natgillin/translations-raw huggingface dataset:
In vitro, ketoconazole, classified as a strong CYP3A4 and P-glycoprotein (P-gp) inhibitor, has been shown to be a multi-pathway CYP and P-gp/breast cancer resistance protein (BCRP) inhibitor for riociguat metabolism and excretion (see section 5.2).
In vitro je ketokonazol, močan zaviralec CYP3A4 in glikoproteina-P (P-gp), zaviral več presnovnih poti ali izločanja riociguata preko CYP in P-gp/protein odpornosti na raka dojke (BCRP - breast cancer resistance protein) (glejte poglavje 5.2).
In vitro, lamivudine inhibited OCT1 and OCT2.
In vitro je lamivudin zaviral OCT1 in OCT2.
In vitro, levetiracetam and its primary metabolite have been shown not to inhibit the major human liver cytochrome P450 isoforms (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 and 1A2), glucuronyl transferase (UGT1A1 and UGT1A6) and epoxide hydroxylase activities.
In vitro so pokazali, da levetiracetam in njegov primarni presnovek ne zavirata aktivnosti glavnih izooblik človeškega jetrnega citokroma P450 (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 in 1A2), glukuronil- transferaze (UGT1A1 in UGT1A6) in epoksid-hidroksilaze.
In vitro, levetiracetam and its primary metabolite have been shown not to inhibit the major human liver cytochrome P450 isoforms (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 and 1A2), glucuronyl transferase (UGT1A1 AND UGT1A6]) and epoxide hydroxylase activities.
In vitro so pokazali, da levetiracetam in njegov primarni presnovek ne zavirata aktivnosti glavnih izooblik človeškega jetrnega citokroma P450 (CYP3A4, 2A6, 2C9, 2C19, 2D6, 2E1 in 1A2), glukuronil-transferaze (UGT1A1 in UGT1A6) in epoksid-hidroksilaze.
In vitro, liraglutide has shown very low potential to be involved in pharmacokinetic interactions with other active substances related to cytochrome P450 and plasma protein binding.
V poskusih in vitro je bila ugotovljena zelo majhna možnost medsebojnega farmakokinetičnega delovanja liraglutida in drugih zdravilnih učinkovin, ki bi bilo povezano s citokromom P450 ali vezavo na beljakovine v plazmi.
In vitro, lurasidone demonstrated no direct, or weak inhibition (direct or time-dependent) (IC50>5.9 μM) of the enzymes cytochrome P450 (CYP)1A2, CYP2B6, CYP2C8, CYP2C9,
Lurasidon in vitro ni neposredno ali šibko zaviral (neposredno ali v odvisnosti od časa) (IC50 > 5,9 μM) encimov citokroma P450 (CYP)1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19,
In vitro, N-desmethyl enzalutamide is metabolized to the carboxylic acid metabolite by carboxylesterase 1, which also plays a minor role in the metabolism of enzalutamide to the carboxylic acid metabolite.
N-desmetil enzalutamid se in vitro presnovi v presnovek karboksilne kisline s karboksilesterazo 1, ki ima tudi manjšo vlogo pri presnovi enzalutamida v presnovek karboksilne kisline.
In vitro, olaparib has been shown to be an inhibitor of OATP1B1, OCT1, OCT2, OAT3, MATE1 and MATE2K.
In vitro je ugotovljeno, da olaparib zavira OATP1B1, OCT1, OCT2, OAT3, MATE1 in MATE2K.
In vitro, olaparib inhibits the efflux transporter P-gp (IC50 = 76µM), therefore it cannot be excluded that olaparib may cause clinically relevant drug interactions with substrates of P-gp (e.g. simvastatin, pravastatin, dabigatran, digoxin, colchicine).
In vitro olaparib zavira efluksni prenašalec P-gp (IC50 = 76 µM), zato ni mogoče izključiti klinično pomembnih medsebojnih delovanj olapariba s substrati P-gp (npr. s simvastatinom, pravastatinom, dabigatranom, digoksinom, kolhicinom).
