The fibrinogen cleavage product Aα-Val360, a specific marker of neutrophil elastase activity in vivo

Richard I Carter; Richard A Mumford; Kelly M Treonze; Paul E Finke; Phillip Davies; Qian Si; John L Humes; Asger Dirksen; Eeva Piitulainen; Ali Ahmad; Robert A Stockley

doi:10.1136/thx.2010.154690

The fibrinogen cleavage product Aα-Val360, a specific marker of neutrophil elastase activity in vivo

Richard I Carter, Richard A Mumford, Kelly M Treonze, Paul E Finke, Phillip Davies, Qian Si, John L Humes, Asger Dirksen, Eeva Piitulainen, Ali Ahmad, Robert A Stockley

Pulmonary Medicine

52 Citations (Scopus)

Abstract

Alpha-1-antitrypsin (A1AT) deficiency is the only recognised genetic risk factor for chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Since A1AT is the major inhibitor of neutrophil elastase (NE), this enzyme has become widely implicated in the pathogenesis of COPD in general; however, there is currently no specific biomarker for its pre-inhibition activity. Such a biomarker should be a measure of elastase-specific COPD disease activity with the potential to assess early targeted therapeutic intervention, in contrast to traditional and non-specific disease severity markers such as forced expiratory volume in 1 s.

Original language	English
Journal	Thorax
Volume	66
Issue number	8
Pages (from-to)	686-91
Number of pages	6
ISSN	0040-6376
DOIs	https://doi.org/10.1136/thx.2010.154690
Publication status	Published - 2011

Keywords

Biological Markers
Calcimycin
Dose-Response Relationship, Drug
Double-Blind Method
Fibrinogen
Humans
Leukocyte Elastase
Leukocyte L1 Antigen Complex
Neutrophil Activation
Peptide Fragments
Peroxidase
Pilot Projects
Pulmonary Emphysema
alpha 1-Antitrypsin
alpha 1-Antitrypsin Deficiency

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10.1136/thx.2010.154690

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title = "The fibrinogen cleavage product Aα-Val360, a specific marker of neutrophil elastase activity in vivo",

abstract = "Alpha-1-antitrypsin (A1AT) deficiency is the only recognised genetic risk factor for chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Since A1AT is the major inhibitor of neutrophil elastase (NE), this enzyme has become widely implicated in the pathogenesis of COPD in general; however, there is currently no specific biomarker for its pre-inhibition activity. Such a biomarker should be a measure of elastase-specific COPD disease activity with the potential to assess early targeted therapeutic intervention, in contrast to traditional and non-specific disease severity markers such as forced expiratory volume in 1 s.",

keywords = "Biological Markers, Calcimycin, Dose-Response Relationship, Drug, Double-Blind Method, Fibrinogen, Humans, Leukocyte Elastase, Leukocyte L1 Antigen Complex, Neutrophil Activation, Peptide Fragments, Peroxidase, Pilot Projects, Pulmonary Emphysema, alpha 1-Antitrypsin, alpha 1-Antitrypsin Deficiency",

author = "Carter, {Richard I} and Mumford, {Richard A} and Treonze, {Kelly M} and Finke, {Paul E} and Phillip Davies and Qian Si and Humes, {John L} and Asger Dirksen and Eeva Piitulainen and Ali Ahmad and Stockley, {Robert A}",

year = "2011",

doi = "10.1136/thx.2010.154690",

language = "English",

volume = "66",

pages = "686--91",

journal = "Thorax",

issn = "0040-6376",

publisher = "B M J Group",

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TY - JOUR

T1 - The fibrinogen cleavage product Aα-Val360, a specific marker of neutrophil elastase activity in vivo

AU - Carter, Richard I

AU - Mumford, Richard A

AU - Treonze, Kelly M

AU - Finke, Paul E

AU - Davies, Phillip

AU - Si, Qian

AU - Humes, John L

AU - Dirksen, Asger

AU - Piitulainen, Eeva

AU - Ahmad, Ali

AU - Stockley, Robert A

PY - 2011

Y1 - 2011

N2 - Alpha-1-antitrypsin (A1AT) deficiency is the only recognised genetic risk factor for chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Since A1AT is the major inhibitor of neutrophil elastase (NE), this enzyme has become widely implicated in the pathogenesis of COPD in general; however, there is currently no specific biomarker for its pre-inhibition activity. Such a biomarker should be a measure of elastase-specific COPD disease activity with the potential to assess early targeted therapeutic intervention, in contrast to traditional and non-specific disease severity markers such as forced expiratory volume in 1 s.

AB - Alpha-1-antitrypsin (A1AT) deficiency is the only recognised genetic risk factor for chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Since A1AT is the major inhibitor of neutrophil elastase (NE), this enzyme has become widely implicated in the pathogenesis of COPD in general; however, there is currently no specific biomarker for its pre-inhibition activity. Such a biomarker should be a measure of elastase-specific COPD disease activity with the potential to assess early targeted therapeutic intervention, in contrast to traditional and non-specific disease severity markers such as forced expiratory volume in 1 s.

KW - Biological Markers

KW - Calcimycin

KW - Dose-Response Relationship, Drug

KW - Double-Blind Method

KW - Fibrinogen

KW - Humans

KW - Leukocyte Elastase

KW - Leukocyte L1 Antigen Complex

KW - Neutrophil Activation

KW - Peptide Fragments

KW - Peroxidase

KW - Pilot Projects

KW - Pulmonary Emphysema

KW - alpha 1-Antitrypsin

KW - alpha 1-Antitrypsin Deficiency

U2 - 10.1136/thx.2010.154690

DO - 10.1136/thx.2010.154690

M3 - Journal article

C2 - 21617168

SN - 0040-6376

VL - 66

SP - 686

EP - 691

JO - Thorax

JF - Thorax

IS - 8

ER -

The fibrinogen cleavage product Aα-Val360, a specific marker of neutrophil elastase activity in vivo

Abstract

Keywords

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