natgillin/translations-raw huggingface dataset:
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,
In vitro, lurasidon nije pokazao izravnu, ili slabu inhibiciju (izravnu ili ovisnu o vremenu) (IC50>5,9 μM) citokrom P450 enzima (CYP)1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19,
In vitro, methylthioninium chloride has been shown to reduce motility of human sperm in a dose dependant manner.
Studija in vitro je pokazala da metiltioninijev klorid smanjuje pokretljivost spermija ovisno o dozi lijeka.
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.
In vitro se N-desmetil enzalutamid metabolizira do metabolita karboksilatne kiseline pomoću karboksilesteraze 1, koja također ima manju ulogu u metabolizmu enzalutamida do metabolita karboksilatne kiseline.
In vitro, olaparib has been shown to be an inhibitor of OATP1B1, OCT1, OCT2, OAT3, MATE1 and MATE2K.
In vitro olaparib se pokazao inhibitorom OATP1B1, OCT1, OCT2, OAT3, MATE1 i 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 inhibira efluksni prijenosnik P-gp (IC50 = 76 µM), stoga se ne može isključiti mogućnost da olaparib može uzrokovati klinički značajne interakcije lijeka sa supstratima P-gp-a (npr. simvastatina, pravastatina, dabigatrana, digoksina i kolhicina).
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 neznatno inhibirao ili nije inhibirao CYP1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6 i 2E1 pa se ne očekuje da bi mogao djelovati kao klinički značajan i o vremenu ovisan inhibitor nekoga od tih enzima citokroma P450.
In vitro, osimertinib does not inhibit OAT1, OAT3, OATP1B1, OATP1B3 and MATE2K at clinically relevant concentrations.
In vitro, osimertinib ne inhibira OAT1, OAT3, OATP1B1, OATP1B3 i MATE2K pri klinički relevantnim koncentracijama.
In vitro, perampanel inhibited AMPA- induced (but not NMDA-induced) increase in intracellular calcium.
In vitro je perampanel inhibirao povećanje unutarstaničnog kalcija koje inducira AMPA (ali ne ono koje inducira 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, siltuksimab je ovisno o dozi inhibirao rast murinske plazmocitomske stanične linije ovisne o IL-6, kao odgovor na ljudski IL-6.
In vitro, slow metabolic turnover of velpatasvir by CYP2B6, CYP2C8, and CYP3A4 was observed.
In vitro je opažena spora metabolička izmjena velpatasvira putem CYP2B6, CYP2C8 i CYP3A4.
In vitro, some macrolide antibiotics like erythromycin inhibited the activity of bovine Cytochrom P 450-enzymes (CYP3A4-subclass).
In vitro su neki makrolidni antibiotici, kao eritromicin, inhibirali aktivnost goveđih enzima citokroma P450 (podvrsta CYP3A4).
In vitro, T-cells are more sensitive than B-cells to the cytotoxic effects of nelarabine.
U in vitro uvjetima T-limfociti pokazuju veću osjetljivost na citotoksično djelovanje nelarabina nego B-limfociti.
In vitro, the lenvatinib blood-to-plasma concentration ratio ranged from 0.589 to 0.608 (0.1 – 10 μg/mL, mesilate).
In vitro, omjer koncentracije lenvatiniba u krvi i plazmi bio je u rasponu od 0,589 do 0,608 (0,1 - 10 μg/ml, mesilat).
In vitro, the lenvatinib blood-to-plasma concentration ratio ranged from 0.589 to 0.608 (0.1 – 10 μg/mL, mesilate).
In vitro, omjer koncentracije lenvatiniba u krvi i plazmi bio je u rasponu od 0,589 do 0,608 (0,1 – 10 μg/ml, mesilat).
In vitro, there is an inverse correlation between the degree of resistance to tipranavir and the capacity of viruses to replicate.
In vitro postoji inverzna korelacija između stupnja otpornosti na tipranavir i kapaciteta replikacije virusa.
In vitro, topotecan did not inhibit human P450 enzymes CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A, of CYP4A nor did it inhibit the human cytosolic enzymes dihydropyrimidine or xanthine oxidase.
In vitro topotekan ne inhibira ljudske P450 enzime CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A ili CYP4A, niti inhibira ljudske citosolne enzime dihidropirimidin ili ksantin oksidazu.
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.
In vitro topotekan ne inhibira ljudske P450 enzime CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A ili CYP4A niti inhibira citosolne enzime dihidropirimidin ili ksantin oksidazu.
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.
In vitro topotekan ne inhibira ljudske P450 enzime CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A ili CYP4A, niti inhibira citosolne enzime dihidropirimidin ili ksantin oksidazu.
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.
In vitro topotekan ne inhibira ljudske P450 enzime CYP1A2, CYP2A6, CYP2C8/9, CYP2C19, CYP2D6, CYP2E, CYP3A ili CYP4A, niti inhibira ljudske citosolne enzime dihidropirimidin ili ksantin oksidazu.
