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INTRODUCTION

Successful medical management of the lung transplant patient requires manipulation of the immune system to prevent graft rejection while avoiding an increased risk for infection. This balance between rejection and infection is a key determinant of the long-term survival of these patients. The pharmacologic management of lung transplant recipients varies by institution, and the optimal regimen has not yet been defined. Currently, a variety of induction and maintenance regimens are used.1

IMMUNOSUPPRESSION

To attenuate graft injury resulting from immunologic rejection, all lung transplant patients require lifelong systemic immunosuppression. Immunosuppression of lung transplant recipients can be divided into three parts: induction phase, maintenance phase, and management of rejection. The drugs used for the induction phase and maintenance phase are summarized in Table 113-1.

Table 113-1IMMUNOSUPPRESSIVE DRUGS

Induction Therapy

Acute cellular rejection remains a significant problem in lung transplantation and is strongly associated with the development of chronic rejection. More than one-third of patients require treatment for acute cellular rejection during the first year after transplant.1 Induction therapy, defined as augmented immunosuppression given during the perioperative or immediate postoperative period, is added to the maintenance immunosuppression regimen to attenuate the risk of early rejection and thereby improve survival. However, induction therapy is not universally adopted by all transplant centers, with approximately 60 percent of adults undergoing lung transplantation receiving induction therapy.1 Because early allograft injury is thought to result from T-cell responses, induction strategies focus on inhibition of T cells.2

In recent years, more than 80% of patients receiving induction therapy in the United States received basiliximab, an IL-2 receptor antagonist. Basiliximab acts by blocking T-cell activation thus preventing T cell proliferation and differentiation. Because it acts only on activated T cells, it does not result in T-cell depletion and is generally well tolerated. With increased use of IL-2 receptor ...

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