Immunosuppressants

Agents that block lymphocyte activation and proliferation. Reduce acute transplant rejection by suppressing cellular immunity (used as prophylaxis). Frequently combined to achieve greater efficacy with ¯ toxicity. Chronic suppression ­ risk of infection and malignancy.

DRUG MECHANISM OTHER USE TOXICITY NOTES
Cyclosporine Calcineurin inhibitor; binds cyclophilin. Blocks T-cell activation by preventing IL-2 transcription. Psoriasis, rheumatoid arthritis. Nephrotoxicity (arteriolar hyalinization, tubular vacuolization), hypertension, hyperlipidemia, neurotoxicity, gingival hyperplasia, hirsutism. Both calcineurin inhibitors are highly nephrotoxic
Tacrolimus (FK506) Calcineurin inhibitor; binds FK506 binding protein (FKBP). Blocks T-cell activation by preventing IL-2 transcription.   Similar to cyclosporine, ­ risk of diabetes and neurotoxicity; no gingival hyperplasia or hirsutism. Both calcineurin inhibitors are highly nephrotoxic
Sirolimus (Rapamycin) mTOR inhibitor; binds FKBP. Blocks T-cell activation and B-cell differentiation by preventing response to IL-2. Kidney transplant rejection prophylaxis specifically. “PanSirtopenia” (pancytopenia), insulin resistance, hyperlipidemia; not nephrotoxic. Kidney “sir-vives.” Synergistic with cyclosporine. Also used in drug-eluting stents.
Basiliximab Monoclonal antibody; blocks IL-2R. Kidney transplant rejection prophylaxis specifically. Edema, hypertension, tremor.  
Azathioprine Antimetabolite precursor of 6-mercaptopurine. Inhibits lymphocyte proliferation by blocking nucleotide synthesis. Rheumatoid arthritis, Crohn disease, glomerulonephritis, other autoimmune conditions. Pancytopenia. 6-MP degraded by xanthine oxidase to oxidized metabolites, toxicity ­ by allopurinol. 6-MP is also degrated by thiopurine methyltransferase to 6-methylmercaptopurine; Pronounce “azathiopurine.”
Mycophenolate Mofetil Reversibly inhibits IMP dehydrogenase, preventing purine synthesis of B and T cells. Lupus nephritis. GI upset, pancytopenia, hypertension, hyperglycemia. Less nephrotoxic and neurotoxic. Associated with invasive CMV infection.
Glucocorticoids Inhibit NF-κB. Suppress both B- and T-cell function by ¯ transcription of many cytokines. Induce T cell apoptosis. Many autoimmune and inflammatory disorders, adrenal insufficiency, asthma, CLL, non-Hodgkin lymphoma. Cushing syndrome, osteoporosis, hyperglycemia, diabetes, amenorrhea, adrenocortical atrophy, peptic ulcers, psychosis, cataracts, avascular necrosis (femoral head). Demargination of WBCs causes artificial leukocytosis. Adrenal insufficiency may develop if drug is stopped abruptly after chronic use.

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