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Article: Mannose-binding protein in preterm infants: Developmental profile and clinical significance

TitleMannose-binding protein in preterm infants: Developmental profile and clinical significance
Authors
Keywordsdevelopment
intrauterine growth retardation
mannose-binding protein
mutations
prematurity
preterm infants
Issue Date1995
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEI
Citation
Clinical And Experimental Immunology, 1995, v. 102 n. 3, p. 649-654 How to Cite?
AbstractThe aim of this study was to determine the developmental profile of mannose-binding protein (MBP) in preterm infants. MBP was measured in 885 longitudinally collected serum samples from 168 preterm infants, and 63 were genotyped with respect to the codon 54 mutation in the MBP gene. MBP level/codon 54 genotyping were also determined on the cord blood of 146/123 term infants and 138/123 adults, respectively. The best cut-off values of MBP for dividing preterm, term infants and adults into 'low' and 'high' MBP groups were 400 ng/ml (55 low, 113 high), 700 ng/ml (35 low, 111 high) and 750 ng/ml (33 low, 105 high), respectively, by achieving the least number of misclassifications according to the codon 54 mutation. The relative risk of the 'low' groups for presence of the codon 54 mutation compared with 'high' groups were 42.4, 67.9 and 22.9 for preterm, term infants and adults, respectively (P < 0.00001). The gestational age and birth weight of the 'low' (n = 55) and 'high' (n = 113) MBP groups of the 168 preterm infants were 29.5 ± 2.8 weeks, 30.5 ± 2.8 weeks (P = 0.03) and 1230 ± 317 g, 1277 ± 289 g (P = 0.35), respectively. The mean MBP levels of these two groups of preterm infants were different (P < 0.001) at all ages measured. As a whole group, the MBP level rose from a mean of 500 ng/ml at 25 weeks gestation to 1700 ng/ml at 20 weeks post full-term. The mortality rates of 'low' and 'high' MBP groups of preterm infants were 22% and 12%, respectively (P = 0.113). This difference in mortality was due to gestational age and birth weight standard deviation score (SDS) after adjusting for length of gestation and gender (P = 0.0001) rather than to low MBP levels (P = 0.65). MBP levels were not related to birthweight SDS score (P = 0.26). The mean ± s.d. MBP levels for preterm, term infants and adults without the codon 54 mutation were 1225 ± 701 ng/ml (n = 45), 2064 ± 829 ng/ml (n = 88) and 2473 ± 1395 ng/ml (n = 95), respectively; the corresponding values for those with the codon 54 mutation were 130 ± 275 ng/ml (n = 18), 533 ± 665 ng/ml (n = 35) and 330 ± 225 ng/ ml (n = 28), respectively. Intra-uterine growth retardation in preterm infants does not influence MBP levels. For those without the codon 54 mutation, there is a significant difference in MBP level between the three age groups. For those with the codon 54 mutation, there is a significant difference between preterm and term infants, but not between term infants and adults. We conclude that there is a maturation in MBP levels for preterm infants. and that a moderately low MBP phenotype does not affect survival. We cannot exclude an effect of profoundly reduced MBP levels (characteristic of homozygous for the codon 54 mutation). Since no such preterm infant was identified in this study.
