Open Access

Plasma antioxidant capacity in critical polytraumatized patients?: methods, severity, and anatomic location

  • Luis Serviá1,
  • Javier Trujillano1Email author,
  • José Carlos Enrique Serrano2,
  • Reinald Pamplona2,
  • Mariona Badia1,
  • Mariona Jové2,
  • Margarida Justes1,
  • Joana Domingo1 and
  • Manuel Portero-Otin2Email author
Critical Care201418:434

https://doi.org/10.1186/cc13917

Published: 12 June 2014

Findings

Oxidative stress (OS) has been invoked as a relevant factor in the evolution and outcome of critical care patients. Indeed, antioxidant therapies have been used in critical care patients [1] but with controversial results [2]. This may be explained by assuming OS as a homeostatically regulated parameter and both its excess and its deficit influencing severity progression. Nonetheless, antioxidant agents could mask an OS signaling role, blocking otherwise physiological responses aimed at recovery of homeostasis [3]. We have evaluated plasma total antioxidant capacity (TAC) in traumatized patients in an ICU, and we determined its potential relationship with severity and trauma location. In a prospective observational study of ICU polytraumatized patients (n = 73, mean Acute Physiology and Chronic Health Evaluation II (APACHE II) score of 11 ± 6) of the Hospital Arnau de Vilanova (Lleida, Spain), we measured (in the first 48 hours) plasma TAC by two different methods: the ferric reducing activity/antioxidant power (FRAP) and the capacity for neutralization of the free radical 2,2′-azino-bis (3-ethylbenzothiazoline)-6-sulphonic acid (ABTS) as previously described [4]. For control subjects, we used age- and gender-matched volunteers (n = 102). We also evaluated the contribution of antioxidant molecules (uric acid, bilirubin, and albumin) to these values. The protocol was approved by the institutional ethics committee of the Arnau de Vilanova Hospital and followed Declaration of Helsinki guidelines for studies with human individuals. All participants (or their legal representatives) gave their consent for the study.

Results

As shown in Figure 1, polytraumatized patients show differences in TAC with reference to control subjects, but these differences are dependent on the technique used. Thus, ICU polytraumatized patients show higher FRAP values but lower ABTS capacity. Notably, APACHE II score influenced FRAP values (Table 1). Indeed, we found that FRAP values were inversely correlated with APACHE II score (r = -0.266, P <0.01) suggesting that, in trauma patients, increased antioxidant response, as measured by FRAP assay, could be a pathophysiological response to stress. Albumin and uric acid concentrations reproduced the FRAP trend with severity. Reinforcing the importance of the technique and the specificities across different antioxidant assessment methods, data for the relationship of APACHE II score with ABTS do not show a significant trend (r = 0.040, P = 0.568). These results also contrast with those obtained in other ICU patients, such as those with sepsis [5].
Figure 1

FRAP and ABTS values in plasma of ICU polytrauma patients (n = 73) are significantly different from those of an age- and gender-matched population (CONTROL) (n = 102). Asterisk indicates statistical differences according to Mann-Whitney test (P <0.05). FRAP and ABTS in plasma were measured as described [4] by using, respectively, 2,4,6-tri(2-piridil)-s-triazine, FeCl3, and acetate buffer (300 mM, pH 3.6) and the ABTS radical cation (ABTS + ·) as reagents and by using a Beckman DU-640 spectrophotometer (Beckman Instruments Inc., Fullerton, CA, USA). Both capacities were referenced to standards containing known concentrations of 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid (Trolox) and expressed as micromolar trolox equivalents (TE). ABTS, 2,2′-azino-bis (3-ethylbenzothiazoline)-6-sulphonic acid; APACHE II, Acute Physiology and Chronic Health Evaluation II; FRAP, ferric reducing/antioxidant power; OS, oxidative stress; TAC, total antioxidant capacity.

Table 1

Study population characteristics of ICU polytraumatized patients

Study population characteristics

APACHE II score

P value

≤7 (n = 28)

8-14 (n = 23)

≥15 (n = 22)

 

Age, yearsa

42.4 ± 14

49.9 ± 20

49.2 ± 19

0.186

Male gender

78.6

82.6

81.8

0.761

AIS (≥3)

    

 Head

17.9

43.5

54.5

0.045

 Chest

57.1

65.2

40.9

0.297

 Abdomen

10.7

8.7

18.2

0.503

FRAP, μM TEb

1,093 (1,013-1,286)

1,072 (856-1,222)

825 (649-1,250)

0.044

ABTS, μM TEb

1,763 (1,555-2,035)

1,765 (1,054-2,008)

1,825 (1,405-1,982)

0.852

Uric acid, mg/dLb

3.8 (2.0-5.9)

2.5 (1.5-4.6)

2.1 (1.2-4.6)

0.056

Bilirrubin, mg/dLb

0.6 (0.4-0.9)

0.8 (0.5-1.4)

0.6 (0.5-1.2)

0.104

Albumin, mg/dLb

3.6 (3.1-3.7)

3.3 (2.7-3.6)

3.0 (2.6-3.4)

0.016

ICU mortality

0.0

0.0

13.6

0.027

Severity was staged according to Acute Physiology and Chronic Health Evaluation II (APACHE II) score. Values are presented as a percentage unless indicated otherwise. aMean ± standard deviation; bmedian (interquartile range). P according to χ2 or Kruskal-Wallis test between different APACHE II groups. ABTS, 2,2′-azino-bis (3-ethylbenzothiazoline)-6-sulphonic acid; AIS, abbreviated injury scale; FRAP, ferric reducing/antioxidant power; ICU, intensive care unit; TE, micromolar trolox equivalents.

In the multiple linear regression, FRAP values in trauma ICU patients are independently influenced by age (β = 0.271, P <0.021), APACHE II score (β = -0.356, P <0.002), and head trauma (β = -0.219, P <0.045). These results accentuate the influence of trauma location and severity in TAC changes.

Our results not only stress the importance of the method used for TAC measurement but also show that age, status severity, and anatomical location of trauma influence TAC response in ICU patients, reinforcing the need for an adequate tailoring of treatments aimed at their recovery, such as antioxidant therapies.

Abbreviations

ABTS: 

2,2′-azino-bis (3-ethylbenzothiazoline)-6-sulphonic acid

APACHE II: 

Acute physiology and chronic health evaluation II

FRAP: 

Ferric reducing/antioxidant power

OS: 

Oxidative stress

TAC: 

Total antioxidant capacity.

Declarations

Acknowledgments

This work was supported by IRBLleida biobank and RETICS BIOBANCOS RD09/0076/00059 and in part by ISCIII (FIS 011-1532) and Generalitat of Catalonia (2009-SGR735). We are indebted to the ICU nurses for their help in sample extraction.

Authors’ Affiliations

(1)
Department of Critical Care Unit, University Hospital Arnau de Vilanova
(2)
NUTREN-Nutrigenomics, Biomedical Research Institute (IRB) of Lleida-UdL

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Copyright

© Serviá et al.; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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