Plasma Adiponectin, clinical factors, and patient outcomes during the acute respiratory distress syndrome.

Pubmed ID: 25259893

Pubmed Central ID: PMC4178176

Journal: PloS one

Publication Date: Sept. 26, 2014

Affiliation: Center for Translational Medicine and Korman Lung Center, Thomas Jefferson University, Philadelphia, Pennsylvania, United States of America.

MeSH Terms: Humans, Male, Adult, Female, Aged, Middle Aged, Treatment Outcome, Prognosis, Severity of Illness Index, Survival Rate, Retrospective Studies, APACHE, Adiponectin, Cardiac Catheterization, Respiratory Distress Syndrome

Grants: R01HL105490, R21HL112672, R21 HL112672, R01 HL105490, R21 AA023571

Authors: Walkey AJ, Demissie S, Shah D, Romero F, Puklin L, Summer RS

Cite As: Walkey AJ, Demissie S, Shah D, Romero F, Puklin L, Summer RS. Plasma Adiponectin, clinical factors, and patient outcomes during the acute respiratory distress syndrome. PLoS One 2014 Sep 26;9(9):e108561. doi: 10.1371/journal.pone.0108561. eCollection 2014.

Studies:

Abstract

OBJECTIVE: Adiponectin (APN) is an anti-inflammatory hormone derived from adipose tissue that attenuates acute lung injury in rodents. In this study, we investigated the association between circulating APN and outcomes among patients with acute respiratory distress syndrome (ARDS). METHODS: We performed a retrospective cohort study using data and plasma samples from participants in the multicenter ARDS Network Fluid and Catheter Treatment Trial. RESULTS: Plasma APN concentrations were measured in 816 (81.6%) trial participants at baseline and in 568 (56.8%) subjects at both baseline and day 7 after enrollment. Clinical factors associated with baseline APN levels in multivariable-adjusted models included sex, body mass index, past medical history of cirrhosis, and central venous pressure (model R2 = 9.7%). We did not observe an association between baseline APN and either severity of illness (APACHE III) or extent of lung injury (Lung Injury Score). Among patients who received right heart catheterization (n = 384), baseline APN was inversely related to mean pulmonary artery pressure (β = -0.015, R2 1.5%, p = 0.02); however, this association did not persist in multivariable models (β = -0.009, R2 0.5%, p = 0.20). Neither baseline APN levels [HR per quartile1.04 (95% CI 0.91-1.18), p = 0.61], nor change in APN level from baseline to day 7 [HR 1.04 (95% CI 0.89-1.23), p = 0.62)] were associated with 60 day mortality in Cox proportional hazards regression models. However, subgroup analysis identified an association between APN and mortality among patients who developed ARDS from extra-pulmonary etiologies [HR per quartile 1.31 (95% CI 1.08-1.57)]. APN levels did not correlate with mortality among patients developing ARDS in association with direct pulmonary injury [HR 0.96 (95% CI 0.83-1.13)], pinteraction = 0.016. CONCLUSIONS: Plasma APN levels did not correlate with disease severity or mortality in a large cohort of patients with ARDS. However, higher APN levels were associated with increased mortality among patients developing ARDS from extra-pulmonary etiologies.