In vitro, olaparib produced little/no inhibition of CYPs 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6 or 2E1 and is not expected to be a clinically significant time dependent inhibitor of any of these P450 enzymes.
In vitro je olaparib le malo ali sploh nič zavrl CYP 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6 ali 2E1 in ni pričakovati, da bi bil klinično pomemben časovno odvisen zaviralec katerega od encimov P450.
In vitro, oritavancin 46.6 μg/mL did not affect an assay for activated protein C resistance (APCR), suggesting that there is a low likelihood that oritavancin will interfere with this test.
In vitro oritavancin v odmerku 46,6 μg/ml ni vplival na preizkus odpornosti proti aktiviranemu proteinu C (APCR, activated protein C resistance), kar kaže na majhno verjetnost, da bo oritavancin vplival na ta preizkus.
In vitro, osimertinib does not inhibit OAT1, OAT3, OATP1B1, OATP1B3 and MATE2K at clinically relevant concentrations.
In vitro osimertinib v klinično pomembnih koncentracijah ne zavira OAT1, OAT3, OATP1B1, OATP1B3 ali MATE2K.
In vitro, perampanel inhibited AMPA- induced (but not NMDA-induced) increase in intracellular calcium.
In vitro je perampanel zavrl povečanje intracelularnega kalcija, ki ga sproži AMPA (vendar ga ne sproži NMDA).
In vitro, siltuximab dose-dependently inhibited the growth of an IL-6-dependent murine plasmacytoma cell line in response to human IL-6.
In vitro je siltuksimab (odvisno od odmerka) zaviral z IL-6-stimulirano rast celične linije od IL-6 odvisnega glodalskega plazmacitoma.
In vitro, slow metabolic turnover of velpatasvir by CYP2B6, CYP2C8, and CYP3A4 was observed.
In vitro so zabeležili počasno presnovo velpatasvirja s citokromi CYP2B6, CYP2C8 in CYP3A4.
In vitro, some macrolide antibiotics like erythromycin inhibited the activity of bovine Cytochrom P 450-enzymes (CYP3A4-subclass).
In vitro lahko nekateri makrolidni antibiotiki, kot je eritromicin, zavirajo delovanje govejega Citohroma P 450-encima (CYP3A4-podrazred).
In vitro, strontium ranelate:
In vitro stroncijev ranelat:
In vitro, the binding of cabazitaxel to human serum proteins was 89-92% and was not saturable up to 50,000 ng/ml, which covers the maximum concentration observed in clinical studies.
In vitro je bila vezava kabazitaksela na beljakovine v človeškem serumu 82–92 % in ni bila saturabilna do 50.000 ng/ml; to vključuje največjo koncentracijo, ugotovljeno v kliničnih študijah.
In vitro, the extent of human plasma protein binding for 14C-labeled metabolites was 80.6% to 98.0% for PBA (over 1-250 microgram/ml), and 37.1% to 65.6% for PAA (over 5-500 microgram /ml).
In vitro je stopnja vezave na beljakovine v plazmi za presnovke, označene s 14C, od 80,6 % do 98,0 % za PBA (prek 1–250 mikrogramov/ml) in od 37,1 % do 65,6 % za PAA (prek 5–500 mikrogramov/ml).
In vitro, the lenvatinib blood-to-plasma concentration ratio ranged from 0.589 to 0.608 (0.1 – 10 μg/mL, mesilate).
Razmerje koncentracij lenvatiniba v krvi in plazmi in vitro je bilo v mejah od 0,589 do 0,608 (0,1-10 μg/ml, mesilat).
In vitro, the percent bound to rat albumin, human albumin and human serum was 98.4%, 95.4% and 99.1%, respectively.
In vitro je znašal odstotek zdravila, vezanega na podganje albumine 98,4%, na človeške albumine 95,4% in na humani serum 99,1%.
