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Cyclosporin

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Cyclosporin

Produced by fungus Tolypocladium inflatum Gams.

Mode of action

  • inhibits activation of T-cells without causing myelosuppression
  • exact site of action is not well defined

Pharmacokinetics

Administration: 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

  • Nephrotoxicity. 3 clinical syndromes:
    - 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
  • hypertension

Further reading

Leaker B, Cairns HS. Clinical aspects of cyclosporin nephrotoxicity. Br J Hosp Med, 1994; 52(10): 529-34


© Charles Gomersall December 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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