Busulphan lung in childhood.

Oakhill, A; Green, I D; Knowlson, G. T. G.; Cameron, A. H.; Shah, Kishore; Hill, F. G. H.; J, Mann

doi:10.1136/jcp.34.5.495

Cited by 19 publications

(13 citation statements)

References 18 publications

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“…Although not specifically evaluated, many of the patients in our study were treated with corticosteroids before death suggesting that the pulmonary toxicity was not reversible with corticosteroids. The 3.6% incidence of pulmonary mortality seen in our study is similar to that reported after standard doses of busulfan (10, 11).…”

Section: Discussionsupporting

confidence: 91%

“…Pulmonary toxic reactions after high‐dose BCNU are well described and amenable to treatment with corticosteroids (7, 8). Chronic administration of busulfan in standard doses is also known to cause pulmonary toxicity in approximately 4% of patients and manifests as delayed pulmonary fibrosis not amenable to treatment with corticosteroids (10, 11). Our study suggests that high‐dose busulfan may also be associated with pulmonary mortality after ASCT.…”

Section: Discussionmentioning

confidence: 99%

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High‐dose busulfan and the risk of pulmonary mortality after autologous stem cell transplant

Kalaycio¹,

Pohlman²,

Kuczkowski³

et al. 2006

Clinical Transplantation

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The non-relapse mortality of autologous stem cell transplant is low enough that the procedure has been extended to older patients with non-Hodgkin's lymphoma. We treated 537 non-Hodgkin's lymphoma patients with high-dose chemotherapy consisting of busulfan, cyclophosphamide, and etoposide followed by autologous stem cell transplant. Sixteen patients were identified who died of pulmonary complications at a five-year incidence of 3.6%. Risk factors for pulmonary mortality included older age and lower baseline D(CO) and FEV1. We conclude that high-dose busulfan is associated with pulmonary mortality after autologous transplant, particularly in older patients.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

High‐dose busulfan and the risk of pulmonary mortality after autologous stem cell transplant

Kalaycio¹,

Pohlman²,

Kuczkowski³

et al. 2006

Clinical Transplantation

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“…The action of BU on cells is mainly limited to the bone marrow. However, other reported side effects of BU therapy are interstitial pulmonary fibrosis (busulphan lung), hyperpigmentation of the skin, ovarian suppression and amenorrhea, and cataract formation (Leake et al 1963;Burns et al 1970;Oakhill et al 1981;Reynolds 1993;Dollery 1999). BU is potentially teratogenic and carcinogenic (Feingold and Koss 1969;IARC 1987;Reynolds 1993;Dollery 1999).…”

Section: Discussionmentioning

confidence: 95%

Haemotoxicity of busulphan, doxorubicin, cisplatin and cyclophosphamide in the female BALB/c mouse using a brief regimen of drug administration

et al. 2010

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Many anticancer drugs are myelotoxic and cause bone marrow depression; however, generally, the marrow/blood returns to normal after treatment. Nevertheless, after the administration of some anti-neoplastic agents (e.g. busulphan, BU) under conditions as yet undefined, the marrow may begin a return towards normal, but normality may not be achieved, and late-stage/residual marrow injury may be evident. The present studies were conducted to develop a short-term mouse model (a 'screen') to identify late-stage/residual marrow injury using a brief regimen of drug administration. Female BALB/c mice were treated with BU, doxorubicin (DOX), cisplatin (CISPLAT) or cyclophosphamide (CYCLOPHOS) on days 1, 3 and 5. In 'preliminary studies', a maximum tolerated dose (MTD) for each drug was determined for use in 'main studies'. In main studies, mice were treated with vehicle (control), low and high (the MTD) dose levels of each agent. Necropsies were performed, and blood parameters and femoral/humeral nucleated marrow cell counts (FNCC/HNCC) were assessed on six occasions (from days 1 to 60/61 post-dosing). Late-stage/residual changes were apparent in BU-treated mice at day 61 post-dosing: RBC, Hb and haematocrit were reduced, mean cell volume/mean cell haemoglobin were increased and platelet and FNCC counts were decreased. Mice given DOX, CISPLAT and CYCLOPHOS, in general, showed no clear late-stage/residual effects (day 60/61). It was concluded that a brief regimen of drug administration, at an MTD, with assessment at day 60/61 post-dosing was a suitable short-term method/screen in the mouse for detecting late-stage/residual marrow injury for BU, a drug shown to exhibit these effects in man.

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“…Regarding pulmonary lesions, it has been reported in humans that long-term and/or high-dose busulfan therapy brought about such pulmonary lesions as bronchopulmonary dysplasia and diffuse interstitial pulmonary fibrosis in adults 9 , 10 , 11 and children 1 , 2 . These lesions are known as “busulfan lungs.” In the lungs of fetal 6 and infant rats, only transient apoptotic changes were detected in alveolar and terminal bronchiolar epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…In children, there are several reports of diverse effects of busulfan treatment such as pulmonary fibrosis and acute clinical neurotoxicity (spasm) 1 , 2 , 3 .…”

Section: Introductionmentioning

confidence: 99%

Systemic Histopathology of Infant Rats Exposed to Busulfan

et al. 2014

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Busulfan is an antineoplastic bifunctional alkylating agent. We previously reported the busulfan-induced systemic histopathological changes in fetal rats and the sequence of brain lesions in fetal and infant rats. In the present study, in order to clarify the nature and sequence of busulfan-induced systemic histopathological changes in infant rats, 6-day-old male infant rats were subcutaneously administered 20 mg/kg of busulfan and histopathologically examined at 1, 2, 4, 7 and 14 days after treatment (DAT). As a result, histopathological changes characterized by pyknosis of component cells were observed in the heart, lungs, stomach, intestines, liver, kidneys, testes, epididymides, hematopoietic and lymphoid tissues, dorsal skin and femur as well as in the brain and eyes (data not shown in this paper). Such pyknosis transiently appeared until 7 DAT with prominence at 2 and/or 4 DAT in each tissue, except for the thymus, in which pyknosis peaked at 1 DAT. Most of the pyknotic nuclei were immunohistochemically positive for cleaved caspase-3, indicating that pyknotic cells were apoptotic. Different from the reports of fetal and adult rats, apoptosis was also found in cardiomyocytes and osteoblasts in infant rats.

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Busulphan lung in childhood.

Cited by 19 publications

References 18 publications

High‐dose busulfan and the risk of pulmonary mortality after autologous stem cell transplant

High‐dose busulfan and the risk of pulmonary mortality after autologous stem cell transplant

Haemotoxicity of busulphan, doxorubicin, cisplatin and cyclophosphamide in the female BALB/c mouse using a brief regimen of drug administration

Systemic Histopathology of Infant Rats Exposed to Busulfan

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