Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia

M. C. Bruce, K. E. Wedig, N. Jentoft, R. J. Martin, Pi-Wan Cheng, T. F. Boat, A. A. Fanaroff

Research output: Contribution to journalArticle

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Abstract

In order to determine whether elastin degradation is increased in infants whose respiratory insufficiency requires ventilation with high concentrations of O2, we quantitated, by amino acid analysis, the elastin degradation products (desmosines) excreted in the urine of 14 premature male infants during the first 3 wk of life. Eight of these infants, the 'low-O2' infants, did not have severe lung disease and did not require more than 40% O2 beyond the first 8 h of life. The other 6 infants, selected retrospectively because they developed bronchopulmonary dysplasia (BPD), were ventilated with more than 60% O2 for at least the first 72 h of life. The pattern of desmosine excretion observed in infants who developed BPD differed significantly (p < 0.05) from the excretion pattern seen in 'low-O2' infants during the first 3 wk of life. At the end of the first week of life, desmosine excretion was significantly greater (p < 0.05) in the infants who later developed BPD than in the 'low-O2' infants without severe lung disease. From Days 7-9 to 20-22, desmosine excretion increased in the 'low-O2' infants from 6.9 ± 1.7 μg/kg to 9.0 ± 3.5 μg/kg. In contrast, desmosine excretion did not remain elevated in the BPD infants, decreasing from 10.6 ± 2.2 μg/kg to 6.1 ± 2.9 μg/kg during the same period. In the BPD infants, elevated desmosine excretion through Day 9 is likely to reflect lung injury, whereas decreased desmosine excretion beyond Day 9 suggests that elastin synthesis and turnover is impaired, possibly as a result of nutritional deficiencies. The observed differences between desmosine excretion patterns in the 'low-O2' and BPD infants strongly suggests differences in elastin metabolism in the 2 groups of infants. Elastin is thought to play a critical role in alveolar septal development; therefore, destruction and/or impaired synthesis of elastin might be a causal factor in the impaired lung growth associated with BPD.

Original languageEnglish (US)
Pages (from-to)568-572
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume131
Issue number4
StatePublished - Jul 31 1985

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Bronchopulmonary Dysplasia
Elastin
Premature Infants
Desmosine
Lung Diseases
Lung Injury
Malnutrition
Respiratory Insufficiency
Ventilation

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Bruce, M. C., Wedig, K. E., Jentoft, N., Martin, R. J., Cheng, P-W., Boat, T. F., & Fanaroff, A. A. (1985). Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia. American Review of Respiratory Disease, 131(4), 568-572.

Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia. / Bruce, M. C.; Wedig, K. E.; Jentoft, N.; Martin, R. J.; Cheng, Pi-Wan; Boat, T. F.; Fanaroff, A. A.

In: American Review of Respiratory Disease, Vol. 131, No. 4, 31.07.1985, p. 568-572.

Research output: Contribution to journalArticle

Bruce, MC, Wedig, KE, Jentoft, N, Martin, RJ, Cheng, P-W, Boat, TF & Fanaroff, AA 1985, 'Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia', American Review of Respiratory Disease, vol. 131, no. 4, pp. 568-572.
Bruce, M. C. ; Wedig, K. E. ; Jentoft, N. ; Martin, R. J. ; Cheng, Pi-Wan ; Boat, T. F. ; Fanaroff, A. A. / Altered urinary excretion of elastin cross-links in premature infants who develop bronchopulmonary dysplasia. In: American Review of Respiratory Disease. 1985 ; Vol. 131, No. 4. pp. 568-572.
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abstract = "In order to determine whether elastin degradation is increased in infants whose respiratory insufficiency requires ventilation with high concentrations of O2, we quantitated, by amino acid analysis, the elastin degradation products (desmosines) excreted in the urine of 14 premature male infants during the first 3 wk of life. Eight of these infants, the 'low-O2' infants, did not have severe lung disease and did not require more than 40{\%} O2 beyond the first 8 h of life. The other 6 infants, selected retrospectively because they developed bronchopulmonary dysplasia (BPD), were ventilated with more than 60{\%} O2 for at least the first 72 h of life. The pattern of desmosine excretion observed in infants who developed BPD differed significantly (p < 0.05) from the excretion pattern seen in 'low-O2' infants during the first 3 wk of life. At the end of the first week of life, desmosine excretion was significantly greater (p < 0.05) in the infants who later developed BPD than in the 'low-O2' infants without severe lung disease. From Days 7-9 to 20-22, desmosine excretion increased in the 'low-O2' infants from 6.9 ± 1.7 μg/kg to 9.0 ± 3.5 μg/kg. In contrast, desmosine excretion did not remain elevated in the BPD infants, decreasing from 10.6 ± 2.2 μg/kg to 6.1 ± 2.9 μg/kg during the same period. In the BPD infants, elevated desmosine excretion through Day 9 is likely to reflect lung injury, whereas decreased desmosine excretion beyond Day 9 suggests that elastin synthesis and turnover is impaired, possibly as a result of nutritional deficiencies. The observed differences between desmosine excretion patterns in the 'low-O2' and BPD infants strongly suggests differences in elastin metabolism in the 2 groups of infants. Elastin is thought to play a critical role in alveolar septal development; therefore, destruction and/or impaired synthesis of elastin might be a causal factor in the impaired lung growth associated with BPD.",
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