Lipoprotein abnormalities are highly prevalent in pediatric heart transplant recipients.
The role of hyperlipidemia in graft coronary artery disease (GCAD) is controversial although hyper-triglyceridemia is an independent risk factor. Recent studies show that 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) inhibitors decrease the incidence of GCAD in adults. The incidence of GCAD in pediatric patients is lower than in adults; it is not clear whether age-related differences in lipid metabolism account for some of this protection. This study was performed to: characterize the lipoprotein profile in children after heart transplantation; demonstrate that total cholesterol (TC) is a poor marker for underlying lipoprotein abnormalities; and to compare lipid abnormalities in patients who had been converted from cyclosporin A (CsA) to tacrolimus. Seventy-one determinations of fasting lipoprotein profiles were performed in a cohort of 28 children. Each child had at least two determinations on separate occasions. TC, low-density lipoprotein (LDL), and serum triglyceride (TG) levels were categorized as abnormal if greater than the 75th percentile for age and gender. A high-density lipoprotein (HDL) level less than the 25th percentile was considered abnormal. Immunosuppression included CsA or tacrolimus, azathioprine, and prednisone. We found that 90% of the patients studied had abnormalities of either TG or HDL. In contrast, LDL tended to be normal when adjusted for age and gender. TC was a poor indicator of any underlying abnormality in TG, LDL, or HDL. In patients converted to tacrolimus, no significant differences were found in the levels of TG, LDL or HDL compared with each patient's respective values while receiving CsA. Hence, lipoprotein abnormalities among pediatric heart transplant recipients are highly prevalent. TC is a poor screening tool in the evaluation for lipid abnormalities. Lipoprotein profiles remain statistically unchanged after conversion from CsA to tacrolimus.
Division of Pediatric Cardiology, Stanford University, California, USA. clifford@leland.stanford.edu
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D000293:Adolescent; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D002648:Child; D002675:Child, Preschool; D003327:Coronary Disease / Q000097:blood / Q000209:etiology*; D016572:Cyclosporine / Q000009:adverse effects; D005260:Female; D016027:Heart Transplantation; D006801:Humans; D006949:Hyperlipidemias / Q000139:chemically induced* / Q000453:epidemiology; D007166:Immunosuppressive Agents / Q000009:adverse effects*; D007223:Infant; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D011241:Prednisone / Q000009:adverse effects*; D015995:Prevalence; D012044:Regression Analysis; D012307:Risk Factors; D018709:Statistics, Nonparametric; D016559:Tacrolimus / Q000009:adverse effects
D000893:Anti-Inflammatory Agents; D007166:Immunosuppressive Agents; D008074:Lipoproteins; D016572:Cyclosporine; D011241:Prednisone; D016559:Tacrolimus