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E Albengres

Publications and source records attributed to E Albengres.

85 records · Page 5Linked to original sources
PubMedDate not supplied

[Cyclosporin A and ketoconazole, drug interaction or therapeutical combination?].

Cyclosporin A is potentiated by ketoconazole, mainly by inhibiting its P-450 dependent biotransformations. The other interest of ketoconazole is related to its antifungal effect, which is often used in immunodepressed patients. Thus for both pharmacodynamic and pharmacokinetic reasons, the combination of the two drugs is of interest. Another advantage is that whereas ketoconazole is a cheap drug, cyclosporin A is an expensive one, thus their combination may save a part of the cyclosporin A cost. Various questions remain to be solved: is it useful to combine in the same tablet selected amounts of the two drugs and if so in which ratio? Such a strategy supposes that intra and inter-individual variability of cyclosporin A metabolism in humans can be tightly monitored. Is it without risk to definitely inhibit some P-450 isoenzymes? Could not the expected simplification of drug dosages generate the need for more cyclosporin A blood level assays, thus leading to an additional cost?

Cyclosporine↗
PubMedDate not supplied

[Value of protecting mitochondrial functions during treatment with cyclosporin A].

The use of cyclosporin A is often limited by its nephrotoxicity. This dose-dependent toxicity can occur in all kinds of transplantation and is reversed with drug withdrawal. Cyclosporin A induces a vasoconstriction leading to an increase of renal vascular resistance and a reduction of glomerular filtration. Histochemical studies show mitochondrial alterations and an excess of cytosolic and mitochondrial calcium leading to a decrease of ATP synthesis. Two strategies can be evoked for limiting cyclosporin-A-induced nephrotoxicity. First, the use of drugs counteracting the vasoconstriction has been proposed. Second, drugs acting by restoration of ATP synthesis could also be of interest. For example, calcium channel blockers may be used for limiting the Ca2+ fluxes into cells. Another way to protect ATP synthesis is to inhibit the cyclosporin-A-induced increase of mitochondrial Ca2+ concentrations; Trimetazidine has shown its efficiency in vitro for protecting mitochondria against these modifications of Ca2+ homeostasis and is under clinical evaluation.

Animals↗