In vitro, TNF-induced secretion of interleukin (IL)-6, IL-8 and granulocyte-macrophage colony stimulating factor (GM-CSF) by human endothelial cells was also inhibited by golimumab.
In vitro pa golimumab tudi zavira s TNF sproženo sekrecijo interlevkina (IL)-6, IL-8 in spodbujevalnega faktorja za granulocitno-makrofagne kolonije (GM-CSF) iz človeških endotelijskih celic.
In vitro, topotecan did not inhibit human P450 enzymes CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A, or CYP4A nor did it inhibit the human cytosolic enzymes dihydropyrimidine or xanthine oxidase.
Topotekan in vitro ni zaviral delovanja encimov človeškega P450 (CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A in CYP4A) in tudi ne človeških citosolskih encimov dihidropirimidin- ali ksantin-oksidaze.
In vitro: Inhibition of osteoblast proliferation, direct cytostatic and pro-apoptotic activity on tumour cells, synergistic cytostatic effect with other anti-cancer drugs, anti-adhesion/invasion activity.
In vitro: Inhibicijo proliferacije osteoblastov, neposredno citostatično in pro-apoptotično aktivnost pri tumorskih celicah, sinergističen citostatični učinek z drugimi zdravili proti raku, anti-adhezijsko in anti-invazijsko aktivnost.
In vitroimatinib inhibits the cytochrome P450 isoenzyme CYP2D6 activity at concentrations similar to those that affect CYP3A4 activity.
In vitro imatinib zavira aktivnost izoencima CYP2D6 citokroma P450 pri koncentracijah, ki so podobne tistim, ki vplivajo na aktivnost CYP3A4.
In vivo - treatment of HIV-1: In an open-label randomised clinical study (GS-01-934) in antiretroviral-naïve patients, genotyping was performed on plasma HIV-1 isolates from all patients with confirmed HIV RNA > 400 copies/mL at weeks 48, 96 or 144 or at the time of early study drug discontinuation.
Zdravljenje HIV–1 in vivo: V odprti, randomizirani klinični študiji (GS-01-934) pri bolnikih, še nezdravljenih s protiretrovirusnimi zdravili, je bila genotipizacija opravljena pri izolatih HIV-1 v plazmi vseh bolnikov s potrjenim HIV RNA > 400 kopij/ml v 48., 96. ali 144. tednu ali ob zgodnji prekinitvi jemanja študijskega zdravila.
In vivo and in vitro models have shown a dual mechanism of action for the effects of ingenol mebutate: 1) induction of local lesion cell death and 2) promoting an inflammatory response characterised by local production of proinflammatory cytokines and chemokines and infiltration of immunocompetent cells.
Modeli in vivo ter in vitro so pokazali dvojni mehanizem delovanja za učinke ingenol mebutata: 1) povzročitev smrti celic v lokalni leziji in 2) pospeševanje vnetnega odziva, za katerega sta značilna lokalna tvorba vnetnih citokinov in kemokinov ter infiltracija imunokompetentnih celic.
In vivo antitumour activity is probably based on direct and indirect effects:
Protitumorsko delovanje in vivo verjetno temelji na neposrednih in posrednih učinkih:
In vivo drug interaction studies evaluated the net effect of the combination treatment, including ritonavir.
V študijah medsebojnega delovanja zdravil in vivo so ocenili neto učinek kombiniranega zdravljenja, vključno z ritonavirjem.
In vivo eslicarbazepine showed an inducing effect on the metabolism of medicinal products that are mainly eliminated by metabolism through CYP3A4 (e.g.
Izkazalo se je, da ima eslikarbazepin in vivo spodbujevalni učinek na presnovo zdravil, ki se izločajo predvsem prek sistema CYP3A4 (npr. simvastatin).
In vivo interaction data is not available.
Podatkov in vivo o medsebojnem delovanju ni.
In vivo interaction studies in humans have demonstrated that anagrelide does not affect the pharmacokinetic properties of digoxin or warfarin.
