Growth of Lung Parenchyma in Infants and Toddlers with Chronic Lung Disease of Infancy
Growth of Lung Parenchyma in Infants and Toddlers with Chronic Lung Disease of Infancy
复制标题
DOI：
10.1164/rccm.200908-1190oc
复制
发表时间：
2010-05-15
影响因子：
24.7
通讯作者：
Tepper, Robert S.
中科院分区：
文献类型：
--
作者：
Balinotti, Juan E.;Chakr, Valentina C.;Tepper, Robert S.
基本原理：描述婴儿期慢性肺病（CLDI）婴儿的临床病理学有限，主要来自死亡或需要肺活检的重度肺病婴儿。由于临床稳定的门诊患者的肺组织不可用，生理测量提供了增加我们对这种疾病的肺病理生理学的理解的潜力。目的：我们假设，如果早产和CLDI的发展导致肺泡发育中断，那么患有CLDI的婴儿和幼儿的肺弥散能力相对于其肺泡容积将低于完全肺弥散能力。方法：我们测量肺弥散量和肺泡容积，在肺容积升高时采用单次屏气法。慢性肺部疾病的婴儿期（23-29周的妊娠，n = 39）与足月对照组（n = 61）进行了比较，在校正年龄为11.6（4.8-17.0）和13.6（3.2-33）months. Measures和主要结果：肺泡容积和肺弥散量增加，随着身体长度为两组。调整后的身体长度，受试者与CLDI有显着较低的肺弥散功能（2.88与3.23 ml/min/mm Hg; P = 0.0004），但没有差异的体积（545与555 ml; P = 0.58）。结论：婴幼儿与CLDI肺弥散功能下降，但正常肺泡容积。这些生理学发现与从患有严重肺部疾病的受试者获得的形态测量数据一致，这表明极早产后肺泡发育受损。
Rationale: The clinical pathology describing infants with chronic lung disease of infancy (CLDI) has been limited and obtained primarily from infants with severe lung disease, who either died or required lung biopsy. As lung tissue from clinically stable outpatients is not available, physiological measurements offer the potential to increase our understanding of the pulmonary pathophysiology of this disease.Objectives: We hypothesized that if premature birth and the development of CLDI result in disruption of alveolar development, then infants and toddlers with CLDI would have a lower pulmonary diffusing capacity relative to their alveolar volume compared with full-term control subjects.Methods: We measured pulmonary diffusing capacity and alveolar volume, using a single breath-hold maneuver at elevated lung volume. Subjects with chronic lung disease of infancy (23-29 wk of gestation; n = 39) were compared with full-term control subjects (n = 61) at corrected ages of 11.6 (4.8-17.0) and 13.6 (3.2-33) months, respectively.Measurements and Main Results: Alveolar volume and pulmonary diffusing capacity increased with increasing body length for both groups. After adjusting for body length, subjects with CLDI had significantly lower pulmonary diffusing capacity (2.88 vs. 3.23 ml/min/mm Hg; P = 0.0004), but no difference in volume (545 vs. 555 ml; P = 0.58).Conclusions: Infants and toddlers with CLDI have decreased pulmonary diffusing capacity, but normal alveolar volume. These physiological findings are consistent with the morphometric data obtained from subjects with severe lung disease, which suggests an impairment of alveolar development after very premature birth.