Gastrointestinal and metabolic problems associated with immunosuppression with either CyA or FK 506 in liver transplantation.

Abstract

Since its introduction in 1979, CyA has been the immunosuppression agent of choice in clinical transplantation of all solid organs.1 More recently, a novel new immunosuppressive agent, FK 506, has been introduced in experimental transplantation.2 Most recently, it also has been introduced into clinical liver transplantation. Both agents appear to be T cell-specific and induce their immunosuppressive effects by impairing interleukin-2 production and receptor expression.3 Presumably, CyA initiates its immunosuppressive actions by an intracellular protein (receptor), cyclophillin, and by interacting with one or more calcium-binding proteins.4 In contrast, FK 506 appears to bind to a completely different intracellular protein, putatively called fugiphillin. Because these two drugs act via different binding proteins, and presumably follow different intermediate steps to produce T cell suppression, we have compared the two in terms of their untoward gastrointestinal and metabolic effects in liver transplant patients.