Intrauterine Inflammation as a Risk Factor for Persistent Ductus Arteriosus Patency after Cyclooxygenase Inhibition in Extremely Low Birth Weight Infants

Objectives To test the hypothesis that intrauterine inflammation increases prostaglandin production and may be a risk factor for persistent ductus arteriosus after therapy with indomethacin, a nonselective cyclooxygenase inhibitor. Study design Indomethacin therapy was started after confirming ductu...

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Veröffentlicht in:The Journal of pediatrics 2010-11, Vol.157 (5), p.745-750.e1
Hauptverfasser: Kim, Eun Sun, MD, Kim, Ee-Kyung, MD, Choi, Chang Won, MD, Kim, Han-Suk, MD, Kim, Beyong Il, MD, Choi, Jung-Hwan, MD, Park, Joong Shin, MD, Moon, Kyung Chul, MD
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container_end_page 750.e1
container_issue 5
container_start_page 745
container_title The Journal of pediatrics
container_volume 157
creator Kim, Eun Sun, MD
Kim, Ee-Kyung, MD
Choi, Chang Won, MD
Kim, Han-Suk, MD
Kim, Beyong Il, MD
Choi, Jung-Hwan, MD
Park, Joong Shin, MD
Moon, Kyung Chul, MD
description Objectives To test the hypothesis that intrauterine inflammation increases prostaglandin production and may be a risk factor for persistent ductus arteriosus after therapy with indomethacin, a nonselective cyclooxygenase inhibitor. Study design Indomethacin therapy was started after confirming ductus arteriosus within 24 hours after birth in extremely low birth weight infants. After one cycle of therapy, infants with closed ductus were classified as responders, and those with patent ductus were classified as nonresponders. Multiple logistic regression analysis was used to determine important perinatal factors associated with persistent ductus arteriosus. Immunohistochemistry with cyclooxygenase antibodies and radioimmunoassay by 6-keto prostaglandin F1α kit were used to determine the relationship between intrauterine inflammation and ductal patency. Results Forty-one infants were responders, and 37 infants were nonresponders. Responders were frequently small for gestational age; nonresponders frequently had lower gestational age, respiratory distress syndrome, and intrauterine inflammation. By multiple logistic regression analysis, respiratory distress syndrome and intrauterine inflammation were more frequent in nonresponders. Cyclooxygenase-1 expression in the umbilical arteries and plasma 6-keto prostaglandin F1α levels were higher in nonresponders. Conclusions Respiratory distress syndrome and intrauterine inflammation were independent risk factors for persistent ductus arteriosus after indomethacin therapy in extremely low-birth weight infants. Intrauterine inflammation may have a negative influence on ductus arteriosus closure via increased cyclooxygenase-1 activity.
