Epidemiology of Neonatal Chronic Lung Disease in Japan

Ogawa, Yutaka; Fujimura, Masanori; Goto, Akiko; Kawano, Tsuyoshi; Kondo, Tsutomu; Nakae, Nobuyuki; Nishida, Akira; Ohno, Tsutomu; Takeuchi, Yutaka; Togari, Hajime; Maeta, Haruo; Oguchi, Kouki

doi:10.1111/j.1442-200x.1992.tb01028.x

Cited by 50 publications

(56 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We were convinced that the dose was enough to exhibit affects on lungs of newborn rats similar to postnatal administration, because the dose of postnatal DXM was so much lower than that of clinical use for CLD (15)(16)(17), i.e. 3.3-12.5 g·kg Ϫ1 ·d Ϫ1 versus 0.5 mg·kg Ϫ1 ·d Ϫ1 (18,19).…”

Section: Antenatal Dexamethasone and Rat Lungsmentioning

confidence: 99%

Antenatal Dexamethasone Administration Impairs Normal Postnatal Lung Growth in Rats

et al. 2001

View full text Add to dashboard Cite

Our purpose was to determine the influences of antenatal dexamethasone administration on neonatal lung development in rats. Dexamethasone (0.4 mg/kg maternal body weight per day) was administered i.p. on the 21st d (group 1) or on the 20th and 21st d (group 2) of gestation in Sprague Dawley rats with timed pregnancies. After natural deliveries, the lungs of the pups 1-60 d of age were removed and processed for morphometric analysis. In 60-d-old pups, groups 1 and 2 both showed a lower numerical density of alveoli and a larger mean alveolar radius than control pups. Antenatal administration of dexamethasone to rats impairs the normal postnatal lung growth. Some aspects of the use of antenatal glucocorticoid therapy in humans may require reconsideration. Antenatal glucocorticoid therapy, including the administration of DXM and betamethasone, is widely used in the perinatal care of premature infants (1-3) The effects of antenatal glucocorticoid therapy include a reduction in the severity of respiratory distress syndrome, reductions in the incidences of several other complications associated with prematurity (hypotension, intracranial hemorrhage, etc.), and a reduction in mortality. In animal experiments, glucocorticoid administration appears to accelerate not only the establishment of the surfactant system, but also the activities of antioxidant enzymes (4) and, via surfactant-independent mechanisms, an increase in alveolar wall compliance (5).The growth of the lung during the human perinatal period consists of several phases (6): 1) the establishment of a surfactant system, 2) an increase in the number of alveoli through division of the existing alveoli (alveolarization), and 3) alveolar wall thinning and capillary fusion (microvascular maturation). The latter two phases are accompanied by structural changes. Alveolarization occurs mainly between the 35th wk of gestation and approximately the third postnatal year. Microvascular maturation begins after birth and is completed by 5 y of age. Alveolarization is said to occur only in the presence of immature thick septa (6).These three phases of lung growth have been observed in most mammals (6), but the times at which the phases occur differ among species. For example, the pulmonary ultrastructure of newborn rats corresponds to that of humans at about the 28th wk of gestation. In other words, rats are born before the process of alveolarization has begun. Alveolarization in the rat lung takes place predominantly within the first 2 wk of life, with microvascular maturation occurring during the third wk (7).Postnatal administration of DXM (1 g/d, i.e. 3.3-12.5 g·kg Ϫ1 ·d Ϫ1 , from d 2 to 15) is known to impair subsequent alveolarization in rats (8,9) During the first 2 wk, DXM accelerates microvascular maturation and suppresses alveolarization. One week after drug withdrawal, the trend toward precocious maturation is reversed. The alveolar wall returns to a more immature state, and a delayed burst of alveolarization begins. At d 60, the lungs appear emphysematous, with l...

show abstract

Section: Antenatal Dexamethasone and Rat Lungsmentioning

confidence: 99%

Antenatal Dexamethasone Administration Impairs Normal Postnatal Lung Growth in Rats

