1996 Abstracts The American Pediatric Society and The Society for Pediatric Research

Pediatric Research (1996) 39, 23–23; doi:10.1203/00006450-199604001-00145


Veneracion G Cabana1, Samuel S Gidding1, Godfrey S Getz1 and Stanford T Shulman1

1Children's Memorial Hospital, University of Chicago and Northwestern University Medical Schools, Chicago, IL.

Lipoproteins participate in the acute response to inflammation. In animal models of acute inflammation and in adult humans with acute myocardial infarction, high density lipoprotein (HDL) levels decrease and serum amyloid A(SAA) increases and is incorporated into HDL. We previously showed that HDL cholesterol and apolipoprotein A1 (apoA1) levels are dramatically low in acute Kawasaki disease (KD) and that the decline is associated with increased SAA. In this study we prospectively assessed the time course of changes in HDL composition in children with acute KD. 12 KD children had plasma obtained before initiation of treatment; 7 had follow-up specimens obtained 2 weeks(n=6) or 6 weeks later. Total cholesterol, triglycerides (TG), HDL cholesterol total and SAA in HDL, core TG in HDL (as%), and apoA1 were measured in each specimen. SAA increased and was present in HDL acutely but not at follow-up. At diagnosis, mean total cholesterol (133 mg/dl), HDL cholesterol (20 mg/dl), and apoA1 (52 mg/dl) levels were below the normal range while core TG was increased (52%). In paired comparisons, total cholesterol, HDL cholesterol and apoA1 all increased (+29 mg/dl, p<0.05; +14 mg/dl, p< 0.0001; +48 mg/dl, p<0.0001 respectively), whereas core TG decreased by 12% (p<0.05) despite no change in plasma TG levels. These studies describe participation of HDL in the acute phase response of KD; this response includes incorporation of SAA into HDL and the recruitment of core TG in exchange for cholesterol ester in the particle. Recovery towards normal begins within 2 weeks of therapy. This is the first demonstration of the participation of HDL in the acute phase response in children.