction, and is a terminal event. The hypercalcemia most probably resulted from bone resorption, either directly by the megakaryoblasts or by secretion of osteolytic substances.
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PMID:Hypercalcemia complicating a megakaryoblastic crisis of chronic myelocytic leukemia. 316 88

High risk splenectomy is often encountered in cases of hypersplenism with massive splenomegaly (10 times usual weight of 150-200 g) resulting from myelophthisic processes. Intra-operative ligation of the splenic artery through the lesser sac is a technically useful method of gaining vascular control prior to mobilizing the challenging spleen. However, a massive or inaccessible spleen imposes mechanical limitations during surgery and may be complicated by torrential intra-operative hemorrhage in the setting of severe thrombocytopenia refractile to platelet transfusions. The authors describe pre-operative intravascular proximal splenic artery control in four adult patients (3 men, 1 woman) with extreme splenomegaly (2,250-10,000 g). The massive splenomegaly in this group resulted from chronic myelogenous leukemia (n = 2), isolated splenic lymphoma (n = 1), and agnogenic myeloid metaplasia (n = 1). Chief symptom manifestations included left upper quadrant abdominal pain, early satiety, post-prandial emesis, dyspnea, petechiae, and associated easy bruising. Prior to surgery, all the patients were taken to the radiology suite where either detachable silastic balloons or stainless steel coils were placed selectively into the splenic artery under fluoroscopic guidance requiring approximately 35 minutes. Splenic artery occlusion aided normalization of thrombocytopenia (average increases 19,000/microliter to 215,000/microliter) with prolongation in survival of platelets. Successful splenectomy was subsequently performed with no additional transfusion requirements and was made technically easier by reducing splenic bulk. There were no adverse consequences of intravascular occlusion and no peri-operative morbidity or mortality. Preoperative intravascular selective splenic artery occlusion, used as an important potential adjunct to anticipated high risk splenectomy, is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preoperative splenic artery occlusion as an adjunct for high risk splenectomy. 317 46

Busulfan or Misulban is considered by many the treatment of choice in chronic myeloid leukemia, for which it is used as a single agent. An interstitial fibrosing lung disease occurring after Busulfan was first described in 1961 and to date 56 cases have been published and are the object of this review. The clinical picture of this drug induced disease is well characterised. The disorder has an estimated incidence of 6% and begins gradually, marked by non-specific signs (dyspnoea, cough) and by an alteration in the clinical state, often severe, and is frequently accompanied by skin pigmentation. As a rule it occurs after prolonged treatment (on average 41 months, cumulative dose 2.900 mg). The respiratory function pattern is that of an interstitial fibrosis characterised by reduced volumes and hypoxaemia and hypocapnic respiratory failure. The radiology reveals interstitial and predominantly basal shadows. The histology is often obtained, either by lung biopsy or frequently at necropsy, because the prognosis is poor with an 84% mortality from respiratory failure. As for numerous interstitial pneumopathies, it poses questions as to the pathogenesis and early detection, problems which at present are imperfectly resolved.
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PMID:[Busulfan-induced pneumopathy]. 347 80

A 34-year-old woman with typical chronic myelogenous leukemia was treated with daily busulfan (total dose, 1600 mg approximately) from July 1978 to June 1981. In February 1981, she noticed a progressive deterioration of her clinical status, characterized by increasing dyspnea and productive cough. In July 1981, an open lung biopsy revealed pulmonary alveolar proteinosis. The patient died of progressive respiratory failure in August 1981. The association between chronic myelogenous leukemia and pulmonary alveolar proteinosis is briefly reviewed. The report discusses the possible etiologic role of busulfan therapy in the development of pulmonary alveolar proteinosis.
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PMID:A case of pulmonary alveolar proteinosis complicating chronic myelogenous leukemia. A peculiar pathologic aspect of busulfan lung? 658 57


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