Improved phagocyte response by co-amoxiclav in renal transplant recipients

Infectious diseases are a major source of morbidity and mortality for immunosuppressed transplant recipients and the antimicrobial chemotherapy can be often less effective in these individuals, because the contribution of underlying host defenses is absent. The influence of co-amoxiclav on the funct...

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Veröffentlicht in:Transplantation 2001-02, Vol.71 (4), p.575-577
Hauptverfasser: CUFFINI, Anna Maria, TULLIO, Vivian, GIACCHINO, Franca, BONINO, Alessandro, MANDRAS, Narcisa, BIANCHI, Nicoletta, ROANA, Janira, SCALAS, Daniela, BONELLO, Franco, CARLONE, Nicola A
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Sprache:eng
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Zusammenfassung:Infectious diseases are a major source of morbidity and mortality for immunosuppressed transplant recipients and the antimicrobial chemotherapy can be often less effective in these individuals, because the contribution of underlying host defenses is absent. The influence of co-amoxiclav on the functions of polymorphonuclear granulocytes (PMNs) from renal transplant recipients were investigated. PMNs from renal transplant recipients showed a diminished phagocytic activity with reduced phagocytosis and bactericidal activity against intracellular Klebsiella pneumoniae, compared to that seen with PMNs from healthy subjects. Co-amoxiclav significantly elicited the functions of PMNs from uremic patients, resulting in an increased percentage of ingested klebsiellae and in a higher bactericidal effect (98-99%), compared with the drug-free control system. When PMNs were collected from renal transplant recipients treated with co-amoxiclav a significant high increase in both phagocytosis and killing activity were detected, showing the co-amoxiclav capability of "restoring" even in vivo the depressed primary functions of PMNs. The interesting beneficial properties of co-amoxiclav, which result in restoring the phagocyte-dependent response in renal transplant patients both in vitro and in vivo, may make this drug more suitable for the treatment of infections in patients with defects of phagocyte functions.
ISSN:0041-1337
1534-6080
DOI:10.1097/00007890-200102270-00016