Intravenously administered glucocorticoids, such as prednisone, are the standard of care in acute<unk> D and chronic<unk> D. The use of these glucocorticoids is designed to suppress the T-cell-mediated immune onslaught on the<unk>  tissues; however, in high doses, this immune-suppression raises the risk of infections and cancer relapse. Therefore, it is desirable to taper off the post-transplant high-level steroid doses to lower levels, at which point the appearance of mild<unk> D may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect.. Cyclosporine and tacrolimus are calcineurin inhibitors. Both substances are structurally different but have the same mechanism of action. Cyclosporin binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase A (known as cyclophilin), while tacrolimus binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase FKBP12. These complexes inhibit calcineurin, block dephosphorylation of the transcription factor NFAT of activated T-cells and its translocation into the nucleus. Standard prophylaxis involves the use of cyclosporine for six months with methotrexate. Cyclosporin levels should be maintained above 200 ng/ml. Other substances that have been studied for<unk> D treatment include, for example: sirolimus, pentostatin, etanercept, and alemtuzumab. In August 2017 the US FDA approved ibrutinib to treat chronic<unk> D after failure of one or more other systemic treatments.
Graft-versus-host disease
Transplant rejection
Cardiac allograft vasculopathy
Vasculogenic mimicry
Infectious tolerance
Disseminated disease
Chronic allograft nephropathy
Post-transplant lymphoproliferative disorder