Approach to the genetic epidemiology of acute lung injury

Michelle Ng Gong, David C. Christiani

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Since the initial description of ARDS in 1967(1), much research has been focused on defining the pathogenesis, clinical presentation, course, and outcome of the syndrome. Initially, early studies investigated the role of complement and endotoxin in lung injury (2). In the past decade, research has focused more on the role of pro-inflammatory and anti-inflammatory response in the pathogenesis and course of acute lung injury and acute respiratory distress syndrome (ALI/ARDS) (3). At the same time, clinical studies were conducted evaluating variables that influence the development and outcome of ALI/ARDS. While many of the animal studies have been consistent, many of the in vivo studies have been heterogeneous. Consequently, efforts to find clinical factors or biomarkers to predict, diagnose, or prognosticate outcomes in ARDS have often been disappointing. Our current understanding of why some patients develop and die from ARDS while others do not is incomplete. For example, while major risk factors for ARDS have been identified, the majority of patients with these risk factors do not develop ARDS. Only 3.8% of patients with documented bacteremia, 41.2% of patients with sepsis syndrome, and 11.9% of intensive care unit patients with pneumonia developed ARDS (4, 5). While smoking has been found to be associated with an increased risk of ARDS in one study, more than half of the ARDS patients were never or ex-smokers (6). Other clinical factors in ARDS have mixed results in the literature. While some studies report an increased risk of developing or dying from ARDS with older age, comorbid conditions such as alcohol-related diseases, and severity of illness, other studies did not find the same (5, 7–10).

Original languageEnglish (US)
Title of host publicationAcute Respiratory Distress Syndrome
PublisherCRC Press
Pages335-356
Number of pages22
ISBN (Electronic)9780203912034
ISBN (Print)9780824740764
StatePublished - Jan 1 2003
Externally publishedYes

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Molecular Epidemiology
Acute Lung Injury
Adult Respiratory Distress Syndrome
Systemic Inflammatory Response Syndrome
Lung Injury
Bacteremia
Research
Endotoxins
Intensive Care Units
Pneumonia
Anti-Inflammatory Agents
Biomarkers
Smoking
Alcohols

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Gong, M. N., & Christiani, D. C. (2003). Approach to the genetic epidemiology of acute lung injury. In Acute Respiratory Distress Syndrome (pp. 335-356). CRC Press.

Approach to the genetic epidemiology of acute lung injury. / Gong, Michelle Ng; Christiani, David C.

Acute Respiratory Distress Syndrome. CRC Press, 2003. p. 335-356.

Research output: Chapter in Book/Report/Conference proceedingChapter

Gong, MN & Christiani, DC 2003, Approach to the genetic epidemiology of acute lung injury. in Acute Respiratory Distress Syndrome. CRC Press, pp. 335-356.
Gong MN, Christiani DC. Approach to the genetic epidemiology of acute lung injury. In Acute Respiratory Distress Syndrome. CRC Press. 2003. p. 335-356
Gong, Michelle Ng ; Christiani, David C. / Approach to the genetic epidemiology of acute lung injury. Acute Respiratory Distress Syndrome. CRC Press, 2003. pp. 335-356
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