In vivo študije medsebojnega delovanja pri ljudeh so pokazale, da anagrelid ne vpliva na farmakokinetične lastnosti digoksina in varfarina.
In vivo interaction studies in humans have demonstrated that digoxin and warfarin do not affect the pharmacokinetic properties of anagrelide.
In vivo raziskave medsebojnega delovanja pri ljudeh so pokazale, da digoksin in varfarin ne vplivata na farmakokinetične lastnosti anagrelida.
In vivo resistance (antiretroviral-naïve patients): In a 144-week open-label randomised clinical study (GS-01-934) in antiretroviral-naïve patients, where efavirenz, emtricitabine and tenofovir disoproxil fumarate were used as individual formulations (or as efavirenz and the fixed combination of emtricitabine and tenofovir disoproxil fumarate (Truvada) from week 96 to 144), genotyping was performed on plasma HIV-1 isolates from all patients with confirmed HIV RNA > 400 copies/ml at week 144 or early study drug discontinuation (see section on Clinical experience).
Odpornost in vivo (pri bolnikih, ki še niso prejemali protiretrovirusnih zdravil): V 144-tedenski odprti randomizirani klinični študiji (GS-01-934), v kateri so pri bolnikih, ki še niso bili zdravljeni s protiretrovirusnimi zdravili, uporabili efavirenz, emtricitabin in dizoproksiltenofovirijev fumarat v ločenih formulacijah (ali kot efavirenz in fiksna kombinacija emtricitabina in dizoproksiltenofovirijevega fumarata (Truvada) od 96. do 144. tedna), opravili genotipizacijo izolatov virusa HIV-1 iz plazme vseh bolnikov s potrjeno koncentracijo HIV RNA > 400 kopij/ml v 144. tednu ali pri zgodnji prekinitvi jemanja študijskega zdravila (glejte poglavje Klinične izkušnje).
In vivo resistance (Therapy naïve patients)
Odpornost in vivo (bolniki, ki še niso bili zdravljeni)
In vivo resistance (Therapy-naïve patients)
Odpornost in vivo (bolniki, ki še niso bili zdravljeni)
In Vivo resistance to enfuvirtide: In phase III clinical studies HIV recombinants containing the env genes from HIV RNA samples taken up to week 24 from 187 patients showed > 4 fold reduced susceptibility to enfuvirtide compared with the corresponding pre-treatment samples.
In vivo odpornost proti enfuvirtidu: v kliničnih študijah faze III so rekombinante HIV, vsebujoče env- gene iz vzorcev HIV-RNA, odvzetih do 24. tedna pri 187 bolnikih, pokazale > 4-krat zmanjšano dovzetnost za enfuvirtid v primerjavi z ustreznimi vzorci, odvzetimi pred zdravljenjem.
In vivo results show that ulipristal acetate (administered as a single 10 mg tablet) 1.5 hour before administration of the P-gP substrate fexofenadine (60 mg) has no clinically relevant effects on the pharmacokinetic of fexofenadine.
In vivo rezultati kažejo, da ulipristalacetat (uporaba v obliki ene 10 mg tablete) 1,5 ure pred uporabo substrata P–gp feksofenadina (60 mg) nima klinično pomembnih učinkov na farmakokinetiko feksofenadina.
In vivo studies and population pharmacokinetic analysis
Raziskave in vivo in analiza populacijske farmakokinetike
In vivo studies and population pharmacokinetic analysis
Raziskave in vivoin analiza populacijske farmakokinetike
In vivo studies have demonstrated that nalmefene reduces alcohol consumption, possibly by modulating cortico-mesolimbic functions.
Študije in vivo so pokazale, da nalmefen zmanjšuje uživanje alkohola, verjetno z uravnavanjem kortiko-mezolimbičnih funkcij.
In vivo studies have shown tylvalosin to be present in higher concentrations in the mucous lining of the respiratory and gut tissues compared to the plasma.
