Factors Affecting the Pulmonary Toxicity of Bleomycin

Parvinen, L.-M.; Kilkku, P.; Mäkinen, Eero; Liukko, P.; Grönroos, M.

doi:10.3109/02841868309135964

Cited by 26 publications

(10 citation statements)

References 10 publications

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“…We used M-CSF Ϫ/Ϫ mice because they have fewer numbers of monocytes and macrophages (40), and bleomycin was used to generate pulmonary fibrosis (28)(29)(30)(31)41). In patients with IPF, lung infiltrates are predominantly subpleural and bibasilar (37).…”

Section: M-csf ؊/؊ Mice Are Protected From Bleomycin-induced Pulmonarmentioning

confidence: 99%

Important Roles for Macrophage Colony-stimulating Factor, CC Chemokine Ligand 2, and Mononuclear Phagocytes in the Pathogenesis of Pulmonary Fibrosis

Baran¹,

Opalek²,

McMaken³

et al. 2007

Am J Respir Crit Care Med

165

159

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Section: M-csf ؊/؊ Mice Are Protected From Bleomycin-induced Pulmonarmentioning

confidence: 99%

Important Roles for Macrophage Colony-stimulating Factor, CC Chemokine Ligand 2, and Mononuclear Phagocytes in the Pathogenesis of Pulmonary Fibrosis

Baran¹,

Opalek²,

McMaken³

et al. 2007

Am J Respir Crit Care Med

165

159

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“…As in our study, there are studies reporting no effect of smoking on development of pulmonary fibrosis and studies reporting inhibitory or positive effect of cigarette smoke on development of fibrosis. Parvinen et al 17 investigated the factors affecting the pulmonary toxicity of bleomycin and found that advanced age, high total dose of bleomycin, and intravenous bolus injections of the drug seemed to be major factors responsible for the development of lung fibrosis whereas smoking had no obvious effect. An earlier report by Osanai et al 12 evaluating the effect of cigarette smoke on the development of bleomycin (BLM)-induced pulmonary fibrosis in hamsters found that tobacco smoke reduced the fibrotic response to bleomycin, however caused derangement of alveolar architecture.…”

Section: It It-s Inh Inh-s Pmentioning

confidence: 99%

The Effect of Cigarette Smoke in Bleomicyn Induced Pulmonary Fibrosis in the Rat Model

Maden¹

2011

UHOD

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The role of cigarette smoking in the development and outcome of pulmonary fibrosis is uncertain. In this study, we aimed to assess the effect of route of bleomycin exposure in the development of pulmonary fibrosis and the effects of cigarette smoke on bleomycin-induced lung fibrosis. We studied five groups of rats; 1-control group, 2-intratracheal bleomycin (IT), 3-intratracheal bleomycin plus cigarette smoke for 4 wk (IT-S), 4-inhaled bleomycin (IN), 5-inhaled bleomycin plus cigarette smoke for 4 wk (IN-S). According to Aschoft's criteria, fibrosis score was higher in IT and IT-S compared to control, IN and IN-S groups. There was no significant difference between IT and IT-S groups. Histopathological evaluation of the lungs of rats revealed that neutrophils, macrophages, plasma cells and lymphocytes in alveolar interstitial space were significantly higher in IT and IT-S compared to IN and IN-S (p< 0.001). IT and IT-S showed a severe collagen, laminin, elastin, fibronectin and proteoglican levels in alveolar, vascular, airway and interstitial space. IN and IN-S showed mild inflammation in lung. There were alveolitis, edema, peribronchial fibrosis, fibroblast proliferation and emphysematous lesions in all groups except for the control group. In this study, we showed that in the development of pulmonary fibrosis in rats, intratracheal administration of bleomycin is more effective than bleomycin inhalation and smoking has no additional effect on development of fibrosis. Keywords: Bleomycin, Pulmonary fibrosis, Cigarette smoking ÖZET S›çan Modelinde Bleomisine Ba¤l› Pulmoner Fibroziste Sigara Duman›n›n EtkisiSigaran›n pulmoner fibrozis geliflimindeki ve sonuçlar›na etkisi net de¤ildir. Bu çal›flmada bleomisin uygulama yolunun pulmoner fibrosis geliflimine ve sigaran›n bleomisine ba¤l› pulmoner fibrosis geliflimi üzerine etkisini de¤erlendirmeyi amaçlad›k. Befl grup fare ile çal›flt›k; 1-kontrol grubu, 2-intratrakeal bleomisin (IT), 3-intratrakeal bleomisin ve 4 hafta süreyle sigara duman› (IT-S), 4-inhale bleomisin(IN), 5-4 hafta süreyle inhale bleomisinle birlikte sigara duman› (IN-S). Aschoft kriterlerine gö-re fibrosis skoru IT ve IT-S gruplar›nda kontrol, IN ve IN-S gruplar›yla karfl›laflt›r›ld›¤›nda daha yüksek bulundu. IT ve IT-S gruplar› aras›nda belirgin fark yoktu. Farelerin akci¤erlerinin histopatolojik incelemesinde alveol ve interstisyel boflluktaki nötrofil, makrofaj, plazma hücreleri ve lenfositler IN ve IN-S grubuna k›yasla IT ve IT-S grubunda belirgin olarak daha yüksekti (p<0.001). IT ve IT-S gruplar›nda alveolar, vasküler, havayolu ve interstisyel bofllukta yo¤un kollajen, laminin, elastin, fibronektin ve proteoglikan düzeyleri izlendi. IN ve IN-S gruplar›nda akci¤erde hafif inflamasyon izlendi. Kontrol grubu d›fl›nda tüm gruplarda alveolit, ödem, peribronflial fibrozis, fibroblast ço¤almas› ve amfizematöz lezyonlar mevcuttu. Bu çal›flmada farelerde pulmoner fibrozis oluflumunda intratrakeal bleomisin uygulaman›n inhale bleomisin inhalasyonundan daha etkili oldu¤u ve sigaran›n pulmoner fibr...