Persistent Identifierhttp://hdl.handle.net/10722/49394
ISSN
2015 Impact Factor: 3.148
2015 SCImago Journal Rankings: 1.369
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLau, YLen_HK
dc.contributor.authorChan, SYen_HK
dc.contributor.authorTurner, MWen_HK
dc.contributor.authorFong, Jen_HK
dc.contributor.authorKarlberg, Jen_HK
dc.date.accessioned2008-06-12T06:41:20Z-
dc.date.available2008-06-12T06:41:20Z-
dc.date.issued1995en_HK
dc.identifier.citationClinical And Experimental Immunology, 1995, v. 102 n. 3, p. 649-654en_HK
dc.identifier.issn0009-9104en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49394-
dc.description.abstractThe aim of this study was to determine the developmental profile of mannose-binding protein (MBP) in preterm infants. MBP was measured in 885 longitudinally collected serum samples from 168 preterm infants, and 63 were genotyped with respect to the codon 54 mutation in the MBP gene. MBP level/codon 54 genotyping were also determined on the cord blood of 146/123 term infants and 138/123 adults, respectively. The best cut-off values of MBP for dividing preterm, term infants and adults into 'low' and 'high' MBP groups were 400 ng/ml (55 low, 113 high), 700 ng/ml (35 low, 111 high) and 750 ng/ml (33 low, 105 high), respectively, by achieving the least number of misclassifications according to the codon 54 mutation. The relative risk of the 'low' groups for presence of the codon 54 mutation compared with 'high' groups were 42.4, 67.9 and 22.9 for preterm, term infants and adults, respectively (P < 0.00001). The gestational age and birth weight of the 'low' (n = 55) and 'high' (n = 113) MBP groups of the 168 preterm infants were 29.5 ± 2.8 weeks, 30.5 ± 2.8 weeks (P = 0.03) and 1230 ± 317 g, 1277 ± 289 g (P = 0.35), respectively. The mean MBP levels of these two groups of preterm infants were different (P < 0.001) at all ages measured. As a whole group, the MBP level rose from a mean of 500 ng/ml at 25 weeks gestation to 1700 ng/ml at 20 weeks post full-term. The mortality rates of 'low' and 'high' MBP groups of preterm infants were 22% and 12%, respectively (P = 0.113). This difference in mortality was due to gestational age and birth weight standard deviation score (SDS) after adjusting for length of gestation and gender (P = 0.0001) rather than to low MBP levels (P = 0.65). MBP levels were not related to birthweight SDS score (P = 0.26). The mean ± s.d. MBP levels for preterm, term infants and adults without the codon 54 mutation were 1225 ± 701 ng/ml (n = 45), 2064 ± 829 ng/ml (n = 88) and 2473 ± 1395 ng/ml (n = 95), respectively; the corresponding values for those with the codon 54 mutation were 130 ± 275 ng/ml (n = 18), 533 ± 665 ng/ml (n = 35) and 330 ± 225 ng/ ml (n = 28), respectively. Intra-uterine growth retardation in preterm infants does not influence MBP levels. For those without the codon 54 mutation, there is a significant difference in MBP level between the three age groups. For those with the codon 54 mutation, there is a significant difference between preterm and term infants, but not between term infants and adults. We conclude that there is a maturation in MBP levels for preterm infants. and that a moderately low MBP phenotype does not affect survival. We cannot exclude an effect of profoundly reduced MBP levels (characteristic of homozygous for the codon 54 mutation). Since no such preterm infant was identified in this study.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CEIen_HK
dc.relation.ispartofClinical and Experimental Immunologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsClinical and Experimental Immunology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subjectdevelopmenten_HK
dc.subjectintrauterine growth retardationen_HK
dc.subjectmannose-binding proteinen_HK
dc.subjectmutationsen_HK
dc.subjectprematurityen_HK
dc.subjectpreterm infantsen_HK
dc.titleMannose-binding protein in preterm infants: Developmental profile and clinical significanceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0009-9104&volume=102&issue=3&spage=649&epage=654&date=1995&atitle=Mannose-binding+protein+in+preterm+infants:+developmental+profile+and+clinical+significanceen_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.emailChan, SY: sychan@hkucc.hku.hken_HK
dc.identifier.emailKarlberg, J: jpekarl@hkucc.hku.hken_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.identifier.authorityChan, SY=rp00356en_HK
dc.identifier.authorityKarlberg, J=rp00400en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid8536386-
dc.identifier.pmcidPMC1553372-
dc.identifier.scopuseid_2-s2.0-0029613269en_HK
dc.identifier.hkuros8406-
dc.identifier.volume102en_HK
dc.identifier.issue3en_HK
dc.identifier.spage649en_HK
dc.identifier.epage654en_HK
dc.identifier.isiWOS:A1995TM10000032-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridChan, SY=7404255082en_HK
dc.identifier.scopusauthoridTurner, MW=7403215582en_HK
dc.identifier.scopusauthoridFong, J=36790905200en_HK
dc.identifier.scopusauthoridKarlberg, J=7005218406en_HK

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