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)

In a 49 year old man with blast crisis and massive leukocytosis due to chronic myelogenous leukemia, severe hypoxic respiratory failure developed despite a normal chest film. Correction of hypoxemia was observed after reduction of the white blood cell count by hydroxy-urea therapy. A similar episode occurred prior to death, and necropsy examination revealed extensive plugging of the pulmonary vasculature by leukemic blast cells but no infection or pulmonary edema. An inverse linear correlation was demonstrated between the peripheral white blood cell count and the efficiency of oxygen transfer in the lung as determined by the arterial to alveolar oxygen tension ratio. We postulate that mechanical obstruction and/or leukocyte mediated capillary endothelial injury caused the severe leukocyte mediated capillary endothelial injury caused the severe hypoxemia. Abnormalities of pulmonary gas exchange may be common in leukemic patients with markedly increased leukocyte counts.
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PMID:Reversible respiratory failure due to intravascular leukostasis in chronic myelogenous leukemia. Relationship of oxygen transfer to leukocyte count. 29 38

A 24-year-old woman with chronic granulocytic leukemia and alveolar proteinosis required extracorporeal membrane oxygenator support for respiratory failure refractory to conventional therapy. During perfusion, each lung was lavaged with 10 L. of normal saline. The lavage led to marked clearing of the lungs and improvement in pulmonary function. Extracorporeal support was terminated successfully after 54 hours. The patient died 2 weeks later with bone marrow insufficiency and overwhelming sepsis. Pulmonary lavage is technically feasible during venovenous oxygenator bypass, and may be of value, since such lavage debrides alveoli as well as the bronchial tree. Because pulmonary lavage provides a possible means of improving pulmonary function, it seems worthy of consideration as an adjunct to membrane oxygenator support.
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PMID:Combination of membrane oxygenator support and pulmonary lavage for acute respiratory failure. 106 Aug 93

Twenty-one patients (median age = 34, range = 10-49; F:M = 7:14) received a preparative regimen consisting of busulfan 4 mg/kg/day x 4, cytosine arabinoside 2 g/m2/12 h x 4 and cyclophosphamide 60 mg/kg/day x 2 ('BAC' regimen) for allogeneic bone marrow transplantation. Out of 12 patients with acute myeloid leukemia (AML), two were in first remission, six were in second remission and four had resistant, relapsed disease or prolonged marrow aplasia after induction chemotherapy. Five of the 12 patients with AML had secondary AML. Four patients had transfusion-dependent myelodysplastic syndrome. Three patients with chronic myeloid leukemia were in the accelerated phase and two were in the blastic phase. Organ toxicities related to the preparative regimen were graded. Liver toxicity occurred in 11 patients, two of these were fatal veno-occlusive disease (VOD) (10%). Nineteen of the 21 patients had grade 2 or less diarrhea, and 13 also had mucositis. One patient developed grade 3 cardiac toxicity, and one other patient had grade 1 skin toxicity. Four patients had gross hematuria related to treatment (19%). No renal, pulmonary or CNS toxicities were encountered. Ten patients have died, two from regimen-related hepatic VOD. Of the remaining eight deaths, four were from respiratory failure in four patients (one case each of Pneumocystis pneumonia, CMV pneumonia, bronchiolitis obliterans associated with chronic graft-versus-host disease, and interstitial pneumonitis complicated pulmonary emboli), and one patient each from GI bleeding, cardiac arrhythmia, sepsis and CNS bleeding. Thus far, only one patient transplanted for secondary AML in second remission relapsed at day 230.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Allogeneic bone marrow transplantation in high-risk myeloid disorders using busulfan, cytosine arabinoside and cyclophosphamide (BAC). 154 49

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 32-year-old Japanese man with chronic granulocytic leukemia died of respiratory failure. Autopsy revealed alveolar proteinosis and pulmonary fibrosis, complicated by disseminated atypical mycobacteriosis. Epithelial hyperplasia caused by busulfan therapy was probably responsible for the induction of excessive surfactant production, resulting in alveolar proteinosis, and the immunosuppressive state due to chronic granulocytic leukemia was probably related to the induction of disseminated atypical mycobacteriosis.
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PMID:Pulmonary alveolar proteinosis and disseminated atypical mycobacteriosis in a patient with busulfan lung. 231 73

We prospectively followed a well characterized cohort of patients post-bone marrow transplantation for changes in pulmonary function. Thirty-four recipients without respiratory symptoms were available for follow up with a mean of two years. Spirometry and other measures of lung volume were well preserved following bone marrow transplantation. A progressive 11.9 percent decline in percent predicted diffusing capacity per year occurred. Age, cigarette smoking, type of cytoreductive therapy, type of GVHD prophylaxis, and the occurrence of AGVHD did not affect longitudinal changes in pulmonary function. Patients receiving transplants for CML developed a highly significant fall in diffusing capacity. Asymptomatic patients with CGVHD developed evidence of progressive obstructive ventilatory impairment. This suggests a subclinical spectrum of patients who may progress to the development of bronchiolitis obliterans and respiratory failure post-bone marrow transplantation.
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PMID:Longitudinal changes in pulmonary function following bone marrow transplantation. 266 44

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

In the absence of preexisting pulmonary disease, progressive respiratory failure caused by leukostasis associated with uncontrolled chronic granulocytic leukemia developed in two patients. The conditions of both patients improved dramatically with aggressive leukapheresis. Clinical improvement correlated with decreased pulmonary wedge pressure, while vascular volume remained constant. Continuous-flow cell separation removed numerous immature myeloid cells, replaced them with oxygen-carrying erythrocytes, and maintained a constant blood volume. The course of these two patients demonstrates the use of continuous-flow leukapheresis in an intensive care unit to reduce leukocyte count and manifestations of leukostasis rapidly, while improving the oxygen-carrying capacity of blood, without exposing the patients to dangerously large shifts in fluid volume.
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PMID:Chronic granulocyte leukemia with respiratory distress. Efficacy of emergency leukapheresis. 694 85

Microangiopathic disease and diffuse alveolar haemorrhage (DAH) are uncommon serious complications of bone marrow transplantation (BMT), but an association between these two conditions has not been previously recognised. We report 4 patients in whom these two complications occurred after allogeneic BMT for haematological malignancy. The patients were 16-39 years of age, and received transplants for acute myeloid leukemia, chronic myeloid leukemia and non-Hodgkin's lymphoma (n = 2). Donors were HLA-identical siblings (n = 3), and a matched unrelated volunteer. The patient with AML was receiving a second transplant for relapse 3 years after her first BMT, and was prepared with busulphan and melphalan; other patients received total body irradiation and cyclophosphamide. Microangiopathy occurred 20-48 days after BMT, and was associated with renal impairment in all cases, and mental confusion in 3. Cyclosporin levels were in the toxic range in 2 cases. DAH occurred 18-55 days after BMT, in 3 cases 2-7 days after the onset of microangiopathy, but preceding it by 14 days in the other case. Patients were treated with fresh frozen plasma, plasma exchange, supplemental oxygen and ventilation in 2 cases. Two patients died of progressive respiratory failure, while 2 patients recovered with evidence of continuing microangiopathic disease, and died of myocardial infarction or fungal infection. We report an association between microangiopathic disease and DAH in these BMT patients, and suggest that damage to the pulmonary vascular endothelium may be the common pathophysiological event, although no specific causative factor could be identified.
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PMID:Diffuse alveolar haemorrhage associated with microangiopathy after allogeneic bone marrow transplantation. 758 Oct 82


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