Interstitial Pneumonitis Associated with Bleomycin Therapy

Luna, Mario A.; Bedrossian, Carlos W.M.; Lichticer, Benjamin; Salem, Philip A.

doi:10.1093/ajcp/58.5.501

Cited by 157 publications

(34 citation statements)

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“…The pathology of bleomycin-induced lung injury in FIGURE 6 Section of right lower lobe of lung taken at necropsy from baboon which died after 95 U/kg of bleomycin. man initially consists of interstitial edema and mononuclear inflammatory cell infiltration which progresses with larger doses to fibrinous exudation into alveolar spaces and proliferation of fibroblasts and type II alveolar epithelial cells (23)(24)(25). Our observations and those of others (26,27) indicate that similar lesions may develop in experimental animals treated with bleomycin.…”

Section: Discussionsupporting

confidence: 79%

“…Our observations and those of others (26,27) indicate that similar lesions may develop in experimental animals treated with bleomycin. The histopathology of bleomycin pulmonary toxicity mimics many features of "usual interstitial pneumonitis" (23) and appears to provide a suitable model for investigating the relationship of altered lung histology, biochemistry, and mechanical function associated with usual interstitial pneumonitis.…”

Section: Discussionmentioning

confidence: 99%

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Bleomycin-Induced Diffuse Interstitial Pulmonary Fibrosis in Baboons

McCullough¹,

Collins²,

Johanson³

et al. 1978

J. Clin. Invest.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Bleomycin-Induced Diffuse Interstitial Pulmonary Fibrosis in Baboons

McCullough¹,

Collins²,

Johanson³

et al. 1978

J. Clin. Invest.

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“…3,5 Our present study showed that administration of IL-18 plus IL-2 induced acute lung injury, usually within 4 days, when a For personal use only. on April 4, 2019. by guest www.bloodjournal.org From high dose of IL-18 (more than 1 g) along with 50 000 IU IL-2 was administered to juvenile B6 mice.…”

Section: Discussionmentioning

confidence: 51%

Interleukin 18 (IL-18) in synergy with IL-2 induces lethal lung injury in mice: a potential role for cytokines, chemokines, and natural killer cells in the pathogenesis of interstitial pneumonia

Okamoto

2002

Blood

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IntroductionInterstitial pneumonia represents a heterogeneous group of idiopathic interstitial lung diseases that have a grave prognosis. It can be clinically classified as an acute and a chronic form (Bouros et al 1 ; Michaelson et al 2 ). Acute interstitial pneumonia (AIP) is clinically characterized by a rapid onset of respiratory failure and has a grave prognosis, with greater than 70% mortality in 3 months, despite mechanical ventilation. AIP is thought to be synonymous with Hamman-Rich syndrome, occurring in patients without preexisting lung diseases. It also physiologically resembles acute respiratory distress syndrome (ARDS) and occurs in a subset of patients with idiopathic ARDS. Chronic interstitial pneumonia is also known as usual interstitial pneumonia (UIP). It is characterized clinically by the insidious onset of a cough and shortness of breath that slowly progresses to respiratory failure and is characterized histopathologically by the random, nonuniform foci of inflammation and fibrosis of the lung. UIP is often observed in aged adults and in patients with a variety of conditions, including viral infections, rheumatoid diseases, and radiation treatment. Additionally, lethal UIP is often found in patients treated with chemotherapy. Bleomycin-and busulphan-induced 3,4 lung fibrosis has been reported in patients undergoing treatment for malignancies, such as squamous cell carcinoma and myeloid leukemia. Prevention of interstitial pneumonia/lung fibrosis is one of the most important issues in patients treated with chemotherapy.Histologically, diffuse infiltration of mononuclear and polymorphonuclear leukocytes into the lung is observed in the early stage of human interstitial pneumonia. Following the interstitial inflammation, florid fibroblast proliferation within both the interstitium and the alveolar space is found (proliferative stage). The same pathology is observed in the lung fibrosis animal model. [1][2][3][4][5][6][7][8] Thus, the interstitial inflammation is thought to be essential for the fibroblast proliferation of lung fibrosis. It has become clear that multiple mediators may be involved in establishing interstitial pneumonia/ lung fibrosis, including cytokines, chemokines, oxygen radicals, eicosanoids, prostaglandin, and apoptosis-related genes. 1-8 However, the pathogenesis of interstitial pneumonia is not well understood. Supported by Kurume University School of Medicine Alumni Foundation (Japan), the Ishibashi Foundation for the Promotion of Science (Tokyo, Japan), Kaibara Morikazu Medical Science Promotion Foundation (Fukuoka, Japan), Mitsui Medical Science Promotion Foundation (Tokyo, Japan), The Promotion and Mutual Aid Corporation for Private Schools of Japan, and Grant-in-Aid for Scientific Research on Priority Areas (C) "Medical Genome Science" from the Ministry of Education, Science, Sports and Culture of Japan (T.H.). Reprints:Tomoaki Hoshino, Department of Internal Medicine 1, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830-0011, Japan; email: hoshino@med.ku...

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“…Paraquat ingestion usually results in diffuse alveolar damage, but hyaline membranes were not present in a fatal case with intra-alveolar fibrosis [310]. Organising pneumonia has been Amiodarone [90,230,[233][234][235][236][237][238][239][240] Amphotericin B [241] Bleomycin [18,[242][243][244][245][246][247][248][249][250][251][252] Busulfan [230,253,254] Busulfan and cyclophosphamide [230] Carbamazepine [255,256]; in association with carbamazepine induced lupus [257] Cephalosporin (cefradin) [258] Chlorambucil [259] Doxorubicin Possible recall after radiation to the breast [260] Fluvastatin [261] Gold salts [262,263] Hexamethonium [264] Interferon-a [264,265] Interferon-a2b, pegylated interferon a2b [266] Interferon-a + cytosine arabinoside [267] Interferon + ribavirin [266] Interferon-b1a [268,…”

Section: Fungimentioning

confidence: 99%

Cryptogenic organising pneumonia

Jf¹

2006

European Respiratory Journal

478

466

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Organising pneumonia is defined histopathologically by intra-alveolar buds of granulation tissue, consisting of intermixed myofibroblasts and connective tissue. Although nonspecific, this histopathological pattern, together with characteristic clinical and imaging features, defines cryptogenic organising pneumonia when no cause or peculiar underlying context is found. Rapid clinical and imaging improvement is obtained with corticosteroid treatment, but relapses are common after stopping treatment.

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Interstitial Pneumonitis Associated with Bleomycin Therapy

Cited by 157 publications

References 0 publications

Bleomycin-Induced Diffuse Interstitial Pulmonary Fibrosis in Baboons

Bleomycin-Induced Diffuse Interstitial Pulmonary Fibrosis in Baboons

Interleukin 18 (IL-18) in synergy with IL-2 induces lethal lung injury in mice: a potential role for cytokines, chemokines, and natural killer cells in the pathogenesis of interstitial pneumonia

Cryptogenic organising pneumonia

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