The value of edema fluid protein measurement in patients with pulmonary edema

Fein, Alan M.; Grossman, Ronald F.; Jones, J.G.; Overland, E. S.; Pitts, Lawrence H.; Murray, John F.; Staub, Norman C.

doi:10.1016/0002-9343(79)90066-4

Cited by 259 publications

(95 citation statements)

References 18 publications

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“…Measurement of protein concentration in pulmonary edema fluid obtained by sampling the distal airspaces provided the first direct evidence in patients to support the conclusion that ARDS resulted from increased lung microvascular and epithelial permeability (54). BALF has been the second most common source of samples for searching for ARDS biomarkers.…”

Section: Balfmentioning

confidence: 98%

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

García‐Laorden¹,

Lorente²,

Flores³

et al. 2017

Ann. Transl. Med.

102

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Abstract:The acute respiratory distress syndrome (ARDS) is an acute inflammatory process of the lung caused by a direct or indirect insult to the alveolar-capillary membrane. Currently, ARDS is diagnosed based on a combination of clinical and physiological variables. The lack of a specific biomarker for ARDS is arguably one of the most important obstacles to progress in developing novel treatments for ARDS. In this article, we will review the current understanding of some appealing biomarkers that have been measured in human blood, bronchoalveolar lavage fluid (BALF) or exhaled gas that could be used for identifying patients with ARDS, for enrolling ARDS patients into clinical trials, or for better monitoring of patient's management. After a literature search, we identified several biomarkers that are associated with the highest sensitivity and specificity for the diagnosis or outcome prediction of ARDS: receptor for advanced glycation end-products (RAGE), angiopoietin-2 (Ang-2), surfactant protein D (SP-D), inteleukin-8, Fas and Fas ligand, procollagen peptide (PCP) I and III, octane, acetaldehyde, and 3-methylheptane. In general, these are cell-specific for epithelial or endothelial injury or involved in the inflammatory or infectious response. No biomarker or biomarkers have yet been confirmed for the diagnosis of ARDS or prediction of its prognosis.However, it is anticipated that in the near future, using biomarkers for defining ARDS, or for determining those patients who are more likely to benefit from a given therapy will have a major effect on clinical practice.

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Section: Balfmentioning

confidence: 98%

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

García‐Laorden¹,

Lorente²,

Flores³

et al. 2017

Ann. Transl. Med.

102

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“…8,9 Increases in lung microvascular permeability have since been confirmed using radiolabeled tracer proteins in patients with ALI/ARDS 18 and by comparing simultaneous concentrations of protein in the pulmonary edema fluid and the plasma from patients with ALI/ARDS. 15,[19][20][21] A variety of circulating markers of endothelial cell injury and activation have been studied in patients with ALI/ARDS. 22 Endothelin-1, a vasoconstrictor and proinflammatory peptide that is released by endothelial cells as a result of injury, [23][24][25][26] is increased in the plasma of patients with ALI/ARDS 27-29 as is von Willebrand factor (VWF) antigen, another marker of endothelial cell activation and injury.…”

Section: Endothelial Injurymentioning

confidence: 99%

Pathophysiology of Acute Lung Injury and the Acute Respiratory Distress Syndrome

Ware¹

2006

Semin Respir Crit Care Med

430

324

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Since the adult respiratory distress syndrome was first described substantial progress has been made in understanding the pathogenesis of this complex syndrome. This review summarizes our current understanding of the pathophysiology of what is now termed the acute respiratory distress syndrome (ARDS) and its less severe form acute lung injury (ALI), with an emphasis on cellular and molecular mechanisms of injury that may represent potential therapeutic targets. Although it is difficult to synthesize all of these abnormalities into a single, unified, pathogenetic pathway, a theme that emerges repeatedly is that of imbalance, be it between pro-and anti-inflammatory cytokines, oxidants and antioxidants, procoagulants and anticoagulants, neutrophil recruitment and activation and mechanisms of neutrophil clearance, or proteases and protease inhibitors. Future therapies aimed at restoring the overall balance of cytokines, oxidants, coagulants, and proteases may ultimately be successful where therapies that target individual cytokines or other mediators have not.

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“…have been shown to cause a loss of endothelial integrity as a barrier to water and protein flux in the lung, resulting in edema formation in the presence of normal microvascular pressures (1)(2)(3)(4)(5). Clinically, this "noncardiogenic" pulmonary edema is documented with increasing frequency (6)(7)(8).…”

mentioning

confidence: 99%

Release of angiotensin converting enzyme by the lung after Pseudomonas bacteremia in sheep.

Gorin¹,

Hasagawa²,

Hollinger³

et al. 1981

J. Clin. Invest.

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A B S T R A C T We studied release of angiotensin-converting enzyme (ACE) by the lung after acute injury associated with an increase in pulmonary vascular permeability. In eight adult sheep with chronic lung lymph fistulas, we measured lymph flow (QL), and both ACE activity and total protein content in lymph and plasma under base-line conditions and during 24 h after an infusion of live pseudomonas organisms.Under base-line conditions, ACE activity in plasma was 4.93+0.43 U/ml (mean±SEM ml/h before pseudomonas bacteremia, and rose to 6.7 ± 1.2 ml/h by 2 h after onset of the infusion (mean ±SEM, P < 0.05). CTP remained significantly elevated for at least 10 h after the infusion. Release of ACE into lung lymph doubled after acute lung injury and equaled 22.3 ± 13.8 U/h at 4 h after onset of the infusion. ACE secretion into lung lymph had returned to baseline levels by 24 h after bacteremia. We did not observe a significant rise in plasma ACE activity after acute lung injury.Pseudomonas bacteremia in sheep results in acute, reversible lung injury associated with increased pulmonary vascular permeability, and increased release of Address reprint requests to Dr.

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The value of edema fluid protein measurement in patients with pulmonary edema

Cited by 259 publications

References 18 publications

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

Biomarkers for the acute respiratory distress syndrome: how to make the diagnosis more precise

Pathophysiology of Acute Lung Injury and the Acute Respiratory Distress Syndrome

Release of angiotensin converting enzyme by the lung after Pseudomonas bacteremia in sheep.

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