Pulmonary Complications of Drug Therapy

Brettner, Alfred; Er, Heitzman; Wg, Woodin

doi:10.1148/96.1.31

Cited by 47 publications

(7 citation statements)

References 34 publications

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“…Godell et al [19] reported 44% of 18 patients under immunosuppressive therapy and Walzer et al [71], 83% of 22 children with ALL, as suffering from P. carinii infection. MTX-induced toxic allergic reactions have been reported by Clarysse et al [9] in 38 of 93 patients with ALL, and subsequently by others [6,8,16,53].…”

Section: Thymus Mediastinum Arid Retroperitonea] Lymphatic Tissuesmentioning

confidence: 89%

“…Therapeutic attempts to prevent late manifestations of leukaemia, especially leukaemic infiltration of the central nervous system (CNS) [2,21,24,48,50], give rise to toxic side-effects, and a protracted suppression of immunodefences. Today, the fatal outcome of the disease is determined less by haemorrhage than by infection [18,22] as may be seen in the recent literature [5,6,8,16,51,52]. During the period of complete remission, abacterial opportunist infections cause lethal complications [17,23,36].…”

Section: Introductionmentioning

confidence: 99%

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Radiological aspects of leukaemia in childhood

1976

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Absfract. The change in radiological features of leukaemia, treated with modern methods, were studied in a retrospective investigation. Of 108 patients with leukaemia treated between 1964 and 1974 at the Children's Hospital, Heidelberg, 89 were studied. Radiological findings were divided into three groups: (i) alterations due to acute leukaemia in the initial phase (ii) late manifestations of leukaemia and (iii) alterations due to side-effects of antileukaemic therapy.It became apparent that, with prolonged survival, there was an increase in the late manifestations of leukaemia, especially in the central nervous system. This was followed by a decrease after the introduction of the therapeutic regime described by Pinkel. The immunosuppressive effect of this antileukaemic therapy gave rise to life-threatening infections, notably with Pneumocystis carinii. Besides the leukaemic manifestations in bones, kidney, and the viscera of the thorax, there were steroid-induced osteoporosis, platyspondyly and aseptic bone necrosis, and, inflammatory gastrointestinal lesions. In addition, ileus sometimes followed administration of vincristine and toxic-allergic pneumonia after methotrexate therapy occurred.

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Section: Thymus Mediastinum Arid Retroperitonea] Lymphatic Tissuesmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Radiological aspects of leukaemia in childhood

1976

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“…Multiple drugs possess pulmonary fibrosis-inducing activities, and iatrogenic pulmonary fibrosis has occasionally been observed (18,19). In these drugs, bleomycin and its derivative PLM are well known as the strongest inducers (1,2).…”

Section: Discussionmentioning

confidence: 99%

The Upregulation by Peplomycin of Signal Transduction in Human Cells

Yamamoto

Yoneda

Ueta

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-To explore the mechanism of pulmonary fibrosis by bleomycin and its derivative, peplomycin (PLM), we examined the influence of PLM on signal transduction in human peripheral blood lymphocytes (HL), monocytes (HM) and fibroblasts (HF). Tyrosine phosphorylation of multiple proteins in HL and HM were induced by 0.001 to 0.05 mg/ ml and by 0.01 to 0.5 mg/ml of PLM, respectively. In HF, 116-kDa protein was phosphorylated 0.2 to 5 mg/ ml of PLM. When HL were treated with 0.01 mg/ ml of PLM, phosphorylation of p56 lck and activation of extracellular-signal related kinase-2 (ERK2) were induced. ERK2 was also activated in HM. Coordinately, the ratio of p21 ras -binding GTP/ GDP was increased by PLM. As well as interleukin-2, PLM induced tyrosine phosphorylation of JAK-3. In addition, PLM upregulated the nuclear translocation of nuclear factor-kappa B and the expression of c-myc-mRNA in HL, HM and HF. Furthermore, 0.01 to 0.001 mg / ml PLM enhanced the cytokine generation by HL and HM, and 1 to 5 mg / ml PLM increased cytokine generation and collagen synthesis by HF. These upregulatory effects of PLM were abrogated by pretreatment of the cells with a tyrosine kinase inhibitor. These results indicate that PLM upregulates signal transduction in a variety of cell types and the upregulation may induce pulmonary fibrosis.

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“…Pulmonary fibrosis is most often idiopathic; an immune mechanism is postulated as the cause (16)(17)(18). Human lung collagen can induce macrophage inhibitor factor production and cytotoxicity in lymphocytes of patients with idiopathic pulmonary fibrosis (19).…”

Section: Discussionmentioning

confidence: 99%