In vivo raziskave so pokazale, da se tilvalozin nahaja v višjih koncentracijah v sluznici dihal in črevesja kot v plazmi.
In vivo studies have shown tylvalosin to be present in higher concentrations in the mucous lining of the respiratory and gut tissues compared to the plasma.
Študije in vivo so pokazale, da je tilvalozin prisoten v višjih koncentracijah v sluzničnem epiteliju tkiv dihal in črevesja kot v plazmi.
In vivo studies in cell line-derived xenograft models of human cancer, including non-small cell lung carcinoma, demonstrate that necitumumab has antitumor activity both in monotherapy and in combination with gemcitabine and cisplatin.
Študije in vivo s ksenografskimi modeli, pridobljenimi iz celic raka pri ljudeh, vključno z nedrobnoceličnim rakom pljuč, so pokazale, da ima necitumumab protitumorsko delovanje tako v monoterapiji kot v kombinaciji z gemcitabinom in cisplatinom.
In vivo –-pre-exposure prophylaxis: Plasma samples from 2 clinical studies of HIV-1 uninfected subjects, iPrEx and Partners PrEP, were analysed for 4 HIV-1 variants expressing amino acid substitutions (i.e.
Zaščita pred izpostavitvijo in vivo: Vzorci plazme iz 2 kliničnih študij, iPrEx in Partners PrEP, pri osebah, ki niso bile okužene s HIV–1, so bili analizirani za 4 različice HIV–1 z izraženo substitucijo za aminokisline (tj.
In vivo, co-administration of Numient with up to 40% volume-to-volume (v/v) alcohol did not result in dose- dumping of levodopa or carbidopa.
Sočasna uporaba zdravila Numient in alkohola pri volumski koncentraciji do 40 % (v/v) in vivo ni povzročila sprostitve celotnega odmerka levodope ali karbidope.
In vivo, correlation was assessed in end-of-life patients between florbetapir (18F) uptake in cortical grey matter and the total β-amyloid burden using 4G8 anti-amyloid antibody that stains β-amyloid found in both neuritic and diffuse plaques.
In vivo so povezavo med privzemom florbetapirja (18F) v kortikalni sivi možganovini in skupnim β-amiloidnim bremenom ocenjevali pri bolnikih ob koncu življenja z uporabo protiamiloidnega protitelesa 4G8, ki obarva β-amiloide v nevritičnih in difuznih lehah.
In vivo, docetaxel is schedule independent and has a broad spectrum of experimental antitumour activity against advanced murine and human grafted tumours.
In vivo docetaksel ni odvisen od režima in ima širok spekter eksperimentalnega protitumorskega delovanja proti napredovalim mišjim in humanim transplantiranim tumorjem.
In vivo, dolutegravir may increase plasma concentrations of medicinal products in which excretion is dependent upon OCT2 or MATE-1 (e.g. dofetilide, metformin) (see Table 1 and section 4.3).
In vivo lahko dolutegravir zviša plazemske koncentracije zdravil, katerih izločanje je odvisno od OCT2 ali MATE-1 (npr. dofetilid, metformin) (glejte Preglednico 1 in poglavje 4.3).
In vivo, flutemetamol (18F) can detect β-amyloid diffuse plaques when they are frequent.
In vivo lahko s flutemetamolom (18F) odkrijemo difuzne lehe, ko so te pogoste.
In vivo, ibandronic acid prevents bone destruction experimentally induced by cessation of gonadal function, retinoids, tumours or tumour extracts.
In vivo ibandronska kislina preprečuje eksperimentalno povzročeno razgradnjo kosti zaradi prenehanja delovanja žlez, retinoidov, tumorjev ali ekstraktov tumorjev.
In vivo, ibandronic acid prevents experimentally induced bone destruction caused by cessation of gonadal function, retinoids, tumours or tumour extracts.
In vivo ibandronska kislina preprečuje eksperimentalno povzročeno razgradnjo kosti zaradi prekinitve gonadne funkcije, retinoidov, tumorjev ali ekstraktov tumorjev.
