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Albumin administration prevents neurological damage and death in a mouse model of
severe neonatal hyperbilirubinemia
#MMPMID26541892
Vodret S
; Bortolussi G
; Schreuder AB
; Ja?prová J
; Vitek L
; Verkade HJ
; Muro AF
Sci Rep
2015[Nov]; 5
(?): 16203
PMID26541892
show ga
Therapies to prevent severe neonatal unconjugated hyperbilirubinemia and
kernicterus are phototherapy and, in unresponsive cases, exchange transfusion,
which has significant morbidity and mortality risks. Neurotoxicity is caused by
the fraction of unconjugated bilirubin not bound to albumin (free bilirubin, Bf).
Human serum albumin (HSA) administration was suggested to increase plasma
bilirubin-binding capacity. However, its clinical use is infrequent due to
difficulties to address its potential preventive and curative benefits, and to
the absence of reliable markers to monitor bilirubin neurotoxicity risk. We used
a genetic mouse model of unconjugated hyperbilirubinemia showing severe
neurological impairment and neonatal lethality. We treated mutant pups with
repeated HSA administration since birth, without phototherapy application. Daily
intraperitoneal HSA administration completely rescued neurological damage and
lethality, depending on dosage and administration frequency. Albumin infusion
increased plasma bilirubin-binding capacity, mobilizing bilirubin from tissues to
plasma. This resulted in reduced plasma Bf, forebrain and cerebellum bilirubin
levels. We showed that, in our experimental model, Bf is the best marker to
determine the risk of developing neurological damage. These results support the
potential use of albumin administration in severe acute hyperbilirubinemia
conditions to prevent or treat bilirubin neurotoxicity in situations in which
exchange transfusion may be required.
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