Placental vascular maldevelopment, intrauterine growth restriction, and pulmonary hypertension.

Placental vascular maldevelopment, intrauterine growth restriction, and pulmonary hypertension.
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DOI:
10.1177/2045894020970056
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发表时间:
2020-10
影响因子:
2.6
通讯作者:
Mestan K
Mestan K
中科院分区:
医学4区
文献类型:
--
作者:
Mathias M;Bitar M;Aldulescu M;Birkett R;Perez M;Mestan K

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一名33岁的孕妇,2,帕拉妇女被发现有早期宫内生长限制在22周妊娠,随后发展为严重的先兆子痫。她在28周时分娩了一名460 g的男性新生儿。婴儿接受无创性消化道支持治疗,出生后前8周通过肠内喂养体重增加,此时他患上了坏死性小肠结肠炎。然后,他出现了严重的肺动脉高压,最大限度的医疗管理难以奏效。他在出生10周时死于低氧性呼吸和心力衰竭。胎盘病理学显示一系列结果与母体血管灌注不良一致。肺部尸检显示肺小动脉肌化和肥大,符合重度肺动脉高压。尸检标本的血管性血友病因子免疫荧光染色表明内皮损伤程度相似。这个病例研究说明了我们对新生儿肺部疾病的胎儿起源的不断发展的知识。
A 33-year-old gravida 2, para 1 woman was noted to have early intrauterine growth restriction at 22 weeks gestation and subsequently developed severe pre-eclampsia. She delivered a 460 g male neonate at 28 weeks. The infant was managed on non-invasive ventilatory support and was gaining weight on enteral feeds for the first eight weeks of life, at which point he developed necrotizing enterocolitis. He then developed severe pulmonary hypertension that was refractory to maximal medical management. He died at 10 weeks of life due to hypoxemic respiratory and heart failure. Placental pathology revealed a constellation of findings consistent with maternal vascular malperfusion. Lung autopsy revealed muscularized and hypertrophied pulmonary arterioles consistent with severe pulmonary hypertension. Von Willebrand factor immunofluorescent staining of autopsy specimens suggest parallels in extent of endothelial injury. This case study illustrates our evolving knowledge of the fetal origins of neonatal lung diseases.
DOI: 10.1016/j.placenta.2014.05.003
发表时间: 2014-08-01
期刊: PLACENTA
影响因子: 3.8
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