doi_str_mv 10.1016/j.jpeds.2010.05.020
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Study design Indomethacin therapy was started after confirming ductus arteriosus within 24 hours after birth in extremely low birth weight infants. After one cycle of therapy, infants with closed ductus were classified as responders, and those with patent ductus were classified as nonresponders. Multiple logistic regression analysis was used to determine important perinatal factors associated with persistent ductus arteriosus. Immunohistochemistry with cyclooxygenase antibodies and radioimmunoassay by 6-keto prostaglandin F1α kit were used to determine the relationship between intrauterine inflammation and ductal patency. Results Forty-one infants were responders, and 37 infants were nonresponders. Responders were frequently small for gestational age; nonresponders frequently had lower gestational age, respiratory distress syndrome, and intrauterine inflammation. By multiple logistic regression analysis, respiratory distress syndrome and intrauterine inflammation were more frequent in nonresponders. Cyclooxygenase-1 expression in the umbilical arteries and plasma 6-keto prostaglandin F1α levels were higher in nonresponders. Conclusions Respiratory distress syndrome and intrauterine inflammation were independent risk factors for persistent ductus arteriosus after indomethacin therapy in extremely low-birth weight infants. Intrauterine inflammation may have a negative influence on ductus arteriosus closure via increased cyclooxygenase-1 activity.</description><identifier>ISSN: 0022-3476</identifier><identifier>EISSN: 1097-6833</identifier><identifier>DOI: 10.1016/j.jpeds.2010.05.020</identifier><identifier>PMID: 20598319</identifier><identifier>CODEN: JOPDAB</identifier><language>eng</language><publisher>Maryland Heights, MO: Mosby, Inc</publisher><subject>Biological and medical sciences ; Cardiology. Vascular system ; Congenital heart diseases. Malformations of the aorta, pulmonary vessels and vena cava ; Cyclooxygenase Inhibitors - therapeutic use ; Ductus Arteriosus, Patent - drug therapy ; Ductus Arteriosus, Patent - epidemiology ; Ductus Arteriosus, Patent - etiology ; Epidemiology ; Female ; Fetal Diseases ; General aspects ; Heart ; Humans ; Indomethacin - therapeutic use ; Infant, Extremely Low Birth Weight ; Infant, Newborn ; Inflammation - complications ; Male ; Medical sciences ; Pediatrics ; Pilot Projects ; Public health. Hygiene ; Public health. Hygiene-occupational medicine ; Risk Factors ; Treatment Failure</subject><ispartof>The Journal of pediatrics, 2010-11, Vol.157 (5), p.745-750.e1</ispartof><rights>Mosby, Inc.</rights><rights>2010 Mosby, Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 Mosby, Inc. 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Study design Indomethacin therapy was started after confirming ductus arteriosus within 24 hours after birth in extremely low birth weight infants. After one cycle of therapy, infants with closed ductus were classified as responders, and those with patent ductus were classified as nonresponders. Multiple logistic regression analysis was used to determine important perinatal factors associated with persistent ductus arteriosus. Immunohistochemistry with cyclooxygenase antibodies and radioimmunoassay by 6-keto prostaglandin F1α kit were used to determine the relationship between intrauterine inflammation and ductal patency. Results Forty-one infants were responders, and 37 infants were nonresponders. Responders were frequently small for gestational age; nonresponders frequently had lower gestational age, respiratory distress syndrome, and intrauterine inflammation. By multiple logistic regression analysis, respiratory distress syndrome and intrauterine inflammation were more frequent in nonresponders. Cyclooxygenase-1 expression in the umbilical arteries and plasma 6-keto prostaglandin F1α levels were higher in nonresponders. Conclusions Respiratory distress syndrome and intrauterine inflammation were independent risk factors for persistent ductus arteriosus after indomethacin therapy in extremely low-birth weight infants. Intrauterine inflammation may have a negative influence on ductus arteriosus closure via increased cyclooxygenase-1 activity.