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Most definitions of BPD are solely based on the requirement for oxygen therapy (1-3), but oxygen dependence per se does not necessarily mean the presence of lung injury. Additional radiographic criteria do not necessarily indicate the extent of lung damage either, and are too subjective for consistent interpretation to be achieved (4,5). Accordingly, there is still no well-accepted definition of BPD.…”

mentioning

confidence: 99%

Plasma KL-6 Predicts the Development and Outcome of Bronchopulmonary Dysplasia

et al. 2006

View full text Add to dashboard Cite

Circulating KL-6 is a specific indicator of pulmonary injury affecting the alveolar epithelium and interstitium. Our preliminary study suggested the usefulness of plasma KL-6 as a marker of bronchopulmonary dysplasia (BPD). To confirm the diagnostic value of KL-6 for BPD as well as to determine the reference range, we conducted a larger prospective study in 135 preterm infants Ͻ32 wk GA. Among the infants without oxygen dependence at a postconceptional age of 36 wk, the plasma KL-6 level showed no significant association with GA at any time. Among 42 infants Ͻ28 wk GA, plasma KL-6 levels were significantly higher in those with moderate/ severe BPD compared with those with no/mild BPD. A plasma level of 199 U/mL at 1 wk or 232 U/mL at 2 wk was an excellent predictor of moderate/severe BPD Ͻ28 wk GA (positive predictive value of 83% and 80%, respectively). Unlike nonspecific markers of inflammation or fibrosis, KL-6 objectively reflects the severity of pulmonary injury irrespective of the treatment or the radiographic changes. Therefore, not only as a good marker, measurement of KL-6 may also help to provide new insights into the pathogenesis of BPD.

show abstract

“…With both methods, the arterial oxygen tension was maintained between 60 and 80 mm Hg with monitoring using a transcutaneous oxygen monitor for at least the first 6 days of life. CLD was defined as the requirement for extra oxygen supplementation beyond 28 days of age associated with symptoms of persistent respiratory distress and hazy lung fields on chest X-ray films [14]. None of the infants had a plasma IgM level of 1 20 mg/ dl, or a positive acute phase reactants score at birth.…”

Section: Subjectsmentioning

confidence: 99%

Oxidation Products of Uric Acid and Ascorbic Acid in Preterm Infants with Chronic Lung Disease

Ogihara¹,

Kim²,

Hirano³

et al. 1997

Neonatology

View full text Add to dashboard Cite

Allantoin, the oxidation product of uric acid (UA), can be used as an in vivo marker of free radical generation. The aims of the present study were to evaluate the allantoin changes in plasma and bronchoalveolar lavage fluid (BALF) as well as to examine plasma levels of ascorbic acid (AA) and its oxidation product, dehydroascorbic acid (DHAA), in infants with or without chronic lung disease (CLD) during the first week of life. The study population was 20 infants of 24–30 weeks gestation, comprising 10 who subsequently developed CLD and 10 without CLD. In the CLD infants, the plasma allantoin/UA ratio showed a significant increase after day 1 and continued to increase gradually to reach a peak on day 6 (6.5 ± 4.1% for CLD and 2.1 ± 0.9% for non-CLD infants). The allantoin/UA ratio in BALF was also higher in CLD infants and the difference reached significance on days 4–6 (41.2 ± 15.8% for CLD and 11.7 ± 9.9% for non-CLD infants). In contrast to allantoin, the plasma DHAA/AA ratio did not differ between the 2 groups throughout the study period. Our findings that the allantoin/UA ratios were significantly higher in CLD than non-CLD infants not only in plasma but also in BALF, and that the intergroup differences of this ratio in both plasma and BALF was more prominent in the latter half of the first week of life further confirm our previous speculation that oxygen radicals are involved in the development of neonatal CLD.

show abstract

Epidemiology of Neonatal Chronic Lung Disease in Japan

Cited by 50 publications

References 5 publications

Antenatal Dexamethasone Administration Impairs Normal Postnatal Lung Growth in Rats

Antenatal Dexamethasone Administration Impairs Normal Postnatal Lung Growth in Rats

Plasma KL-6 Predicts the Development and Outcome of Bronchopulmonary Dysplasia

Oxidation Products of Uric Acid and Ascorbic Acid in Preterm Infants with Chronic Lung Disease

Contact Info

Product

Resources

About