S100B testing in pregnancy

Michetti, Fabrizio; Gazzolo, Diego

doi:10.1016/s0009-8981(03)00243-2

Cited by 40 publications

(29 citation statements)

References 76 publications

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“…9,75,76 One such biomarker is S100␤. 77,78 We found that in human preterm fetuses, HMGB1 is a very strong predictor of systemic S100␤ levels, independently of gestational age, birth weight, or cord blood IL-6 levels. This finding is consistent with the intracellular location of these two DAMP molecules and absence of the classical NF-B and AP1 response elements on the S100␤ promoter.…”

Section: Damps and Fetal Inflammation 971mentioning

confidence: 75%

Characterization of RAGE, HMGB1, and S100β in Inflammation-Induced Preterm Birth and Fetal Tissue Injury

Buhimschi

Baumbusch

Dulay

et al. 2009

The American Journal of Pathology

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Immune activation represents an adaptive reaction triggered by both noxious exogenous (microbes) and endogenous [high mobility group box-1 protein (HMGB1), S100 calcium binding proteins] inducers of inflammation. Cell stress or necrosis lead the release of HMGB1 and S100 proteins in the extracellular compartment where they act as damage-associated molecular pattern molecules (or alarmins) by engaging the receptor for advanced glycation end-products (RAGE). Although the biology of RAGE is dictated by the accumulation of damage-associated molecular pattern molecules at sites of tissue injury, the role of RAGE in mediating antenatal fetal injury remains unknown. First, we studied the relationships at birth between the intensity of human fetal inflammation and sRAGE (an endogenous RAGE antagonist), HMGB1, and S100␤ protein. We found significantly lower sRAGE in human fetuses that mounted robust inflammatory responses. HMGB1 levels correlated significantly with levels of interleukin-6 and S100␤ in fetal circulation. We then evaluated the levels and areas of tissue expression of RAGE, HMGB1, and S100␤ in specific organs of mouse fetuses on E16. Using an animal model of endotoxin-induced fetal damage and preterm birth, we determined that inflammation induces a significant change in expression of RAGE and HMGB1, but not S100␤, at sites of tissue damage. Our findings indicate that RAGE and Conventional wisdom holds that the primary causes of the high neonatal morbidity and mortality attendant preterm birth are complications of immature organ systems.1-4 However, a growing body of investigation suggests that the poor outcome observed in many preterm children is not entirely dependent on their gestational age at birth. 2,5,6 After correcting for gestational age, several risk factors remain significantly associated with an increased risk of cerebral palsy, such as intra-amniotic infection, histological chorioamnionitis, prolonged rupture of the membranes, and hypoxemic fetal growth re-

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Section: Damps and Fetal Inflammation 971mentioning

confidence: 75%

Characterization of RAGE, HMGB1, and S100β in Inflammation-Induced Preterm Birth and Fetal Tissue Injury

Buhimschi

Baumbusch

Dulay

et al. 2009

The American Journal of Pathology

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“…A recent study demonstrated that a few parameters (out of 36 tested) were unaffected during uncomplicated pregnancy, delivery, and the early postpartum period, suggesting a need to implement gestational age-specific reference intervals [23]. S100B has already been tested in pregnancy in amniotic fluid or cord blood to evaluate the fetal brain damages or the presence of a protein's gradient between fetal and maternal bloodstreams [24,25], but not in maternal blood during physiological pregnancy. Both the Roche Diagnostics ® and DiaSorin ® methods found that S100B levels in pregnant women were not significantly different between trimesters and largely comparable to the general population (p < 0.001).…”

Section: Discussionmentioning

confidence: 99%

Preanalytical, analytical, gestational and pediatric aspects of the S100B immuno-assays

Bouvier

Duret

Rouzaire

et al. 2016

Clinical Chemistry and Laboratory Medicine (CCLM)

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Background: Traumatic brain injury management is a tricky issue in children and pregnant women (due to adverse effects of computer tomography). To facilitate management, we report the main analytical performances and reference ranges for blood tests for the wellestablished S100B biomarker in under-16 children on a DiaSorin ® Liaison XL analyzer and in pregnant women on DiaSorin ® Liaison XL and Roche Diagnostics ® Cobas e411 analyzers. Methods: Serum S100B concentrations were determined by chemiluminescent immunoassay on a DiaSorin ® analyzer in a population of 409 healthy children aged 0-16 years and on DiaSorin

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“…An either suppressive or promoting role has been documented for S100 proteins, with regard to multiple tumor types, especially of solid nature (Table 1) [7,[12][13][14][15]. Based on these findings, it is not surprising that S100 proteins are being determined in various biological fluids (sputum, blood, urine, synovial, pleural [4], cerebrospinal [18], and amniotic fluid [16]) in feces [4] and in biopsy specimens, including placental [16].…”

Section: S100 Proteins and Extradigestive Diseasesmentioning

confidence: 99%

Calprotectin, Calgranulin C, and Other Members of the S100 Protein Family in Inflammatory Bowel Disease

et al. 2011

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S100B testing in pregnancy

Cited by 40 publications

References 76 publications

Characterization of RAGE, HMGB1, and S100β in Inflammation-Induced Preterm Birth and Fetal Tissue Injury

Characterization of RAGE, HMGB1, and S100β in Inflammation-Induced Preterm Birth and Fetal Tissue Injury

Preanalytical, analytical, gestational and pediatric aspects of the S100B immuno-assays

Calprotectin, Calgranulin C, and Other Members of the S100 Protein Family in Inflammatory Bowel Disease

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