title: [Markers of brain injury in non-invasive biological fluids].
abstract: Hypoxia-ischemia (H-I) constitutes the main phenomenon responsible for brain-blood barrier permeability modifications leading to cerebral vascular autoregulation loss in newborns. Hypotension, cerebral ischemia, and reperfusion are the main events involved in vascular auto-regulation loss leading to cell death and tissue damage. Reperfusion could be critical since organ damage, particularly of the brain, may be amplified during this period. An exaggerated activation of vasoactive agents, of calcium mediated effects could be responsible for reperfusion injury (R-I), which, in turns, leads to cerebral hemorrhage and damage. These phenomena represent a common repertoire in newborns complicated by perinatal acute or chronic hypoxia treated by risky procedures such as mechanical ventilation, nitric oxide supplementation, brain cooling, and extracorporeal membrane oxygenation (ECMO). Despite accurate monitoring, the post-insult period is crucial, as clinical symptoms and standard monitoring parameters may be silent at a time when brain damage is already occurring and the therapeutic window for pharmacological intervention is limited. Therefore, the measurement of circulating biochemical markers of brain damage, such as vasoactive agents and nervous tissue peptides is eagerly awaited in clinical practice to detect high risk newborns. The present article is aimed at investigating the role of dosage biochemical markers in non-invasive biological fluids such as S100B, a calcium binding protein, activin A, a protein expressed in Central nervous System (CNS).
authors.affiliation: Department of Fetal, Maternal and Neonatal Medicine, C. Armgo, Alessandria, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Moresco
authors.forename: V
authors.initials: V
authors.lastname: Bellissima
authors.forename: M
authors.initials: M
authors.lastname: Colivicchi
authors.forename: S
authors.initials: S
authors.lastname: Crivelli
authors.forename: F
authors.initials: F
authors.lastname: Guerriero
authors.forename: A
authors.initials: A
authors.lastname: Ricotti
authors.forename: M
authors.initials: M
authors.lastname: Sabatini
authors.forename: M C
authors.initials: MC
authors.lastname: Strozzi
authors.forename: F
authors.initials: F
authors.lastname: Temporini
authors.forename: D
authors.initials: D
authors.lastname: Gazzolo
mesh_terms: D028341:Activins / Q000652:urine*; D015415:Biomarkers / Q000032:analysis; D001925:Brain Damage, Chronic / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D016022:Case-Control Studies; D019281:Dimerization; D006801:Humans; D020925:Hypoxia-Ischemia, Brain / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D007231:Infant, Newborn; D007232:Infant, Newborn, Diseases / Q000378:metabolism; D009414:Nerve Growth Factors / Q000032:analysis* / Q000737:chemistry / Q000652:urine; D015427:Reperfusion Injury / Q000517:prevention & control; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000032:analysis* / Q000737:chemistry / Q000652:urine; D012463:Saliva / Q000737:chemistry*; D016482:Urinalysis
chemical_list: D015415:Biomarkers; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; C579160:S100B protein, human; C422405:activin A; D028341:Activins