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Original Research: Asthma |

Asymmetric Dimethylarginine in Exhaled Breath Condensate and Serum of Children With AsthmaExhaled ADMA in Children With Asthma

Silvia Carraro, MD; Giuseppe Giordano, PhD; Giorgio Piacentini, MD; Ahmad Kantar, MD; Serena Moser, MD; Laura Cesca, MD; Mariangela Berardi, MD; Iole M. Di Gangi, PhD; Eugenio Baraldi, MD
Author and Funding Information

From the Women’s and Children’s Health Department (Drs Carraro, Giordano, Cesca, Berardi, Di Gangi, and Baraldi), University of Padova, Padova; the Department of Pediatrics (Drs Piacentini and Moser), University of Verona, Verona; and the Paediatric Asthma Centre (Dr Kantar), Misurina Pio XII Institute, Belluno, Italy.

Correspondence to: Eugenio Baraldi, MD, Unit of Pediatric Respiratory Medicine and Allergy, Women’s and Children’s Health Department, University of Padova, Via Giustiniani 3, 35128 Padova, Italy; e-mail: baraldi@pediatria.unipd.it


For editorial comment see page 367

Drs Carraro and Giordano contributed equally to the work.

This study was previously presented at the European Respiratory Society Annual Congress 2012, Vienna, Austria, September 1-5, 2012.

Funding/Support: The study was supported by the Salus Pueri Fundation, Padova, Italy.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;144(2):405-410. doi:10.1378/chest.12-2379
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Background:  Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor and uncoupler of nitric oxide synthase. By promoting the formation of peroxynitrite, ADMA is believed to contribute to several aspects of asthma pathogenesis (ie, airway inflammation, oxidative stress, bronchial hyperresponsiveness, and collagen deposition). The aim of the present study was to compare this mediator in healthy children and children with asthma using the completely noninvasive exhaled breath condensate (EBC) technique.

Methods:  We recruited 77 children with asthma (5-16 years of age) and 65 healthy children (5-15 years of age) who underwent EBC collection and spirometry. Serum ADMA levels and fractional exhaled nitric oxide levels were measured on the same day in a subgroup of children with asthma. EBC was collected using the Turbo-Deccs (Medivac). ADMA levels were measured using the ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) technique.

Results:  ADMA could be detected in the EBC of 71 subjects with asthma and 64 healthy subjects. ADMA levels in the EBC of children with asthma were significantly higher than in the healthy control subjects (median, 0.12 [interquartile range, 0.05-0.3] vs 0.07 [0.05-0.12]; P = .017), whereas no difference emerged between the children with asthma who were or were not receiving inhaled steroid treatment. No correlation was found between serum and EBC ADMA levels (P > .5).

Conclusions:  We measured ADMA in EBC by UPLC-MS/MS, a reference analytical technique. Higher ADMA levels were found in children with asthma, supporting a role for this mediator in asthma pathogenesis. This oxidative stress-related mediator also seems to be scarcely affected by steroid therapy. We speculate that ADMA might be a target for new therapeutic strategies designed to control oxidative stress in asthma.

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