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PII‐9
Author(s) -
Graff J.,
Reiche C.,
Gossmann J.,
Harder S.
Publication year - 2006
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2005.12.134
Subject(s) - platelet , immunosuppression , flow cytometry , mycophenolate , platelet activation , sirolimus , renal function , monocyte , integrin alpha m , pharmacology , medicine , immunology , transplantation , endocrinology , chemistry
BACKGROUND Rapamycin (RAPA) is a new makrolide type immunosuppressive drug that has been controversial discussed to induce platelet hyperreagibility. In contrast to mycofenolate mofetil (MMF) platelet activation has been confirmed under azathioprin (AZA) therapy. METHODS In a substudy of a clinical trial platelet function of renal transplant patients treated with AZA (n=6) or MMF (n=6) was investigated before and 3 months after conversion to rapamycin. CD 62P, PAC1, platelet‐monocyte interaction[CD41, CD11b (all as mean fluorescence intensity, MFI)] and CD40L (%+ platelets) was assessed by flow cytometry. RESULTS In AZA treated patients CD 62P decreases significantly (p<0,05) from 193±56 to 139±81 and CD41 (MFI) from 1530±260 to 576±218. CD11b (505±128 to 327±78) and CD40L (34±4 to 28±11) were also reduced but did not reach statistical significance. In an additional vitro investigation incubation of whole blood with increasing doses of rapamycin (from 50 to 1000ng/ml) did not result in any significant changes of platelet activation parameters. Platelet function in former MMF treated patients was unchanged after conversion to RAPA. CONCLUSION The conversion of immunosuppression from AZA to RAPA leads to a slight decrease of previous platelet activation. We found no evidence for increased platelet activation in RAPA patients. Clinical Pharmacology & Therapeutics (2005) 79 , P37–P37; doi: 10.1016/j.clpt.2005.12.134