{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T11:21:33Z","timestamp":1790767293618,"version":"4.1.0"},"reference-count":19,"publisher":"European Respiratory Society (ERS)","issue":"5","license":[{"start":{"date-parts":[[2019,10,24]],"date-time":"2019-10-24T00:00:00Z","timestamp":1571875200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.ersjournals.com\/user-licence"}],"content-domain":{"domain":["publications.ersnet.org"],"crossmark-restriction":true},"short-container-title":["Eur Respir J"],"accepted":{"date-parts":[[2019,8,13]]},"published-print":{"date-parts":[[2019,11]]},"abstract":"<jats:sec><jats:title>Introduction<\/jats:title><jats:p>Pulmonary hypertension is a rare but important cause of mortality after haematopoietic stem cell transplantation (HSCT) in children. This complication is poorly characterised in the literature. We report here a series of children who developed pulmonary hypertension after HSCT.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Between January 2008 and December 2015, we retrospectively analysed 366 children who underwent HSCT (age range 0.5\u2013252\u2005months; median 20.3\u2005months). During the post-HSCT course, echocardiography scans motivated by respiratory symptoms identified 31 patients with elevated tricuspid regurgitation velocity (&gt;2.8\u2005m\u00b7s<jats:sup>\u22121<\/jats:sup>), confirmed when possible by right heart catheterisation (RHC).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>22 patients had confirmed pulmonary hypertension with mean\u00b1<jats:sc>sd<\/jats:sc>pulmonary arterial pressure 40.1\u00b110\u2005mmHg (range 28\u201362\u2005mmHg) and pulmonary vascular resistance 17.3\u00b19.2\u2005Wood Units (range 8\u201342\u2005Wood Units). Among the 13 responders at reactivity test, only one patient responded to calcium channel blockers. Seven patients (32%) died. 15 pulmonary hypertension patients were alive after a mean\u00b1<jats:sc>sd<\/jats:sc>follow-up of 6.5\u00b12.3\u2005years (range 2\u201310\u2005years). All survivors could be weaned off pulmonary hypertension treatment after a median follow-up of 5\u2005months (range 3\u201316). The delay between clinical symptoms and initiation of pulmonary hypertension therapy was significantly longer in patients who subsequently died (mean\u00b1<jats:sc>sd<\/jats:sc>33.5\u00b123\u2005days; median 30\u2005days) than in survivors (mean\u00b1<jats:sc>sd<\/jats:sc>7\u00b13\u2005days) (p&lt;0.001).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Pulmonary hypertension is a severe complication of HSCT with an underestimated incidence and high mortality. Aggressive and timely up-front combination therapy allowed normalisation of pulmonary pressure and improved survival.<\/jats:p><\/jats:sec>","DOI":"10.1183\/13993003.00612-2019","type":"journal-article","created":{"date-parts":[[2019,10,24]],"date-time":"2019-10-24T18:15:22Z","timestamp":1571940922000},"page":"1900612","update-policy":"https:\/\/doi.org\/10.1183\/ers-crossmark-policy","source":"Crossref","is-referenced-by-count":20,"title":["Pulmonary hypertension after bone marrow transplantation in 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