Pulmonary hypoplasia in neonatal hypophosphatasia.
Pulmonary hypoplasia in neonatal hypophosphatasia.
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新生儿低磷酸酯酶症中的肺发育不全。
DOI：
10.3109/15513818809022304
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发表时间：
1988
期刊：
影响因子：
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通讯作者：
Kenneth J. Milne
中科院分区：
文献类型：
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作者：
M. Silver;G. Vilos;Kenneth J. Milne
对一例出生后立即窒息死亡的低磷酸酶症男婴进行尸检，研究肺生长的形态学、生物物理学和生化参数。肺发育不良，因为一个显着减少的空气形成，但肺成熟是正常的胎龄的所有参数。通过体重和纤维测量评估的横膈膜发育与胸部缩小一致。这种迟发性肺发育不全的机制归因于胸腔容积减少，与产前超声检查观察到的受影响婴儿的正常胎儿呼吸运动相关。
Morphological, biophysical, and biochemical parameters of lung growth were studied at autopsy on a male infant with hypophosphatasia who died with asphyxia immediately after birth. The lungs were hypoplastic because of a marked decrease in airspace formation but lung maturation was normal for gestational age by all the parameters used. Diaphragmatic development, assessed by weight and fiber measurement, was in keeping with the decreased chest size. The proposed mechanism for this late onset type of pulmonary hypoplasia, attributed to decreased thoracic volume, is correlated with antenatal ultrasonographic observations of normal fetal breathing movements in the affected infant.