P2 Platelet Reactivity as a Potential Biomarker in Idiopathic Pulmonary Fibrosis. (12th November 2015)
- Record Type:
- Journal Article
- Title:
- P2 Platelet Reactivity as a Potential Biomarker in Idiopathic Pulmonary Fibrosis. (12th November 2015)
- Main Title:
- P2 Platelet Reactivity as a Potential Biomarker in Idiopathic Pulmonary Fibrosis
- Authors:
- Crooks, MG
Wright, C
Fraser, S
Morice, AH
Hart, SP - Abstract:
- Abstract : Introduction and objectives: Heterogeneity of idiopathic pulmonary fibrosis (IPF) means it is difficult to identify those at highest risk of progression who are most likely to benefit from treatment. A biomarker that predicts disease activity, prognosis and treatment response would be beneficial. We previously reported increased platelet reactivity in IPF, 1 and here we explore whether platelet reactivity warrants further investigation as a biomarker. Methods: Data were obtained from two studies: Study 1. a study of platelet reactivity in IPF; and Study 2. a pilot randomised-controlled trial of an investigational IPF treatment. Standard protocols were used to measure platelet-monocyte aggregate (PMA) formation, P-selectin expression, and fibrinogen binding in blood samples. Platelet reactivity in IPF was compared with controls. Correlation between platelet reactivity and forced vital capacity (FVC) was assessed. Study 2 data were used to assess the change in platelet reactivity in response to the intervention and correlation between baseline platelet reactivity, symptoms (KBILD) and exercise capacity (6MWD). Results: Study 1 included 13 IPF patients (mean± SD, Age 70.3 ± 5.8 years, 69% male, FVC 91.9 ± 17.8% predicted) and 12 controls (Age 66.2 ± 10.2, 66.7% males). Study 2 included 19 IPF patients (Age 71.5 ± 8.7, 72% males, FVC 84.4 ± 16.8% predicted). IPF patients demonstrated significantly increased platelet reactivity compared to controls (P < 0.01). PlateletAbstract : Introduction and objectives: Heterogeneity of idiopathic pulmonary fibrosis (IPF) means it is difficult to identify those at highest risk of progression who are most likely to benefit from treatment. A biomarker that predicts disease activity, prognosis and treatment response would be beneficial. We previously reported increased platelet reactivity in IPF, 1 and here we explore whether platelet reactivity warrants further investigation as a biomarker. Methods: Data were obtained from two studies: Study 1. a study of platelet reactivity in IPF; and Study 2. a pilot randomised-controlled trial of an investigational IPF treatment. Standard protocols were used to measure platelet-monocyte aggregate (PMA) formation, P-selectin expression, and fibrinogen binding in blood samples. Platelet reactivity in IPF was compared with controls. Correlation between platelet reactivity and forced vital capacity (FVC) was assessed. Study 2 data were used to assess the change in platelet reactivity in response to the intervention and correlation between baseline platelet reactivity, symptoms (KBILD) and exercise capacity (6MWD). Results: Study 1 included 13 IPF patients (mean± SD, Age 70.3 ± 5.8 years, 69% male, FVC 91.9 ± 17.8% predicted) and 12 controls (Age 66.2 ± 10.2, 66.7% males). Study 2 included 19 IPF patients (Age 71.5 ± 8.7, 72% males, FVC 84.4 ± 16.8% predicted). IPF patients demonstrated significantly increased platelet reactivity compared to controls (P < 0.01). Platelet reactivity and FVC did not correlate. In study 2, stimulated platelets expressed significantly less P-selectin in response to the intervention (P = 0.03). Unstimulated PMA formation moderately correlated with KBILD (r = 0.38. P = 0.01), but other platelet markers showed no correlation with symptoms or exercise capacity. Conclusion: IPF patients exhibit increased platelet reactivity compared to controls. The reduction in platelet reactivity in response to an intervention may indicate responsiveness to treatment effect. Although there was no correlation between FVC and platelet activation, further investigation is warranted to assess associations between platelet reactivity and lung function decline and mortality. Reference: 1 Crooks MG, Fahim A, Naseem KM, Morice AH, Hart SP. Increased platelet reactivity in idiopathic pulmonary fibrosis is medicated by a plasma factor. PLoS One 2014;9 (10):e111347 … (more)
- Is Part Of:
- Thorax. Volume 70(2015)Supplement 3
- Journal:
- Thorax
- Issue:
- Volume 70(2015)Supplement 3
- Issue Display:
- Volume 70, Issue 3 (2015)
- Year:
- 2015
- Volume:
- 70
- Issue:
- 3
- Issue Sort Value:
- 2015-0070-0003-0000
- Page Start:
- A75
- Page End:
- A75
- Publication Date:
- 2015-11-12
- Subjects:
- Chest -- Diseases -- Periodicals
Thorax
Chest -- Diseases
Periodicals
Periodicals
617.54 - Journal URLs:
- http://thorax.bmjjournals.com/contents-by-date.0.shtml ↗
http://www.bmj.com/archive ↗ - DOI:
- 10.1136/thoraxjnl-2015-207770.139 ↗
- Languages:
- English
- ISSNs:
- 0040-6376
- Deposit Type:
- Legaldeposit
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- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - BLDSS-3PM
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