Surgical biology for the clinician: vascular effects of immunosuppression.

摘要: Transplantation is the accepted treatment of end-stage organ failure. The introduction cyclosporine (CsA) in early 1980s greatly improved outcome solid transplantation, with an increase 3-year survival from almost 40% to 70%.1 Substantial advances development additional immunosuppressants have allowed transplant physicians more specifically modulate immune response according precise requirements both transplanted and patient receiving allograft.2 Although immunosuppressive agents are sufficient minimize allograft rejection promote short-term after a major limitation longer-term vasculopathy (AV).3–7 Central AV endothelial damage subsequent dysfunction. Endothelial dysfunction contributes intimal hyperplasia progressive plaque buildup that leads AV.8,9 attributable numerous factors, including preservation solutions, ischemia reperfusion injury, acute episodes, dyslipidemia, hypertension, diabetes use drugs.8,10 These factors elicit activation by disrupting homeo-static balance between endothelium-derived relaxing such as nitric oxide (NO) activating endothelin (ET-1).9–11 activated endothelium increases vascular resistance, adhesiveness, thrombogenicity risk atherogenesis.12 Many currently used cause transplantation may further accelerate AV. objective this review provide insight into effects most commonly immunosuppressants: CsA, tacrolimus (Tac), rapamycin (Rapa) its synthetic derivative everolimus (Erl), corticosteroids, azathioprine (AZA) mycophenolate mofetil (MMF). We also comparative discussion drugs’ benefits risks terms side offer preventative strategies emphasize tailoring regimen individual needs modification physiologic changes dictate.