In vivo, in human subjects possessing ineffective mutations of CYP2C19, production of the hydroxy metabolite is decreased 10- fold while brivaracetam itself is increased by 22 % or 42 % in individuals with one or both mutated alleles.
Pri človeških preskušancih, ki so imeli neučinkovite mutacije CYP2C19, se je proizvodnja hidroksi presnovka in vivo zmanjšala za 10-krat, medtem ko se je brivaracetam povečal za 22 % oziroma 42 % pri posameznikih z mutacijo enega ali obeh alelov.
In vivo, quantitative correlation was not assessed in end-of-life patients between florbetaben (18F) uptake in cortical grey matter and the beta-amyloid deposition in autopsied samples.
In vivo pri bolnikih ob koncu življenja niso ocenjevali kvantitativne povezave med privzemom [18F]florbetabena v kortikalni sivi možganovini in β-amiloidnimi oblogami pri obdukcijskih vzorcih.
In vivo, robenacoxib solution for injection produced marked inhibition of COX-2 activity and had no effect on COX-1 activity.
In vivo so priporočeni odmerki robenakoksib raztopine za injiciranje povzročili vidno inhibicijo COX-2 aktivnosti, medtem ko na COX-1 aktivnost niso vplivali.
In vivo, tenofovir alafenamide is hydrolysed within cells to form tenofovir (major metabolite), which is phosphorylated to the active metabolite tenofovir diphosphate.
In vivo se alafenamidtenofovirat hidrolizira v celicah v tenofovir (glavni presnovek), ki se fosforilizira v aktivni presnovek tenofovir difosfat.
In vivo, the ring-opened product is subsequently converted to peptidic degradants and eliminated mainly through biliary excretion.
In vivo se produkt z odprtim obročem nato spremeni v peptidne razgradne produkte in se izloči predvsem z žolčem.
In vivo, the t1/2 of MTIC was similar to that of TMZ, 1.8 hr.
In vivo je bila vrednost t1/2 za MTIC podobna kot za temozolomid, tj.1,8 ure.
In vivo, the t½ of MTIC was similar to that of TMZ, 1.8 hr.
In vivo je bila vrednost t1/2 za MTIC podobna kot za temozolomid – 1,8 ure.
In vivo, the t½ of MTIC was similar to that of TMZ, 1.8 hr.
In vivo je bila vrednost t1/2 za MTIC podobna kot za temozolomid, tj.1,8 ure.
In vivo: Inhibition of osteoclastic bone resorption, which alters the bone marrow microenvironment, making it less conducive to tumour cell growth and anti-angiogenic activity.
In vivo: Inhibicijo osteoklastne resorpcije kosti, ki spremeni mikrookolje kostnega mozga, tako da je le-to manj ugodno za rast tumorskih celic in protiangiogeno aktivnost.
In vivo: Inhibition of osteoclastic bone resorption, which alters the bone marrow microenvironment, making it less conducive to tumour cell growth and anti-angiogenic activity.
In vivo: Inhibicijo osteoklastne resorpcije kosti, ki spremeni mikrookolje kostnega mozga, tako da je le-to manj ugodno za rast tumorskih celic, protiangiogeno aktivnost in protibolečinsko aktivnost.
In vivo: Inhibition of osteoclastic bone resorption, which alters the bone marrow microenvironment, making it less conducive to tumour cell growth, anti-angiogenic activity and anti-pain activity.
In vivo: Inhibicijo osteoklastne resorpcije kosti, ki spremeni mikrookolje kostnega mozga, tako da je le-to manj ugodno za rast tumorskih celic in protiangiogeno aktivnost.
In vivo: Inhibition of osteoclastic bone resorption, which alters the bone marrow microenvironment, making it less conducive to tumour cell growth, anti-angiogenic activity and anti-pain activity.