In vitro, voriconazole displays broad-spectrum antifungal activity with antifungal potency against Candida species (including fluconazole -resistant C. krusei and resistant strains of C. glabrata and C. albicans) and fungicidal activity against all Aspergillus species tested.
Vorikonazol pokazuje širok spektar antifungalne aktivnosti in vitro, sa snažnim djelovanjem protiv vrsta iz roda Candida (uključujući C. krusei rezistentnu na flukonazol i rezistentne sojeve C. glabrata i C. albicans) te fungicidnim djelovanjem protiv svih ispitanih vrsta iz roda Aspergillus.
In vitro: Cysteamine bitartrate is a substrate of P-gp and OCT2, but not a substrate of BCRP, OATP1B1, OATP1B3, OAT1, OAT3 and OCT1.
In vitro: Cisteamin bitartrat je supstrat P-gp-a i OCT2, no nije supstrat BCRP, OATP1B1, OATP1B3, OAT1, OAT3 i OCT1.
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: inhibicija proliferacije osteoblasta, izravno citostatsko i proapoptotska aktivnost na tumorske stanice, sinergistički citostatski učinak s drugim antitumorskim lijekovima, antiadhezivna/antiinvazivna aktivnost.
In vitro: Resistance has been seen in vitro and in some HIV-1 infected patients due to the development of the M184V/I mutation with emtricitabine or the K65R mutation with tenofovir.
In vitro: Rezistencija je opažena in vitro i u nekih bolesnika zaraženih virusom HIV-1, zbog razvoja mutacije M184V/I uz emtricitabin ili mutacije K65R uz tenofovir.
In vitroimatinib inhibits the cytochrome P450 isoenzyme CYP2D6 activity at concentrations similar to those that affect CYP3A4 activity.
Imatinib in vitro inhibira aktivnost CYP2D6 izoenzima citokroma P450 u koncentracijama koje su slične onima što utječu na djelovanje 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.
In vivo – liječenje HIV-1: U otvorenom, randomiziranom kliničkom ispitivanju (GS-01-934) na pacijentima koji prije nisu bili liječeni antiretrovirusnim lijekovima, provedeno je određivanje genotipa na plazmatskim izolatima HIV-1 od svih pacijenata s potvrđenim HIV RNK > 400 kopija/mL u 48., 96. ili 144. tjednu ili u vrijeme prijevremenog prekida uzimanja ispitivanog lijeka.
In vivo antitumour activity is probably based on direct and indirect effects:
In vivo antitumorska aktivnost se vjerojatno temelji na direktnim i indirektnim učincima:
In vivo drug interaction studies evaluated the net effect of the combination treatment, including ritonavir.
Ispitivanja interakcija lijekova in vivo su ocijenila neto učinak kombiniranog liječenja, uključujući ritonavir.
In vivo drug interaction studies evaluated the net effect of the combination treatment, including ritonavir.
U in vivo ispitivanjima interakcije lijekova ocjenjivo se neto učinak kombiniranog liječenja, uključujući ritonavir.
In vivo eslicarbazepine showed an inducing effect on the metabolism of medicinal products that are mainly eliminated by metabolism through CYP3A4 (e.g.
In vivo eslikarbazepin izaziva indicirajući učinak na metabolizam lijekova koji se uglavnom eliminiraju metabolizmom putem CYP3A4 (npr. simvastatin).
In vivo eslicarbazepine showed an inducing effect on the metabolism of medicinal products that are mainly eliminated by metabolism through CYP3A4 (e.g.
In vivo eslikarbazepin izaziva indicirajući učinak na metabolizam lijekova, koji se uglavnom eliminiraju metabolizmom putem CYP3A4 (npr. simvastatin).
In vivo interaction studies in humans have demonstrated that anagrelide does not affect the pharmacokinetic properties of digoxin or warfarin.
In vivo ispitivanja interakcija u ljudi dokazala su da anagrelid ne utječe na farmakokinetička svojstva digoksina i varfarina.
In vivo interaction studies in humans have demonstrated that digoxin and warfarin do not affect the pharmacokinetic properties of anagrelide.
In vivo ispitivanja interakcija u ljudi dokazala su da digoksin i varfarin ne utječu na farmakokinetička svojstva anagrelida.
In vivo resistance (Therapy naïve patients)
Rezistencija in vivo (prethodno neliječeni bolesnici)
In vivo resistance (Therapy-naïve patients)
Rezistencija in vivo (prethodno neliječeni bolesnici)
In vivo results show that administration of ulipristal acetate with a potent and a moderate CYP3A4 inhibitor increased Cmax and AUC of ulipristal acetate with a maximum of 2- and 5.9-fold, respectively.
In vivo rezultati pokazuju da primjena ulipristalacetata s jakim i umjerenim inhibitorima CYP3A4 povećava CRmaxR odnosno AUC ulipristalacetata do najviše 2 odnosno 5,9 puta.
In vivo results show that the administration of ulipristal acetate with a strong CYP3A4 inducer such as rifampicin markedly decreases Cmax and AUC of ulipristal acetate by 90% or more and decreases ulipristal acetate half-life by 2.2-fold corresponding to an approximately 10-fold decrease of ulipristal acetate exposure.
