Recent data suggest that inflammatory processes play a major role in pulmonary vascular remodelling in patients with idiopathic, heritable, and drug-or toxin-induced (ihd) pulmonary arterial hypertension (PAH)[ 1, 2]. Besides gaining insight into the mechanisms of PAH, understanding the link between inflammation and PAH may help to identify future therapeutic targets. Different studies have shown increased levels of cytokines in ihdPAH, including the proinflammatory cytokines interleukin (IL)-1b, IL-2, IL-4, IL-6, IL-8, IL-12p70, tumour necrosis factor (TNF)-a, monocyte chemoattractant protein-1 [ 2, 3], and the cytokine-like hormone leptin [ 4]. Advances in highly sensitive multiplex detection technologies present new opportunities to rapidly and specifically measure many cytokines using a limited sample volume [ 5]; the potential of combining markers rather than focusing on any single biomarker is of considerable interest [ 3, 6]. Using such an approach, SOON et al.[ 7] recently suggested that IL-2, IL-6, IL-8, IL-10 and IL-12p70 levels were associated with mortality in patients with ihdPAH. The French Network of Pulmonary Hypertension recently conducted a multicentre prospective cohort study of incident cases of PAH followed up for 3 years [ 8], from which a biobank of plasma stored as microstraws at-180uC was available. Therefore, we tested our prospective cohort to determine whether cytokines quantified using a highly sensitive multiplex assay predict mortality in patients with ihdPAH.

Briefly, consecutive incident cases of PAH presenting at the University Pulmonary Vascular Departments in Clamart (Paris), Marseille, Grenoble, Strasbourg, Nancy and Toulouse (France) were enrolled between December 2003 and April 2006. Incident cases were defined as PAH patients with a diagnosis of PAH confirmed by right-heart catheterisation, without current or previous treatment with drugs approved for the management of PAH such as endothelin receptor antagonists, type 5 phosphodiesterase inhibitors or prostacyclins.