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RISS 인기검색어
- 검색키워드
- 저자 : ( Carina Ittrich ) (검색결과 2 건)
- 무료
- 기관 내 무료
- 유료
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( Jin Woo Song ),( R Gisli Jenkins ),( Imre Noth ),( Moisés Selman ),( Vincent Cottin ),( Yasuhiko Nishioka ),( Antje Prasse ),( Eric S White ),( Carina Ittrich ),( Claudia Diefenbach ),( Klaus B Rohr 대한결핵 및 호흡기학회 2020 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.128 No.-
Background The INMARK trial investigated effects of nintedanib on blood biomarkers in subjects with IPF. We investigated the effect of nintedanib on markers of epithelial damage. Methods Subjects (n=346) with IPF and FVC ≥80% predicted were randomised 1:2 to receive nintedanib 150 mg bid or placebo double-blind for 12 weeks, followed by open-label nintedanib for 40 weeks. Blood samples were taken at weeks 4, 8, 12, 16, 20, 24, 36, and 52. We assessed the rate of change (slope) in log10-transformed CA-125 and CA19-9 (two markers of epithelial damage) from baseline to week 12 using random coefficient regression and changes in log10-transformed CA-125 and CA19-9 over 52 weeks using a mixed model for repeated measures. Results The adjusted rate of change in CA-125 levels from baseline to week 12 was significantly different for nintedanib vs placebo (difference -0.046 U/mL/month [95% CI 0.056, -0.035]; p<0.001). Adjusted mean CA-125 levels decreased with nintedanib vs placebo from week 4; after week 12 CA-125 levels were similar between groups (Figure). There was no significant difference between nintedanib and placebo in the adjusted rate of change in CA19-9 levels from baseline to week 12 (difference -0.023 U/mL/month [95% CI -0.055, 0.009]; p=0.17). Adjusted mean CA19-9 levels over 52 weeks were similar in both groups. Conclusion CA-125 may be a biomarker of response to nintedanib in patients with IPF.
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Gene Expression Profiling in Patients with Idiopathic Pulmonary Fibrosis (IPF) in the INMARK Trial
( Jin Woo Song ),( Moisés Selman ),( R Gisli Jenkins ),( Eric S White ),( Vincent Cottin ),( Yasuhiko Nishioka ),( Imre Noth ),( Antje Prasse ),( Benjamin Strobel ),( German Leparc ),( Carina Ittrich 대한결핵 및 호흡기학회 2020 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.128 No.-
Background The INMARK trial investigated blood biomarkers as predictors of disease progression in patients with IPF and preserved lung function. In this study, we investigated changes in gene expression levels in patients treated with nintedanib and placebo. Methods Subjects with IPF and FVC ≥80% predicted were randomized 1:2 to receive nintedanib or placebo for 12 weeks followed by open-label nintedanib for 40 weeks. Total RNA was extracted from whole blood samples taken at baseline and week 12. Changes in gene expression levels from baseline to week 12 were analyzed. Data were log2 transformed prior to analysis. Changes in gene expression levels were considered significant if p≤0.05 and |log2fold change|≥0.5. Results Of 116 and 230 subjects randomized to receive nintedanib and placebo, respectively, data from 110 and 217 patients were included in the analysis. Of 60,675 genes evaluated, 14,799 had counts per million ≥1 in at least half the samples from either treatment group per time point and were included in the analysis. In adjusted analyses, compared with baseline levels, no genes were downregulated after 12 weeks’ treatment with placebo, while nine genes were downregulated after 12 weeks’ treatment with nintedanib (Table). No genes were upregulated. In unadjusted analyses, the change from baseline in expression level at week 12 was significantly different between nintedanib and placebo for five genes (SHISA4, LTF, CTSG, OLFM4, DEFA4) (Table). Pathways analysis suggested that the genes downregulated in patients treated with nintedanib were related to neutrophil function and extracellular matrix organization. Conclusions These analyses of the INMARK trial, based on genome-wide transcriptome profiling, identified a small number of genes that were downregulated after 12 weeks of nintedanib treatment in subjects with IPF and preserved lung function. The potential of gene expression profiling as a marker of treatment response in patients with IPF requires further study.
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