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Polymorphisms in cytokine genes do not predict progression to end-stage heart failure in children

Published online by Cambridge University Press:  15 August 2006

Steven A. Webber
Affiliation:
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Gerard J. Boyle
Affiliation:
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Steven Gribar
Affiliation:
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Yuk Law
Affiliation:
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Pamela Bowman
Affiliation:
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Susan A. Miller
Affiliation:
Department of Pediatrics, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Mohammed R. Awad
Affiliation:
Department of Pathology, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Mamun Ahmed
Affiliation:
Department of Pathology, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Joan Martell
Affiliation:
Department of Pathology, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA
Adriana Zeevi
Affiliation:
Department of Pathology, University of Pittsburgh School of Medicine, Children's Hospital of Pittsburgh and Thomas E. Starzl Transplant Institute, Pittsburgh, USA

Abstract

A number of cytokines have been implicated in the pathophysiology of congestive heart failure. Genetic polymorphisms of several cytokine genes are known to result in altered gene expression, enabling us to characterize patients as "high" or "low" producers of specific cytokines. We speculate that the cytokine genotypes for a population of children who underwent heart transplantation for end-stage ventricular failure due to cardiomyopathy or congenital heart disease would be enriched for "high producers" of pro-inflammatory cytokines and "low producers" of anti-inflammatory cytokines. Methods: Cytokine genotyping was performed for the following cytokines on 94 transplanted children using polymerase chain reaction-sequence specific technique: tumor necrosis factor-α (−308), interleukin 10 (−1082, −819, −592), interleukin 6 (−174), transforming growth factor-β1(codons 10 & 25), and interferon-γ (+874). Patients with ventricular failure after transplantation for dilated cardiomyopathy, numbering 37, or for congenital heart disease, numbering 34, were compared to 15 children transplanted for structural disease, such as hypoplastic left heart syndrome, without ventricular failure, and to data from healthy children. An additional 8 children with restrictive or hypertrophic cardiomyopathy were also studied. Results: No differences in genotypic distribution were seen between the groups, and all patients were comparable to genotypic distributions as assessed from published normal data. Conclusion: No evidence is found to support the hypothesis that these polymorphisms for cytokine genes influence progression to end-stage heart failure in children undergoing transplantation because of cardiomyopathy or congenital heart disease.

Type
Original Article
Copyright
2002 Cambridge University Press

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