The Dept of Anaesthesia & Intensive Care, CUHK
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CyclosporinProduced by fungus Tolypocladium inflatum Gams. Mode of actionPharmacokineticsAdministration: IV/PO. Bioavailability 20-50%. Peak concentrations 3-4 h after dosing Elimination: t1/2 6 h. Metabolized in liver Drug interactions: phenytoin, phenobarbitone, cotrimoxazole and rifampicin effect liver metabolism causing increased clearance Adverse effects- acute toxicity: occurs in first 7 days of treatment. Usually presents as oliguria in patients who have received a cadaveric renal transplant but may also occur in native kidneys in patients who are treated with high doses. Can only be distinguished from rejection and preservation damage to the transplanted kidney by renal biopsy - subacute: generally occurs after at least 7 days of treatment and is present in varying degrees in all patients treated with cyclosporin. Both acute and subacute forms appear to mediated by a reversible increase in renovascular resistance. Both forms are dose-dependent; peak concentrations may be responsible. Concurrent use of calcium channel blockers may partially prevent acute and subacute toxicity but this has not achieved wide usage - chronic Further readingLeaker B, Cairns HS. Clinical aspects of cyclosporin nephrotoxicity. Br J Hosp Med, 1994; 52(10): 529-34 © Charles Gomersall December 1999 |
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