Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome
Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gest...
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Published in: | Disease markers Vol. 2014; no. 2014; pp. 1 - 7 |
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Cairo, Egypt
Hindawi Puplishing Corporation
01-01-2014
Hindawi Publishing Corporation John Wiley & Sons, Inc |
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Abstract | Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF-α, and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF-α, respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF-α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF-α. Body weight correlated negatively with IL-6 and positively with CRP and TNF-α. Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers. |
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AbstractList | Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF-α, and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF-α, respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF-α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF-α. Body weight correlated negatively with IL-6 and positively with CRP and TNF-α. Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers. Anatomopathologic studies have failed to define the fetal inflammatory response syndrome (FIRS) as a cause of fetal death. Here, liver fragments of perinatal autopsies were collected at a university hospital from 1990 to 2009 and classified according to the cause of death, perinatal stress, and gestational age (GA) of the fetus. IL-6, TNF- α , and C-reactive protein (CRP) expression were immunostained, respectively, with primary antibody. Cases with congenital malformation, ascending infection, and perinatal anoxia showed increased IL-6, CRP, and TNF- α , respectively. Prematures presented higher expression of IL-6 whereas term births showed higher expression of CRP. Cases classified as acute stress presented higher expression of IL-6 and TNF- α and cases with chronic stress presented higher expression of CRP. GA correlated negatively with IL-6 and positively with CRP and TNF- α . Body weight correlated negatively with IL-6 and positively with CRP and TNF- α . Despite the diagnosis of FIRS being clinical and based on serum parameters, the findings in the current study allow the inference of FIRS diagnosis in the autopsied infants, based on an in situ liver analysis of these markers. |
Audience | Academic |
Author | Vinícius da Silva, Marcos Pereira, Lívia Helena M. Guimarães, Camila S. O. Ramalho, Fernando S. Castellano, Lúcio Roberto Machado, Juliana Reis Rocha, Laura Penna Olegário, Janaínna Grazielle Pacheco Reis, Marlene Antônia dos Corrêa, Rosana Rosa Miranda |
AuthorAffiliation | 2 Biological Sciences Department, General Immunology Division, Triangulo Mineiro Federal University, 38025-180 Uberaba, MG, Brazil 3 Human Immunology Research and Education Group, Technical Health School of UFPB, Federal University of Paraiba, 58051-900 João Pessoa, PB, Brazil 1 Biological Sciences Department, General Pathology Division, Triangulo Mineiro Federal University, 38025-180 Uberaba, MG, Brazil 4 Pathology and Forensic Medicine Department, Ribeirão Preto Faculty of Medicine of São Paulo University, 14049-900 Ribeirão Preto, SP, Brazil |
AuthorAffiliation_xml | – name: 2 Biological Sciences Department, General Immunology Division, Triangulo Mineiro Federal University, 38025-180 Uberaba, MG, Brazil – name: 3 Human Immunology Research and Education Group, Technical Health School of UFPB, Federal University of Paraiba, 58051-900 João Pessoa, PB, Brazil – name: 1 Biological Sciences Department, General Pathology Division, Triangulo Mineiro Federal University, 38025-180 Uberaba, MG, Brazil – name: 4 Pathology and Forensic Medicine Department, Ribeirão Preto Faculty of Medicine of São Paulo University, 14049-900 Ribeirão Preto, SP, Brazil |
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CitedBy_id | crossref_primary_10_1159_000496203 crossref_primary_10_1177_0003319719896472 crossref_primary_10_1177_0961203320947154 crossref_primary_10_1016_j_prp_2018_10_016 crossref_primary_10_1155_2014_269681 crossref_primary_10_1590_s2175_97902022e20827x |
Cites_doi | 10.1016/0002-9378(61)90063-1 10.1590/S0021-75572007000700012 10.2223/JPED.2043 10.1515/JPM.2003.009 10.1542/peds.2008-1222 10.1155/2013/340959 10.1067/mob.2000.108885 10.1111/j.1471-0528.1986.tb07854.x 10.1016/S0002-9378(98)70272-8 10.1016/S0165-0378(02)00085-2 10.1515/JPM.2011.100 10.1152/ajpendo.00544.2001 10.1016/j.ajog.2004.06.086 10.1007/978-3-662-09224-8_1 10.1016/S0022-3476(67)80066-0 10.1053/jhep.2003.50009 10.1016/S0895-4356(01)00400-0 10.1055/s-2006-956773 10.1111/j.1651-2227.2000.tb03344.x 10.1111/j.1600-0897.2009.00791.x 10.1016/S0140-6736(95)91327-0 10.3109/10253891003667870 10.1016/0028-2243(90)90138-Q 10.1053/hupa.2001.24992 10.1620/tjem.221.181 10.1159/000076132 10.3109/15513815.2011.650505 10.1155/2010/790605 10.1038/jp.2010.53 10.1016/j.ejogrb.2009.07.015 |
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Contributor | Pereira, Lívia Helena M Vinícius da Silva, Marcos Guimarães, Camila S. O Castellano, Lúcio Roberto Machado, Juliana Reis Rocha, Laura Penna Ramalho, Fernando S Olegário, Janaínna Grazielle Pacheco Reis, Marlene Antônia dos Corrêa, Rosana Rosa Miranda |
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Copyright | Copyright © 2014 Lívia Helena M. Pereira et al. COPYRIGHT 2014 John Wiley & Sons, Inc. Copyright © 2014 Lívia Helena M. Pereira et al. 2014 |
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SubjectTerms | C-reactive protein C-Reactive Protein - genetics C-Reactive Protein - metabolism Female Fetal Death Fetal diseases Fetal Diseases - metabolism Fetal Diseases - mortality Gene Expression Health aspects Humans Infant, Newborn Interleukin-6 Interleukin-6 - genetics Interleukin-6 - metabolism Liver Liver - metabolism Patient outcomes Perinatal Death Physiological aspects Pregnancy Systemic Inflammatory Response Syndrome - metabolism Systemic Inflammatory Response Syndrome - mortality Tumor Necrosis Factor-alpha - metabolism |
Title | Interleukin-6 and C-Reactive Protein Are Overexpressed in the Liver of Perinatal Deaths Diagnosed with Fetal Inflammatory Response Syndrome |
URI | https://search.emarefa.net/detail/BIM-457602 https://dx.doi.org/10.1155/2014/252780 https://www.ncbi.nlm.nih.gov/pubmed/24659848 https://search.proquest.com/docview/1510103088 https://pubmed.ncbi.nlm.nih.gov/PMC3934536 |
Volume | 2014 |
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