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“…Established risk factors for the toxicity are age >70 years, cumulative dose >450 units, thoracic radiotherapy and a high inspired concentration of oxygen. Bleomycin pulmonary toxicity occurs in 10--50% of patients with one or more of these factors (115)(116)(117)(118). Interstitial pneumonitis accompanying bone marrow transplantation is the other example of chemotherapyrelated pulmonary toxicity increasing with age (115,119).…”

Section: Pulmonary Toxicitymentioning

confidence: 99%

“…Among many anticancer drugs causing pulmonary toxicity, only bleomycin is shown to be associated with increased toxicity in the elderly (115)(116)(117)(118). Bleomycin directly injures the pulmonary capillary endothelium and type I pneumocytes, leading to diffuse alveolar damage and interstitial fibrosis (115).…”

Section: Pulmonary Toxicitymentioning

confidence: 99%

Cancer Chemotherapy in the Elderly

Sekine

Fukuda

Kunitoh

et al. 1998

Japanese Journal of Clinical Oncology

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As the geriatric population is growing, it is increasingly important to be familiar with chemotherapy for the elderly. Age-related changes in pharmacokinetics are documented for doxorubicin, etoposide, ifosfamide, daunorubicin, mitomycin, cisplatin and methotrexate. The hematological toxicity of most standard-dose chemotherapy is not affected by age in patients with normal organic functions and good performance status, although increased toxicity with aging is suggested in the use of actinomycin-D, etoposide, vinblastin, methotrexate, methyl-CCNU, doxorubicin and mitomycin, and in dose-intensive chemotherapy. Among non-hematological toxicities, only doxorubicin-induced cardiomyopathy and bleomycin-induced pulmonary toxicity are demonstrated to be accelerated in the elderly. There is no evidence that advanced age decreases the efficacy of chemotherapy for tumors, except for Hodgkin's disease and acute leukemia. These results suggest that advanced chronological age alone is not always associated with severe toxicity and poor prognosis, and that many elderly patients with cancer will benefit from chemotherapy. To answer questions regarding the optimal chemotherapy regimen, dose and intensity in this population, the influence of age should be analyzed in a multivariate approach in future studies.

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Factors Affecting the Pulmonary Toxicity of Bleomycin

Cited by 26 publications

References 10 publications

Important Roles for Macrophage Colony-stimulating Factor, CC Chemokine Ligand 2, and Mononuclear Phagocytes in the Pathogenesis of Pulmonary Fibrosis

Important Roles for Macrophage Colony-stimulating Factor, CC Chemokine Ligand 2, and Mononuclear Phagocytes in the Pathogenesis of Pulmonary Fibrosis

The Effect of Cigarette Smoke in Bleomicyn Induced Pulmonary Fibrosis in the Rat Model

Cancer Chemotherapy in the Elderly

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