Daniel Bernstein

Publication Details

  • Induction therapy for pediatric and adult heart transplantation: Comparison between OKT3 and daclizumab TRANSPLANTATION Chin, C., Pittson, S., Luikart, H., Bernstein, D., Robbins, R., Reitz, B., Oyer, P., Valantine, H. 2005; 80 (4): 477-481

    Abstract:

    Induction therapy can reduce morbidity and early mortality in pediatric and adult heart transplant recipients. Monoclonal and polyclonal agents are most widely used; they nonspecifically deplete the T-cell pool and are thus associated with drug-induced side effects. The cytokine release syndrome is one of the most problematic events associated with induction. Daclizumab, a highly humanized, specific interleukin-2 receptor blocker, may be efficacious to the monoclonal agent, OKT3. Due to its specific action and properties, the safety profile of this agent may be superior to OKT3.Forty subjects received daclizumab and their clinical outcomes were compared against a historical group of 40 subjects who received OKT3. Three- and six-month outcome measures included survival, rejection history, steroid burden, and complications.Mortality was low between the groups with equivalent 6-month survival. No differences in rejection profile or time to the first significant rejection event were detected; no subject had severe acute rejection within the first 180 days. Steroid requirement for maintenance immunosuppression and treatment of rejection was also similar between the groups. Six-month prevalence for complications were significantly different; 55% of OKT3-treated subjects having at least one event compared to 33% of daclizumab-treated subjects (P=0.04). The likelihood of complications occurred within the first month after transplantation.Daclizumab induction therapy is as efficacious as OKT3 in the prevention of early acute rejection after heart transplantation among pediatric and adult subjects. Complications related to the induction agent are significantly lower in the humanized product.

    View details for DOI 10.1097/01.tp.0000168153.50774.30

    View details for Web of Science ID 000231566800008

    View details for PubMedID 16123721

Stanford Medicine Resources:

Footer Links: