吲哚美辛治疗动脉导管未闭后早产高血压

Takahiro Tominaga, S. Omori, M. Awazu
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引用次数: 0

摘要

高血压是成人非甾体抗炎药(NSAIDs)的一种已知并发症。然而,在儿童中很少有报道。在一项对诊断为高血压的新生儿的回顾性研究中,吲哚美辛治疗动脉导管未闭(PDA)与高血压的发展有关。据报道,医疗PDA关闭通常与全身血压升高有关。然而,这些病例的临床过程和实验室结果尚未被描述。我们报告一个早产儿在使用吲哚美辛治疗PDA后出现高血压。虽然我们的病例之前有因吲哚美辛引起的急性肾损伤(AKI),但在尿量开始增加后出现高血压。虽然非甾体抗炎药引起的成人高血压被认为是由于肾脏血管收缩和随后的钠潴持(4),但在我们的病例中,高血压的主要机制被认为是由于血管阻力增加,可能是由血管前列腺素I2 (PGI2)合成的抑制引起的。病例报告
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypertension in a preterm after indomethacin use for patent ductus arteriosus
Hypertension is a known complication of non-steroidal antiinflammatory drugs (NSAIDs) in adults1). However, it has rarely been reported in children. In a retrospective study of neonates diagnosed with hypertension, indomethacin treatment for patent ductus arteriosus (PDA) was described to be associated with the development of hypertension2). It is reported that medical PDA closure is usually associated with an increase in systemic blood pressure3). The clinical course and laboratory findings of such cases, however, have not been described. We report a preterm infant who developed hypertension after the administration of indomethacin for PDA. Although our case had preceding acute kidney injury (AKI) due to indomethacin, hypertension developed after urine output started to increase. While NSAID-induced hypertension in adults has been ascribed to renal vasoconstriction and subsequent sodium retention4), the major mechanism of hypertension in our case was thought to be high after load due to increased vascular resistance, presumably induced by the inhibition of vascular prostaglandin I2 (PGI2) synthesis. Case Report
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