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Immunosuppressive agents drug interactions

Mignat C. Clinically significant drug interactions with new immunosuppressive agents. Drug Saf 1997 16(4) 267-78. [Pg.1746]

Compare and contrast the currently available immunosuppressive agents in terms of mechanisms of action, adverse events, and drug-drug interactions. [Pg.829]

Sirolimus is currently the only FDA-approved ToR inhibitor. One of its derivatives, everolimus, is in phase III clinical trials and has been approved for use in some European countries.30 Sirolimus is a macrolide antibiotic that has no effect on cal-cineurin phosphatase.11,31,32 Sirolimus inhibits T cell activation and proliferation by binding to and inhibiting the activation of the mammalian ToR, which suppresses cellular response to IL-2 and other cytokines (i.e., IL-4 and IL-15J.11,31 Studies have shown that sirolimus may be used safely and effectively with either cyclosporine or tacrolimus as a replacement for either azathioprine or mycophenolate mofetil.33 However, when using both sirolimus and cyclosporine as part of a patient s immunosuppressant therapy, because of a drug interaction between the two resulting in a marked increase in sirolimus concentrations, it is recommended to separate the sirolimus and cyclosporine doses by at least 4 hours. Sirolimus also can be used as an alternative agent for patients who do not tolerate calcineurin inhibitors due to nephrotoxicity or other adverse events.34... [Pg.842]

The following drug classes may have a potential drug interaction with nevirapine Antiarrhythmics, anticonvulsants, antifungals, calcium channel blockers, cancer chemotherapy (cyclophosphamide), ergot alkaloids, immunosuppressants, motility agents, opiate agonists. [Pg.1890]

Drug interactions When using combinations of immunosuppressive agents, the dose of each agent, including Orthoclone OKT3, should be reduced to the lowest level compatible with an effective therapeutic response so as to reduce the potential for and severity of infections and malignant transformations. [Pg.290]

Until the role of echinacea in immune modulation is better defined, this agent should be avoided in patients with immune deficiency disorders (eg, AIDS, cancer), autoimmune disorders (eg, multiple sclerosis, rheumatoid arthritis), and patients with tuberculosis. While there are no reported drug interactions for echinacea, some preparations have a high alcohol content and should not be used with medications known to cause a disulfiram-like reaction. In theory, echinacea should also be avoided in persons taking immunosuppressant medications (eg, organ transplant recipients). [Pg.1356]

Anaizi, N. Drug interactions involving immunosuppressive agents. Graft 2001, 4, 232-247. [Pg.874]

Lake KD, Canafax DM. Important interactions of drugs with immunosuppressive agents used in transplant recipients. J Antimicrob Chemother 1995 36 11-22. [Pg.1641]

Glucocorticoid chemistry, pharmacokitietics, and drug interactions are described in Chapter 59. Prednisone, prednisolone, and other glucocorticoids are used alone and in combination with other immunosuppressive agents for treatment of transplant rejection and autoimmune disorders. [Pg.910]

Hepatic or renal insufficiency does not significantly alter the pharmacokinetics of CP (194). Since immunosuppressive activity resides exclusively in the metabolites of CP (i.e., phosphoromide mustard and acrolein), pharmacokinetics are not predicted by the parent compound. Correlations between CP pharmacokinetics and pharmacodynamics are difficult to demonstrate. Measuring the metabolites is technically difficult (211). Drug interaction with other cytotoxic agents may increase neutropenia. One case report found the combination of CP plus infliximab was more likely to cause T-cell lymphopenia than either agent alone (212). [Pg.136]

Enzymes that are addressed by major drugs have been studied in particular detail. Thus, well above one hundred stmctures have been reported for dihydrofolate reductases from a variety of organisms, including major pathogens such as Mycobacterium tuberculosis, which is the causative agent of tuberculosis, and of Plasmodium falciparum, which is the most important of the Plasmodium spp. that causes malaria. The interaction of mammalian dihydrofolate reductases with inhibitors that are used as cytostatic agents and/or immunosuppressants is also documented extensively by X-ray stmctures. [Pg.256]


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See also in sourсe #XX -- [ Pg.90 , Pg.91 , Pg.93 , Pg.97 , Pg.98 ]




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