%0 Journal Article
%T Significant Differences in Markers of Oxidant Injury between Idiopathic and Bronchopulmonary-Dysplasia-Associated Pulmonary Hypertension in Children
%A Kimberly B. Vera
%A Donald Moore
%A English Flack
%A Michael Liske
%A Marshall Summar
%J Pulmonary Medicine
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/301475
%X While oxidant stress is elevated in adult forms of pulmonary hypertension (PH), levels of oxidant stress in pediatric PH are unknown. The objective of this study is to measure F2-isoprostanes, a marker of oxidant stress, in children with idiopathic pulmonary hypertension (IPH) and PH due to bronchopulmonary dysplasia (BPD). We hypothesized that F2-isoprostanes in pediatric IPH and PH associated with BPD will be higher than in controls. Plasma F2-isoprostanes were measured in pediatric PH patients during clinically indicated cardiac catheterization and compared with controls. F2-Isoprostane levels were compared between IPH, PH due to BD, and controls. Five patients with IPH, 12 with PH due to BPD, and 20 control subjects were studied. Patients with IPH had statistically higher isoprostanes than controls 62£¿pg/mL (37¨C210) versus 20£¿pg/mL (16¨C27), ). The patients with PH and BPD had significantly lower isoprostanes than controls 15£¿pg/mL (8¨C17) versus 20£¿pg/ml (16¨C27), . F2-isoprostanes are elevated in children with IPH compared to both controls and patients with PH secondary to BPD. Furthermore, F2-isoprostanes in PH secondary to BPD are lower than control levels. These findings suggest that IPH and PH secondary to BPD have distinct mechanisms of disease pathogenesis. 1. Introduction It has long been recognized that patients with pediatric idiopathic pulmonary hypertension (IPH) have poor long-term survival. More recently pulmonary hypertension (PH) associated with bronchopulmonary dysplasia (BPD) has been identified as a significant cause of mortality among BPD patients [1, 2]. Few studies have evaluated the mechanisms and optimal treatment of PH due to BPD, resulting in management strategies for these patients which mirror the better studied pharmacologic treatments of IPH. The use of similar therapeutic strategies in these two populations relies on the unproven assumption that the diseases share similar molecular pathophysiologies. Oxidant stress appears to play a role in the molecular mechanism of adult IPH. Multiple studies measuring F2-isoprostanes, a stable marker of oxidant stress resulting from the oxidation of cell-membrane arachidonic acid, have shown adult IPH patients, have higher F2-isoprostane levels than do control patients [3, 4]. Elevated F2-isoprostane levels suggest enhanced oxidant stress in IPH patients and may also directly contribute to pulmonary vasoconstriction [5]. There are no published data on oxidant stress or F2-isoprostane levels in pediatric patients with PH secondary to BPD or IPH. The objective of this study is to
%U http://www.hindawi.com/journals/pm/2012/301475/