</description><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Congenital heart diseases. Malformations of the aorta, pulmonary vessels and vena cava</subject><subject>Cyclooxygenase Inhibitors - therapeutic use</subject><subject>Ductus Arteriosus, Patent - drug therapy</subject><subject>Ductus Arteriosus, Patent - epidemiology</subject><subject>Ductus Arteriosus, Patent - etiology</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Fetal Diseases</subject><subject>General aspects</subject><subject>Heart</subject><subject>Humans</subject><subject>Indomethacin - therapeutic use</subject><subject>Infant, Extremely Low Birth Weight</subject><subject>Infant, Newborn</subject><subject>Inflammation - complications</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Pediatrics</subject><subject>Pilot Projects</subject><subject>Public health. Hygiene</subject><subject>Public health. 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Hygiene-occupational medicine</topic><topic>Risk Factors</topic><topic>Treatment Failure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Eun Sun, MD</creatorcontrib><creatorcontrib>Kim, Ee-Kyung, MD</creatorcontrib><creatorcontrib>Choi, Chang Won, MD</creatorcontrib><creatorcontrib>Kim, Han-Suk, MD</creatorcontrib><creatorcontrib>Kim, Beyong Il, MD</creatorcontrib><creatorcontrib>Choi, Jung-Hwan, MD</creatorcontrib><creatorcontrib>Park, Joong Shin, MD</creatorcontrib><creatorcontrib>Moon, Kyung Chul, MD</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of pediatrics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Eun Sun, MD</au><au>Kim, Ee-Kyung, MD</au><au>Choi, Chang Won, MD</au><au>Kim, Han-Suk, MD</au><au>Kim, Beyong Il, MD</au><au>Choi, Jung-Hwan, MD</au><au>Park, Joong Shin, MD</au><au>Moon, Kyung Chul, MD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intrauterine Inflammation as a Risk Factor for Persistent Ductus Arteriosus Patency after Cyclooxygenase Inhibition in Extremely Low Birth Weight Infants</atitle><jtitle>The Journal of pediatrics</jtitle><addtitle>J Pediatr</addtitle><date>2010-11-01</date><risdate>2010</risdate><volume>157</volume><issue>5</issue><spage>745</spage><epage>750.e1</epage><pages>745-750.e1</pages><issn>0022-3476</issn><eissn>1097-6833</eissn><coden>JOPDAB</coden><abstract>Objectives To test the hypothesis that intrauterine inflammation increases prostaglandin production and may be a risk factor for persistent ductus arteriosus after therapy with indomethacin, a nonselective cyclooxygenase inhibitor. Study design Indomethacin therapy was started after confirming ductus arteriosus within 24 hours after birth in extremely low birth weight infants. After one cycle of therapy, infants with closed ductus were classified as responders, and those with patent ductus were classified as nonresponders. Multiple logistic regression analysis was used to determine important perinatal factors associated with persistent ductus arteriosus. Immunohistochemistry with cyclooxygenase antibodies and radioimmunoassay by 6-keto prostaglandin F1α kit were used to determine the relationship between intrauterine inflammation and ductal patency. Results Forty-one infants were responders, and 37 infants were nonresponders. Responders were frequently small for gestational age; nonresponders frequently had lower gestational age, respiratory distress syndrome, and intrauterine inflammation. By multiple logistic regression analysis, respiratory distress syndrome and intrauterine inflammation were more frequent in nonresponders. Cyclooxygenase-1 expression in the umbilical arteries and plasma 6-keto prostaglandin F1α levels were higher in nonresponders. Conclusions Respiratory distress syndrome and intrauterine inflammation were independent risk factors for persistent ductus arteriosus after indomethacin therapy in extremely low-birth weight infants. Intrauterine inflammation may have a negative influence on ductus arteriosus closure via increased cyclooxygenase-1 activity.</abstract><cop>Maryland Heights, MO</cop><pub>Mosby, Inc</pub><pmid>20598319</pmid><doi>10.1016/j.jpeds.2010.05.020</doi><tpages>6</tpages></addata></record>
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subjects Biological and medical sciences
Cardiology. Vascular system
Congenital heart diseases. Malformations of the aorta, pulmonary vessels and vena cava
Cyclooxygenase Inhibitors - therapeutic use
Ductus Arteriosus, Patent - drug therapy
Ductus Arteriosus, Patent - epidemiology
Ductus Arteriosus, Patent - etiology
Epidemiology
Female
Fetal Diseases
General aspects
Heart
Humans
Indomethacin - therapeutic use
Infant, Extremely Low Birth Weight
Infant, Newborn
Inflammation - complications
Male
Medical sciences
Pediatrics
Pilot Projects
Public health. Hygiene
Public health. Hygiene-occupational medicine
Risk Factors
Treatment Failure
title Intrauterine Inflammation as a Risk Factor for Persistent Ductus Arteriosus Patency after Cyclooxygenase Inhibition in Extremely Low Birth Weight Infants
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