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Biomarkers of Acute Lung Injury: Worth Their Salt? Alastair G Proudfoot1,2†, Matthew Hind1,2† and Mark JD Griffiths1,2*†

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Biomarkers of Acute Lung Injury: Worth Their Salt? Alastair G Proudfoot1,2†, Matthew Hind1,2† and Mark JD Griffiths1,2*† Proudfoot et al. BMC Medicine 2011, 9:132 http://www.biomedcentral.com/1741-7015/9/132 Clinical Biomarkers OPINION Open Access Biomarkers of acute lung injury: worth their salt? Alastair G Proudfoot1,2†, Matthew Hind1,2† and Mark JD Griffiths1,2*† Abstract The validation of biomarkers has become a key goal of translational biomedical research. The purpose of this article is to discuss the role of biomarkers in the management of acute lung injury (ALI) and related research. Biomarkers should be sensitive and specific indicators of clinically important processes and should change in a relevant timeframe to affect recruitment to trials or clinical management. We do not believe that they necessarily need to reflect pathogenic processes. We critically examined current strategies used to identify biomarkers and which, owing to expedience, have been dominated by reanalysis of blood derived markers from large multicenter Phase 3 studies. Combining new and existing validated biomarkers with physiological and other data may add predictive power and facilitate the development of important aids to research and therapy. Introduction The natural history of acute lung injury Thesyndromeacutelunginjury(ALI)anditsmore Regardless of the wide variety of insults that cause or severe counterpart acute respiratory distress syndrome contribute to the development of ALI, the response of (ARDS) are defined by radiographic and physiological the lung is largely stereotypic. A combination of tissue changes that characterize patients with acute lung fail- injury and inflammation affecting the gas exchange sur- ure (Table 1) [1]. All age groups may be affected, face of the lung, the alveolar-capillary membrane, causes although the syndrome has a higher incidence and mor- high permeability pulmonary edema. The presence of a tality in older people. Across all ages the incidence is protein-rich inflammatory exudate in the airspace approximately 200,000 cases per year in the United impairs surfactant function [7]. The resulting collapse States with a mortality of around 35% [2]. Survivors face and consolidation of the lung causes profound hypoxe- a long-term reduction in quality of life; for example, mia because inflammatory mediators induce changes in only 54% of survivors were able to return to work 12 the control of vascular tone that disable hypoxic pul- months after hospital discharge [3]. monary vasoconstriction [8]. Loss of pulmonary capillary The validation of biomarkers, for use in clinical surface area associated with localized lung destruction trials and ultimately in practice, has become a central and occlusion of the vascular bed by intravascular tenet of translational biomedical research [4]. The thrombosis, increases the anatomical dead space, itself purpose of this article is to discuss the role of biomar- associated with a poor outcome [9], giving rise to car- kers in the management of ALI and related research. bon dioxide retention. Host factors, both inherited We shall not present a state of the art review of the [10,11] and acquired, influence individual susceptibility, field of all the biomarkers that have been investigated (for example, excessive alcohol consumption predis- in this field, excellent examples of which have been poses, while diabetes mellitus protects) [12,13]. Precipi- produced recently [5,6]. Rather, we shall question cur- tating causes or risk factors, which often “hunt in rent strategies to identify biomarkers and whether packs”, either affect the lung directly (pneumonia, what has been achieved thus far has advanced the aspiration of stomach contents and thoracic trauma) or field. cause ALI indirectly through a systemic inflammatory response syndrome (SIRS) associated with multiple organ dysfunction, exemplified by severe sepsis and transfusion related ALI [14]. These causes, to a large * Correspondence: [email protected] † Contributed equally part, determine the initial clinical course and outcome, 1Royal Brompton & Harefield NHS Foundation Trust, Adult Intensive Care but most patients subsequently require invasive Unit, Sydney Street, London SW3 6NP, UK Full list of author information is available at the end of the article © 2011 Proudfoot et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Proudfoot et al. BMC Medicine 2011, 9:132 Page 2 of 8 http://www.biomedcentral.com/1741-7015/9/132 Table 1 NAECC definition of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS)[1] Timing Oxygenation Chest Radiograph Exclusion of