Arteritis and increased intracellular calcium as a possible mechanism for tacrolimus-related cardiac toxicity in a pediatric transplant recipient

Transplantation. 1997 Sep 15;64(5):773-5. doi: 10.1097/00007890-199709150-00020.

Abstract

We recently reported partially to wholly reversible hypertrophic cardiomyopathy, including severe hypertrophic obstructive cardiomyopathy, as a side effect in pediatric transplant recipients receiving tacrolimus immunosuppression. This seemed to be dose related. We describe a pediatric patient receiving tacrolimus who died 3 weeks after liver/bowel transplantation. Postmortem findings revealed arteritis of cardiac arteries and extensive calcification of cardiac tissue suggesting a possible mechanism of tacrolimus cardiac toxicity. This is consistent with recent reports of tacrolimus increasing calcium release into the sarcoplasmic reticulum of cardiac and striated muscle.

Publication types

  • Case Reports

MeSH terms

  • Arteritis / chemically induced*
  • Arteritis / metabolism*
  • Calcium / metabolism*
  • Cardiomyopathy, Hypertrophic / chemically induced
  • Cardiomyopathy, Hypertrophic / etiology*
  • Carrier Proteins / metabolism
  • Child, Preschool
  • Humans
  • Immunosuppressive Agents / pharmacology*
  • Immunosuppressive Agents / toxicity
  • Intestine, Small / transplantation*
  • Liver Transplantation / adverse effects*
  • Male
  • Sarcoplasmic Reticulum / chemistry
  • Tacrolimus / metabolism
  • Tacrolimus / pharmacology*
  • Tacrolimus / toxicity
  • Transplantation, Homologous / adverse effects

Substances

  • Carrier Proteins
  • Immunosuppressive Agents
  • Calcium
  • Tacrolimus