In vivo: Inhibicijo osteoklastne resorpcije kosti, ki spremeni mikrookolje kostnega mozga, tako da je le-to manj ugodno za rast tumorskih celic, protiangiogeno aktivnost in protibolečinsko aktivnost.
In vivo: Inhibition of osteoclastic bone resorption, which alters the bone marrow microenvironment, making it less conducive to tumour cell growth, anti-angiogenic activity and anti-pain activity.
In vivo: Zavrtje osteoklastne resorpcije kosti, ki spremeni mikrookolje kostnega mozga, tako da postane manj primerno za rast tumorskih celic, antiangiogeno in protibolečinsko aktivnost.
In volunteers with mild to moderate renal impairment (creatinine clearance 30 – 80 ml/min), the pharmacokinetics of vardenafil were similar to that of a normal renal function control group.
Pri prostovoljcih z blago do zmerno ledvično okvaro (kreatininski očistek 30 do 80 ml/min) je bila farmakokinetika vardenafila podobna kot pri preiskovancih iz kontrolne skupine, pri katerih je bilo delovanje ledvic normalno.
In volunteers with mild to moderate renal impairment (creatinine clearance 30-80 ml/min), the pharmacokinetics of vardenafil were similar to that of a normal renal function control group.
Pri prostovoljcih z blago do zmerno ledvično okvaro (kreatininski očistek 30 do 80 ml/min) je bila farmakokinetika vardenafila podobna kot pri preiskovancih iz kontrolne skupine, pri katerih je bilo delovanje ledvic normalno.
In volunteers with moderate hepatic impairment (Child-Pugh Class B), mean Cmax and AUC values were 175% and 65% higher.
Pri prostovoljcih z zmerno okvaro jeter (Child-Pugh B) je bila povprečna Cmax 175 % večja in povprečna AUC 65 % večja.
In volunteers with normal kidney function, total clearance (Cltot) amounts to 170 ml/min/1.73 m2 and part of total renal clearance is achieved by tubular secretion.
Pri prostovoljcih z normalnim ledvičnim delovanjem je celoten očistek (Cltot) 170 ml/min/1,73 m2; del celotnega ledvičnega očistka je dosežen s tubularno sekrecijo.
In volunteers with severe renal impairment (creatinine clearance <30 mL/min), sildenafil clearance was reduced, resulting in mean increases in AUC and Cmax of 100 % and 88 % respectively compared to age-matched volunteers with no renal impairment.
Pri prostovoljcih s hudo okvaro ledvic (očistek kreatinina < 30 ml/min) se je očistek sildenafila zmanjšal, to pa je povzročilo povprečno zvečanje AUC za 100 % in Cmax za 88 % v primerjavi s prostovoljci primerljive starosti brez okvare ledvic.
In volunteers with severe renal impairment (eGFR-MDRD 15 to 29 mL/min/1.73 m2), mean Cmax and AUC values were 92% and 118% higher.
Pri prostovoljcih s hudo okvaro ledvic (eGFR-MDRD od 15 do 29 ml/min/1,73 m2) je bila povprečna Cmax za 92 % večja in AUC za 118 % večja.
In Waldenström’s macroglobulinaemia, Imbruvica was studied in one main study involving 63 patients who had previously received another treatment for their disease.
Pri Waldenströmovi makroglobulinemiji so zdravilo Imbruvica proučevali v eni glavni študiji, v kateri je sodelovalo 63 bolnikov, ki so bili predhodno zdravljeni z drugim zdravilom za svojo bolezen.
in whom an autonomic neuropathy is present,
imajo avtonomno nevropatijo,
in whom an autonomic neuropathy is present,
ki imajo avtonomno nevropatijo,
in whom glycaemic control is markedly improved,
e jim urejenost glikemije občutno izboljša,
in whom glycaemic control is markedly improved,
ki se jim nadzor nad glikemijo občutno izboljša,
in whom glycaemic control is markedly improved,
ki se jim urejenost glikemije občutno izboljša,