A Transplant Center Experience with Basiliximab Induction Strategies - A Double Edged Sword?

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<h3>Purpose</h3> The benefit of immunosuppression induction for heart transplant (HT) is debated given potential risks of infection and malignancy. Here, we report 18 years of patient outcomes from a large HT center to define the risks and benefits of Interleukin-2 receptor antagonist basiliximab (BX) induction when used as standardized induction or in selected patients only. <h3>Methods</h3> Retrospective single-center analysis of 475 consecutive HT recipients from 2003-2020. Patients were grouped by use of induction strategy in basiliximab group (BG) and no-basiliximab group (NBG). A subgroup analysis by era compared 2003-2015 standard BX induction and 2016-present with selective BX use. <h3>Results</h3> There were no clinically significant differences in gender and age between BG and NBG, though BG patients had lower baseline GFR than the NBG (62.8 vs 73.2, p=0.001) as well as higher PRA (p=0.01) (Fig A). When adjusted for confounders (sex, age, PRA, GFR) the BG was less likely to have acute cellular rejection (ACR) (OR 0.42, p <0.001), but had more antibody mediated rejection (AMR) (OR 11.7, p < 0.001) and more cardiac allograft vasculopathy at 5-years post HT (OR 3.8, p=0.04). There was no difference between BG and NBG in ejection fraction, DSA, malignancies and infections. When stratified by era (2003-2015 vs. 2016-present), ACR remains less common in the BG than NBG (35% vs 50%, p=0.045) while AMR remained more common (9.7 vs 0% p=0.005).In the pre-2016 the BG had more DSA (0 vs 11%, p <0.001). Notably there was no significant difference in survival comparing pre-and post-2016 NBG group, however both pre-2016 BG and post-2016 BG have significantly higher mortality (p=0.045 and 0.03) during post HT year 1-5 (Fig B). <h3>Conclusion</h3> Basiliximab reduces the incidence of ACR but increases AMR and CAV possibly associated with increased mortality both with use of standard and selective induction protocols. Further mechanistic studies are needed to describe a T-cell escape mechanism with enhanced humoral immunity and late complications.