"Norspan se nesm\u00ED pou\u017E\u00EDvat sou\u010Dasn\u011B s\u00A0inhibitory MAO nebo u pacient\u016F, kter\u00FDm byly inhibitory MAO pod\u00E1v\u00E1ny b\u011Bhem uplynul\u00FDch dvou t\u00FDdn\u016F (viz bod 4.3).\n\u00DA\u010Dinky jin\u00FDch l\u00E1tek na farmakokinetiku buprenorfinu:\nBuprenorfin je prim\u00E1rn\u011B metabolizov\u00E1n glukuronidac\u00ED a v\u00A0men\u0161\u00ED m\u00ED\u0159e (p\u0159ibli\u017En\u011B 30\u00A0%) pomoc\u00ED CYP3A4. Sou\u010Dasn\u00E1 l\u00E9\u010Dba inhibitory CYP3A4 m\u016F\u017Ee v\u00E9st ke zv\u00FD\u0161en\u00FDm plazmatick\u00FDm koncentrac\u00EDm se zv\u00FD\u0161enou \u00FA\u010Dinnost\u00ED buprenorfinu.\nVe studii l\u00E9kov\u00E9 interakce s\u00A0inhibitorem CYP3A4 ketokonazolem nebylo zji\u0161t\u011Bno klinicky v\u00FDznamn\u00E9 zv\u00FD\u0161en\u00ED pr\u016Fm\u011Brn\u00E9 hodnoty maxim\u00E1ln\u00ED koncentrace (Cmax) nebo celkov\u00E9 expozice (AUC) buprenorfinu po sou\u010Dasn\u00E9m pod\u00E1n\u00ED p\u0159\u00EDpravku Norspan \uFFFDs ketokonazolem ve srovn\u00E1n\u00ED s\u00A0pod\u00E1n\u00EDm samotn\u00E9ho p\u0159\u00EDpravku Norspan.\nInterakce mezi buprenorfinem a induktory enzymu CYP3A4 nebyly studov\u00E1ny. Sou\u010Dasn\u00E9 pod\u00E1n\u00ED p\u0159\u00EDpravku Norspan a induktor\u016F enzymu (nap\u0159. fenobarbital, karbamazepin, fenytoin a rifampicin) by mohlo v\u00E9st ke zv\u00FD\u0161en\u00ED clearance, a t\u00EDm i ke sn\u00ED\u017Een\u00ED \u00FA\u010Dinnosti.\nRedukce hepat\u00E1ln\u00EDho krevn\u00EDho ob\u011Bhu indukovan\u00E1 n\u011Bkter\u00FDmi celkov\u00FDmi anestetiky (nap\u0159. halothanem) a jin\u00FDmi l\u00E9\u010Div\u00FDmi p\u0159\u00EDpravky m\u016F\u017Ee v\u00E9st ke sn\u00ED\u017Een\u00ED rychlosti eliminace buprenorfinu v j\u00E1trech.\nFarmakodynamick\u00E9 interakce:\nNorspan se mus\u00ED u\u017E\u00EDvat se zvl\u00E1\u0161tn\u00ED opatrnost\u00ED s: \nBenzodiazepiny: Tato kombinace m\u016F\u017Ee potencovat respira\u010Dn\u00ED \u00FAtlum centr\u00E1ln\u00EDho p\u016Fvodu s\u00A0rizikem \u00FAmrt\u00ED (viz bod 4.4). \nOstatn\u00EDmi l\u00E1tkami vyvol\u00E1vaj\u00EDc\u00EDmi \u00FAtlum centr\u00E1ln\u00EDho nervov\u00E9ho syst\u00E9mu: jako jsou ostatn\u00ED opioidn\u00ED deriv\u00E1ty (analgetika a antitusika obsahuj\u00EDc\u00ED nap\u0159. morfin, dextropropoxyfen, kodein, dextromethorfan nebo noskapin). N\u011Bkter\u00E1 antidepresiva, antagonist\u00E9 H1-receptoru se\u00A0sedativn\u00EDm \u00FA\u010Dinkem, alkohol, anxiolytika, neuroleptika, klonidin a podobn\u00E9 l\u00E1tky. Tyto kombinace zvy\u0161uj\u00ED \u00FAtlum CNS.\nBuprenorfin je \u010D\u00E1ste\u010Dn\u00FDm agonistou m\u00ED-receptoru, av\u0161ak uv\u00E1d\u00ED se, \u017Ee p\u0159i typick\u00FDch analgetick\u00FDch d\u00E1vk\u00E1ch funguje jako \u010Dist\u00FD agonista m\u00ED-receptoru. Tyto d\u00E1vky vedou k\u00A0srovnateln\u00E9 nebo vy\u0161\u0161\u00ED expozici buprenorfinu, ne\u017E je expozice produkovan\u00E1 transderm\u00E1ln\u00EDmi n\u00E1plastmi Norspan 5, 10, a 20 \u00B5g/h. V\u00A0klinick\u00FDch studi\u00EDch sleduj\u00EDc\u00EDch Norspan, v\u00A0jejich\u017E r\u00E1mci byly subjekt\u016Fm pod\u00E1v\u00E1ny agonist\u00E9 opioidn\u00EDho m\u00ED-receptoru (a\u017E do d\u00E1vky 90 mg morfinu peror\u00E1ln\u011B nebo ekvivalentn\u00ED denn\u00ED d\u00E1vky), a pot\u00E9 byly subjekty p\u0159evedeny na Norspan, nebyl zaznamen\u00E1n abstinen\u010Dn\u00ED syndrom nebo syndrom z\u00A0vysazen\u00ED opioidu b\u011Bhem p\u0159echodu z opioidu na Norspan (viz bod\u00A04.4).\n \n"@cs . . . . . . . . "4.5\tInterakce s\u00A0jin\u00FDmi l\u00E9\u010Div\u00FDmi p\u0159\u00EDpravky a jin\u00E9 formy interakce"@cs . . "004.005" . . .