title: Soluble Fas (CD95/Apo-1), soluble Fas ligand, and activated caspase 3 in the cerebrospinal fluid of infants with posthemorrhagic and nonhemorrhagic hydrocephalus.
abstract: Hydrocephalus may result in loss of tissue associated with neuronal degeneration, axonal damage, and reactive gliosis. The soluble form of the anti-apoptotic regulator Fas (sFas) and the pro-apoptotic factors soluble FasL (sFasL) and activated caspase 3 were studied in the cerebrospinal fluid of infants with hydrocephalus. Fifteen preterm infants with posthemorrhagic hydrocephalus undergoing serial reservoir puncture and seven term or near-term infants with nonhemorrhagic hydrocephalus and shunt surgery were included in the study. Twenty-four age-matched patients with lumbar puncture for the exclusion of meningitis served as controls. Elevated levels of sFas were observed in infants with posthemorrhagic hydrocephalus [median (range), 131 ng/mL (51-279 ng/mL)] and in nonhemorrhagic hydrocephalus [127 ng/mL (35-165 ng/mL)]. sFas concentrations were highest in a subgroup of eight patients with posthemorrhagic hydrocephalus developing periventricular leukomalacia [164 ng/mL (76-227 ng/mL)]. In contrast, in 24 control infants, sFas was low, in 15 cases below detection limit (0.5 ng/mL) and in nine cases, 24 ng/mL (20-43 ng/mL). sFasL and activated caspase 3 did not differ from control infants in all groups of patients. Increased intrathecal release of sFas in the cerebrospinal fluid of infants with hydrocephalus may serve as an indicator of brain injury from progressive ventricular dilatation.
authors.affiliation: Department of Neonatology, Charité, Children's Hospital, Campus Virchow Klinikum, D-13353 Berlin, Germany. ursula.felderhoff@charite.de
authors.forename: Ursula
authors.initials: U
authors.lastname: Felderhoff-Mueser
authors.forename: Christoph
authors.initials: C
authors.lastname: Buhrer
authors.forename: Peter
authors.initials: P
authors.lastname: Groneck
authors.forename: Michael
authors.initials: M
authors.lastname: Obladen
authors.forename: Peter
authors.initials: P
authors.lastname: Bartmann
authors.forename: Axel
authors.initials: A
authors.lastname: Heep
mesh_terms: D017209:Apoptosis / Q000502:physiology; D053148:Caspase 3; D020169:Caspases / Q000134:cerebrospinal fluid*; D053222:Fas Ligand Protein; D006801:Humans; D006849:Hydrocephalus / Q000134:cerebrospinal fluid* / Q000473:pathology; D007231:Infant, Newborn; D007234:Infant, Premature; D020300:Intracranial Hemorrhages / Q000134:cerebrospinal fluid* / Q000150:complications / Q000473:pathology; D007969:Leukomalacia, Periventricular / Q000209:etiology / Q000473:pathology; D008297:Male; D008562:Membrane Glycoproteins / Q000134:cerebrospinal fluid*; D013129:Spinal Puncture; D019014:fas Receptor / Q000134:cerebrospinal fluid*
chemical_list: C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor; C505407:CASP3 protein, human; D053148:Caspase 3; D020169:Caspases