{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T16:18:27Z","timestamp":1777479507548,"version":"3.51.4"},"reference-count":48,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2016,7,10]],"date-time":"2016-07-10T00:00:00Z","timestamp":1468108800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Clin Appl Thromb Hemost"],"published-print":{"date-parts":[[2017,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>The incidence of neonatal hypoxic\u2013ischemic encephalopathy (HIE) is reportedly high in countries with limited resources. Its pathogenesis is multifactorial. A role for thrombophilia has been described in different patterns of preterm and full-term perinatal brain injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aim:<\/jats:title>\n                    <jats:p>This study aims to identify risk factors associated with neonatal HIE and also to determine the contributions of genetic thrombophilia in the development of neonatal HIE.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Sixty-seven neonates with HIE and 67 controls were enrolled in the study. Clinical history and examination were undertaken. Patients and controls were tested for the presence of factor V G1691A and prothrombin G20210A mutations. In addition, protein S, protein C, and antithrombin III levels were assessed.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>Parental consanguinity and performing emergency cesarean section (CS) were significant risk factors for neonatal HIE (odds ratio [OR] 6.5, 95% confidence interval [CI] 2.6-15.3, P &lt; .001, OR 12.6, 95% CI 2.52-63.3, P = .002, respectively). No significant difference was found regarding maternal age and parity. About 33% of cases and 6% of controls were found to have at least 1 thrombophilic factor ( P &lt; .001). Factor V G1691A mutation significantly increased the risk of neonatal HIE (OR 4.5, 95% CI 1.4-14.5, P = .012), while prothrombin G 20210A mutation and protein C deficiency were not.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Parental consanguinity, emergency CS, and factor V mutation may contribute to the higher risk of developing neonatal HIE.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1076029615607302","type":"journal-article","created":{"date-parts":[[2015,9,23]],"date-time":"2015-09-23T21:19:23Z","timestamp":1443043163000},"page":"266-273","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":6,"title":["Impact of Thrombophilia on the Risk of Hypoxic\u2013Ischemic Encephalopathy in Term Neonates"],"prefix":"10.1177","volume":"23","author":[{"given":"Nafisa H. R.","family":"AbdelAziz","sequence":"first","affiliation":[{"name":"Department of Pediatrics, Assiut University Children Hospital, Assiut, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hanan G.","family":"AbdelAzeem","sequence":"additional","affiliation":[{"name":"Department of Clinical Pathology, Assiut University, Assiut, Egypt"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eman M. 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