cardiogenic pulmonary oedema ALI Acute PaO2/FiO2 ≤ 300 mmHg Bilateral opacities consistent with PAOP ≤ 18 mmHg if measured or no clinical evidence of left ARDS or 40 kPa pulmonary oedema atrial hypertension PaO2/FiO2 ≤ 200 mmHg or 27 kPa PaO2/FiO2, arterial partial pressure of oxygen/inspired oxygen fraction; PAOP, pulmonary artery occlusion pressure mechanical ventilation in an intensive care unit to main- emphasizes the primary role of disordered epithelial tain adequate gas exchange and often other organ repair, which may be contributed to by repeated or per- supports. sistent injury and inflammation, in driving a pathological While the development of pulmonary fibrosis in a fibrotic response [22]. patient with ALI predicts the requirement for prolonged Despite years of concerted effort and very many clini- respiratory support and a poor outcome [15], relatively cal trials, a minority of which have been capable of pro- little is known about the processes that determine the ducing a definitive result, there are no treatments (as resolution of inflammation, injury and subsequent lung opposed to modifications of organ support [23,24]) that repair [16]. The consecutive three-phase pathological improve the outcome of patients with ALI [25]. What model of ALI (exudative, proliferative and fibrotic) is a has become evident, both in this field and in critical gross over-simplification. Fibrosis is evident histologi- care in general, is the extent and importance of iatro- cally as early as a week after the onset of the disorder genic injury. Hence, half of ALI arises in patients who [17] and procollagen III peptide, a precursor of collagen were subjected to mechanical ventilation for another synthesis, is elevated in the broncho-alveolar lavage reason: the four major culprits being mechanical ventila- (BAL) fluid of ARDS patients at the time of tracheal tion that targets normal blood gas parameters, transfu- intubation [18]. Indeed, not only is the injured lung sion of blood products, excessive fluid resuscitation and known to be heterogeneously affected [19], it also seems hospital acquired pneumonia (Figure 1) [26-29]. Accord- likely from the examination of lavage samples from ingly, recent epidemiological evidence suggests that tar- patients that these pathological processes coincide in the geting hospital acquired injury can halve the incidence same lung region [20]. Similarly, while several pro- of ARDS despite an increase in patients’ severity of ill- inflammatory mediators are also pro-fibrotic, distinct ness, the number of comorbidities and the prevalence of patterns of gene expression are associated with acute major ARDS risk factors [30]. inflammation and fibrosis in the injured lung, suggesting Hence, studying patients with ALI is a challenge that fibrosis is not simply an inevitable consequence of because the syndrome is the end result of an almost unresolved inflammation [21]. Indeed, current thinking infinite variety of scenarios. These range from young fit patients with severe pneumonia or thoracic trauma to older patients who fail to recover from routine proce- Precipitating cause or risk factors for ALI dures, suffer complications, require respiratory support because of a combination of a chronic cardio-respiratory condition and hospital-acquired pneumonia, and ulti- Infection mately develop ARDS on a ventilator. As a consequence, Genetic factors VALI the water is muddied both by heterogeneity in the host Comorbidities TRALI and in the risk factors, and by the variety of other co- Fluid overload incident processes. Furthermore, it is often difficult to Inflammation define precisely when the syndrome started, which may Coagulation have a dramatic effect on measured variables in cases Altered cell function where the condition changes rapidly. Finally, variable Tissue injury management regimens may contribute to patient hetero- Fibrogenesis/ Repair geneity, both in the face of clear evidence (for example, poor adherence to low tidal volume ventilation) [31] Figure 1 Process-based pathogenesis of ALI.Traditionalcauses of or risk factors for ALI maybe contributed to in certain patients by and where evidence is lacking(forexample,intheuse hospital-acquired harm (red) and modified in their potency for of adjuncts to respiratory support like prone positioning, causing ALI by multiple patient’s susceptibility (blue). Depending on inhaled nitric oxide and high frequency oscillation). the balance of these factors the processes that determine the Conversely, critically ill patients are closely monitored, natural history of ALI are initiated in the lung. physiological data are electronically stored and their Proudfoot et al. BMC Medicine 2011, 9:132 Page 3 of 8 http://www.biomedcentral.com/1741-7015/9/132 clinical condition
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