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Solid organ transplantation has been accepted as a lifesaving treatment for patients with end-stage kidney, liver, heart, lung, and intestinal disease. The benefit of pancreas or islet cell transplant for type 1 diabetic patients is generally not immediate, however normoglycemia without the need for exogenous insulin following transplantation offers better quality of life and potentially reduces long-term diabetic complications.1,2 In 2007, 27,578 transplants were performed in the United States. Kidney transplant was most commonly performed followed by liver and heart. However, demand far surpasses supply with about 100,000 people on the waiting list to receive an organ.3

The physiologic barrier to solid organ transplant is recognition of the foreign antigens and subsequent orchestrated immune response. When this response is mounted against the allograft, it is referred to as "rejection". There are three types of graft rejection can occur after solid organ transplantation: humoral, acute cellular, and chronic rejection. Humoral rejection is mediated by antibodies against donor antigens present on the vascular endothelium and typically occurs intraoperatively or within days after receiving ABO blood type mismatched or positive crossmatch organ transplant. Avoiding mismatched transplant or desensitizing recipients with donor-specific antibodies may prevent this mode of rejection, but treating humoral rejection remains challenging. Acute cellular rejection is the most common type of rejection and is generally reversible with appropriate treatment. It results from an orchestrated immune response that involves alloantigen presentation by antigen presenting cells that leads to alloreactive T cells. The cytotoxic T cells infiltrate the graft and cause direct tissue damage, whereas the helper T cells produce cytokines to cause subsequent immunological and inflammatory events. Although acute cellular rejection can occur anytime following transplant, the risk is highest in the first several months after transplant. Prevention and treatment of acute cellular rejection is of utmost importance, as it is a significant predictor of chronic rejection. The exact etiology of chronic rejection is unknown. It is a slow process of graft fibrosis and arteriopathy, which results in graft dysfunction, usually manifested years after transplantation. While acute cellular rejection can be treated pharmacologically, the only therapy for chronic rejection is retransplantation.4

Signs and symptoms of rejection are nonspecific pain and tenderness over graft site, fever, and lethargy. If left untreated, rejection leads to clinically significant organ dysfunction. The diagnosis of rejection is made based on histological findings from a biopsy specimen of the transplant organ.4

Immunosuppression Regimen

TABLE 18-1 Commonly Used Immunosuppressive Agents in Solid Organ Transplantation

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