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Drug‐Cytokine Interactions: Focus on Cyclosporine
Author(s) -
Liao Janice S.,
Reiss William G.
Publication year - 1996
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1996.tb02970.x
Subject(s) - immune system , cytokine , nephrotoxicity , interleukin , immunology , tumor necrosis factor alpha , inflammation , drug , biology , pharmacology , transplant rejection , kidney , endocrinology
The immune system is a complex network that regulates and maintains the host's defense system. Changes and alterations in the immune system precipitate a series of reactions to prevent further damage as well as initiate repair. The systems cellular component relies on cytokines (interleukins, tumor necrosis factor, interferons, etc.) to facilitate communication in response to a foreign antigen. Cytokine concentrations are therefore elevated during times of inflammation, such as rejection of a transplanted organ. Recent research suggests that interleukin‐6 may have an inhibitory effect on cytochrome P‐450 3A and thus affect drug metabolism. Cyclosporine, which is administered to prevent rejection of transplanted organs, is metabolized primarily by the P‐450 3A system. Thus, the inhibitory effect of interleukin‐6 may alter cyclosporine concentrations, which in turn may increase its adverse effects, such as nephrotoxicity.