SOMATOSTATIN IN PRETERM INFANTS - POSTNATAL CHANGES AND RESPONSE TO STRESS

Citation
L. Jain et al., SOMATOSTATIN IN PRETERM INFANTS - POSTNATAL CHANGES AND RESPONSE TO STRESS, Biology of the neonate, 68(2), 1995, pp. 81-86
Citations number
15
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00063126
Volume
68
Issue
2
Year of publication
1995
Pages
81 - 86
Database
ISI
SICI code
0006-3126(1995)68:2<81:SIPI-P>2.0.ZU;2-O
Abstract
To determine the chronology of postnatal somatostatin (SRIF) changes i n preterm infants and the relationship of SRIF levels to respiratory a nd gastrointestinal complications, we evaluated sequential SRIF levels in 62 preterm infants in the first month of life. Weekly preprandial plasma samples were obtained and analyzed for SRIF using a radioimmuno assay. Additional blood samples were obtained at the time of abdominal events. Somatostatin levels were highest in week 2 and gradually decl ined in weeks 3 and 4 (mean +/- SD pmol/l, SRIF = 92.3 +/- 30.3 in wee k 2 vs. 79.8 +/- 33.9 in week 3 and 69.7 +/- 54.4 in week 4, p < 0.03) . Birth weight, gestational age and sex were not related to initial SR IF levels. Infants with respiratory distress requiring assisted ventil ation had significantly higher week 1 SRIF levels compared to infants without respiratory problems (97.9 +/- 22.7 vs. 74.9 +/- 21 pmol/l, p < 0.02). Twenty-one of the 62 infants had gastrointestinal complicatio ns. Somatostatin levels preceding (89.0 +/- 25.9 pmol/l), during(91.0 +/- 13.3) and after (79.3 +/- 28.6) the gastrointestinal events were n ot significantly different, nor were they different from SRIF concentr ations of age-matched preterm infants without gastrointestinal complic ations. The results suggest that in preterm infants, postnatal SRIF ch anges follow a definite pattern with peak concentrations in week 2. Re spiratory distress is associated with a significant increase in SRIF. However, subsequent gastrointestinal events do not lead to an increase in SRIF. This lack of SRIF response in gastrointestinal stress may pl ay a role in the pathogenesis of gut injury in the premature neonate.