Lindberg Lars
Institution of Clinical Sciences, PICU, Children's Hospital in Lund, Skane University Hospital, Lund University, Lund, Sweden.
Front Pediatr. 2025 May 19;13:1504180. doi: 10.3389/fped.2025.1504180. eCollection 2025.
This case report highlights the challenges in treating bronchopulmonary dysplasia (BPD) in a premature infant with severe pulmonary hypertension, recurrent pulmonary hypertensive crises, and the need of 100% oxygen to achieve acceptable arterial oxygen saturations. Key factors in the infant's improvement involved switching from pulmonary vasodilation to systemic afterload reduction using losartan, an angiotensin II type 1 receptor blocker. This alteration in treatment strategy led to a pronounced and prompt decrease in pulmonary arterial pressure, reduced oxygen dependency and resolution of pulmonary hypertensive crises. The infant's remarkable clinical response suggests that the pulmonary hypertension in BPD may have a pulmonary post-capillary cause, possibly driven by angiotensin II. A literature review corroborates this revision of the current understanding of the pathophysiologic mechanism involved in BPD and suggests that therapies targeting the renin-angiotensin-aldosterone system rather than pulmonary vasodilation may be an effective treatment strategy.
本病例报告强调了治疗一名患有严重肺动脉高压、复发性肺动脉高压危象且需要100%氧气以达到可接受动脉血氧饱和度的早产儿支气管肺发育不良(BPD)所面临的挑战。婴儿病情改善的关键因素包括使用氯沙坦(一种1型血管紧张素II受体阻滞剂)从肺血管扩张转变为降低体循环后负荷。治疗策略的这种改变导致肺动脉压显著迅速下降,氧依赖减少,肺动脉高压危象得到缓解。婴儿显著的临床反应表明,BPD中的肺动脉高压可能有肺毛细血管后原因,可能由血管紧张素II驱动。文献综述证实了对BPD所涉及病理生理机制的当前理解的这一修正,并表明针对肾素-血管紧张素-醛固酮系统而非肺血管扩张的疗法可能是一种有效的治疗策略。