2004
DOI: 10.1016/j.cardfail.2004.06.271
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The effect of beta blocker use on cyclosporine level in cardiac transplant recipients

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Cited by 3 publications
(5 citation statements)
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“…To our knowledge, these are the first data on the effect of carvedilol on the bioavailability of tacrolimus in liver transplant recipients. Nevertheless, this observation confirms the results of Kaijser et al36 in kidney transplant recipients and those of Bader et al37 in cardiac transplant recipients. In particular, Bader et al recently supposed that carvedilol influences CNI levels through its effect on a membrane protein that regulates CNI absorption.…”
Section: Discussionsupporting
confidence: 91%
“…To our knowledge, these are the first data on the effect of carvedilol on the bioavailability of tacrolimus in liver transplant recipients. Nevertheless, this observation confirms the results of Kaijser et al36 in kidney transplant recipients and those of Bader et al37 in cardiac transplant recipients. In particular, Bader et al recently supposed that carvedilol influences CNI levels through its effect on a membrane protein that regulates CNI absorption.…”
Section: Discussionsupporting
confidence: 91%
“…For example, the inadvertent use of clarithromycin, an inhibitor of the cytochrome P‐450 3A4 pathway, for a simple urinary tract infection can double the serum TAC level and result in significant nephrotoxicity. P‐glycoprotein is a cell membrane‐associated protein that transports a variety of drug substances and influences drug absorption (in the intestine) and elimination (in the liver and kidney) (7). Carvedilol, a nonselective beta‐blocker with alpha‐blocking properties is metabolized by the cytochrome P‐450 2D6, but not the P‐450 3A4 pathway.…”
Section: Immunosuppressive Medicationsmentioning
confidence: 99%
“…Carvedilol, a nonselective beta‐blocker with alpha‐blocking properties is metabolized by the cytochrome P‐450 2D6, but not the P‐450 3A4 pathway. Carvedilol has been shown to increase serum levels of CNIs by inhibiting the P‐glycoprotein pathway (7,8). Other frequent potential interactions include allopurinol (which can increase levels of antimetabolites to toxic levels, especially AZA), nonsteroidal anti‐inflammatory medications (NSAIDs) (which can potentiate CNI‐induced nephrotoxicity) and spironolactone, which can increase CNI‐induced hyperkalemia.…”
Section: Immunosuppressive Medicationsmentioning
confidence: 99%
“…A potential issue with β‐blockade following transplantation is that cyclosporin levels may elevate (specific to carvedilol use) [19]. The proposed interaction is through the modulation of P‐glycoprotein, a membrane bound efflux pump that regulates cyclosporin absorption.…”
Section: Heart Rate Manipulationmentioning
confidence: 99%
“…The proposed interaction is through the modulation of P‐glycoprotein, a membrane bound efflux pump that regulates cyclosporin absorption. Given that raised cyclosporin has been associated with nephrotoxicity [20], in vivo cardiotoxicity [21] and an increased risk of malignancy [22], it has therefore been advised that a 10% dose reduction of cyclosporin should be considered upon the initiation of carvedilol [19].…”
Section: Heart Rate Manipulationmentioning
confidence: 99%