1999
DOI: 10.1056/nejm199910213411703
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A Preliminary Study of Long-Term Treatment with Interferon Gamma-1b and Low-Dose Prednisolone in Patients with Idiopathic Pulmonary Fibrosis

Abstract: In a preliminary study, 12 months of treatment with interferon gamma-1b plus prednisolone was associated with substantial improvements in the condition of patients with idiopathic pulmonary fibrosis who had had no response to glucocorticoids.

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Cited by 543 publications
(314 citation statements)
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“…There were marked improvements in pulmonary function, arterial blood gas, and exercise activity in the patients with IPF who received IFN-␥. 70 These findings are in agreement with the experimental model of bleomycin (BL)-induced pulmonary fibrosis: In hamsters that were treated with BL, an abundant expression of lung TGF-␤ mRNA preceded the overexpression of procollagen I and III mRNA. IFN-␥ treatment of mice that received intratracheal BL significantly reduced lung TGF-␤, procollagen level and hydroxyproline content.…”
Section: Role Of Tgf-␤1 In Disease Conditions Characterized By Excesssupporting
confidence: 86%
See 1 more Smart Citation
“…There were marked improvements in pulmonary function, arterial blood gas, and exercise activity in the patients with IPF who received IFN-␥. 70 These findings are in agreement with the experimental model of bleomycin (BL)-induced pulmonary fibrosis: In hamsters that were treated with BL, an abundant expression of lung TGF-␤ mRNA preceded the overexpression of procollagen I and III mRNA. IFN-␥ treatment of mice that received intratracheal BL significantly reduced lung TGF-␤, procollagen level and hydroxyproline content.…”
Section: Role Of Tgf-␤1 In Disease Conditions Characterized By Excesssupporting
confidence: 86%
“…Ramos et al 69 Human IPF ELISA, RT-PCR Increased Ziesche et al 70 Human IPF ELISA, RT-PCR Increased, inhibited by IFN-␥ Gauldie et al 72 Rat EPF IH, CGT Increased Querfeld et al 74 Human SS IH, ISH Increased Ihn et al 75 Human SS ELISA, IB Increased, inhibited by TGF-␤ Ab Oh et al 83 Rat DN NB, MLEC Increased, inhibited by TGF-␤ Ab Hong et al 86 Mouse DN IH, ISH, SH Increased Sharma et al 87 Human DN ELISA Increased, inhibited by, captopril Helmich et al 88 Human DN SEI Increased Mezzano et al 90 Human MN IH, ISH Increased Honkanen et al 91 Human MN EIA Increased Diamond et al 92 Rat ON NB, IL Increased Isaka et al 96 Rat ON IH, NB, ISH, AODN transfer Increased, inhibited by TGF-␤ AODN Kaneto et al 97 Human ON IH, RT-PCR Increased Sharma et al 100 Human CAN RT-PCR Increased Cuhaci et al 101 Human CAN IH Increased Qi et al 104 Rat LC NB, AdCAT␤-TR transfection Inhibited by AdCAT␤-TR transfection Ueno et al 105 Rat LC IF, ELISA, AdT␤-ExR Inhibited by AdT␤-ExR injection Zhang et al 106 Rat LC ELISA Increased, inhibited by IFN-␥ gene transfer Bacr et al 107 Human LC NB, IH Increased …”
mentioning
confidence: 99%
“…Some of them were retrospective analyses or case series only. Among the drugs tried or on trial are Etanercept, Imatinib, Prednisone (Daniil et al, 1999;Douglas et al, 1997;Douglas, Ryu, & Schroeder, 2000;Douglas et al, 1998;Nicholson AG, 2000;Riha et al, 2002;Ziesche, Hofbauer, Wittmann, Petkov, & Block, 1999), N-Acetylcysteine (Demedts et al, 2005), TGF-β antibody (Genzyme, 2007), Interferon-γ (Antoniou et al, 2006;Raghu et al, 2004;Raghu R, 2001), Interferon-β (Raghu, Bozic, & Brown, 2001), Pirfenidone (Azuma, Nukiwa et al, 2005;S. Nagai et al, 2002;Raghu, Johnson, Lockhart, & Mageto, 1999), Colchicine (Douglas, Ryu, & Schroeder, 2000;Douglas et al, 1998;Selman et al, 1998), Bosentan, Cyclosporin-A (Alton, Johnson, & Turner-Warwick, 1989;Moolman, Bardin, Rossouw, & Joubert, 1991), D-Penicillamin (Chapela, Zuniga, & Selman, 1986;Selman et al, 1998), Heparin (Kubo et al, 2005), Relaxin (ATS, 2002), Angiotensin converting enzyme (ACE) inhibitors (Nadrous, Ryu, Douglas, Decker, & Olson, 2004), and CTGF antibodies (Mageto Y, 2004).…”
Section: Clinical Trialsmentioning
confidence: 99%
“…Chronic expression of type 2 cytokines facilitates the chronic disease process, whereas elevated levels of IFN-g have been hypothesized to antagonize the remodeling aspect of specific chronic lung disease and to cross-regulate the production of type 2 cytokines. The differential activities of these polarized cytokines have been put into play in clinical trials where IFNg1b has been used to treated patients with interstitial pulmonary fibrosis (19,20). However, the end results of this clinical trial were disappointing, as little efficacy was noted (20).…”
Section: Cytokine Phenotype Of Human Chronic Lung Diseasementioning
confidence: 99%