In vivo rezultati pokazuju da primjena ulipristalacetata s jakim induktorima CYP3A4 kao što je rifampicin značajno smanjuje CRmaxR i AUC ulipristalacetata za 90% ili više i smanjuje poluvrijeme eliminacije ulipristalacetata za 2,2 puta što približno odgovara smanjenju izlaganja ulipristalacetatu za 10 puta.
In vivo studies and population pharmacokinetic analysis
Ispitivanja in vivo i analiza populacijske farmakokinetike
In vivo studies have demonstrated that nalmefene reduces alcohol consumption, possibly by modulating cortico-mesolimbic functions.
In vivo ispitivanja pokazala su da nalmefen smanjuje konzumaciju alkohola, moguće moduliranjem kortiko-mezolimbičkih funkcija.
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.
In vivo – predekspozicijska profilaksa: Uzorci plazme ispitanika koji nisu bili zaraženi virusom HIV-1 u 2 klinička ispitivanja, iPrEx i Partners PrEP, bili su analizirani na 4 varijante virusa HIV-1 s ekspresijom supstitucije aminokiselina (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.
In vivo istodobna primjena Numienta s alkoholom do 40 % volumenske koncentracije nije dovela do nakupljanja doze levodope ili karbidope.
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 dolutegravir može povećati plazmatske koncentracije lijekova čije izlučivanje ovisi o OCT2 ili MATE-1 (npr. dofetilid, metformin) (vidjeti Tablicu 1 i dio 4.3).
In vivo, flutemetamol (18F) can detect β-amyloid diffuse plaques when they are frequent.
In vivo, flutemetamol (18F) može detektirati β-amiloidne difuzne plakove kada su učestali.
In vivo, ibandronic acid prevents bone destruction experimentally induced by cessation of gonadal function, retinoids, tumours or tumour extracts.
In vivo, ibandronatna kiselina sprječava eksperimentalno induciranu razgradnju kosti uzrokovanu zaustavljanjem gonadne funkcije, retinoidima, tumorima ili ekstraktima tumora.
In vivo, ibandronic acid prevents experimentally-induced bone destruction caused by cessation of gonadal function, retinoids, tumours or tumour extracts.
In vivo ibandronatna kiselina sprječava eksperimentalno inducirano uništavanje kosti uzrokovano zaustavljanjem gonadnih funkcija, retinoidima, tumorima ili ekstraktima tumora.
In vivo, ibandronic acid prevents experimentally-induced bone destruction caused by cessation of gonadal function, retinoids, tumours or tumour extracts.
In vivo ibandronatna kiselina sprječava eksperimentalno induciranu destrukciju kosti uzrokovanu zaustavljanjem gonadnih funkcija, retinoidima, tumorima ili ekstraktima tumora.
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.
In vivo je u ljudskih ispitanika s neutralnim mutacijama enzima CYP2C19 stvaranje hidroksi metabolita deseterostruko smanjeno, dok je koncentracija brivaracetama povećana za 22% odnosno 42% u osoba s jednim odnosno oba mutirana alela.
In vivo, robenacoxib solution for injection produced marked inhibition of COX-2 activity and had no effect on COX-1 activity.
In vivo, otopina robenakoksiba za injekciju uzrokovala je značajnu inhibiciju aktivnosti COX-2 i nije imala utjecaja na aktivnost COX-1.
In vivo, the t½ of MTIC was similar to that of TMZ, 1.8 hr.
In vivo je t1/2 MTIC-a bio sličan onomu temozolomida, odnosno 1,8 sati.
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: inhibicija osteoklastične resorpcije kosti koja mijenja mikrookoliš koštane srži i čini je manje pogodnom za rast tumorskih stanica, antiangiogeno djelovanje i analgetsko djelovanje
In vivo: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.
In vivo: U otvorenom randomiziranom kliničkom ispitivanju (GS-01-934) s bolesnicima koji prethodno nisu bili liječeni antiretrovirusnim lijekovima, provedeno je određivanje genotipa na plazmatskim izolatima virusa HIV-1 prikupljenima od svih bolesnika s potvrđenim HIV RNK > 400 kopija/ml u 48., 96. ili 144. tjednu ili u trenutku prijevremenog prekida uzimanja ispitivanog lijeka.
In volunteers with mild to moderate hepatic cirrhosis (Child-Pugh class A and B) sildenafil clearance was reduced, resulting in increases in AUC (85 %) and Cmax (47 %) compared to age-matched volunteers with no hepatic impairment.
U dobrovoljaca s blagom do umjerenom cirozom jetre (Child-Pugh stadij A i B) klirens sildenafila je bio smanjen, što je rezultiralo povećanjem AUC-a (85%) i Cmax (47%) u usporedbi s dobrovoljcima bez oštećenja jetre podudarnima s obzirom na dob.
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.
U dobrovoljaca s blagim do umjerenim oštećenjem funkcije bubrega (klirens kreatinina 30-80 ml/min) farmakokinetika vardenafila bila je slična onoj u kontrolnoj skupini s normalnom funkcijom bubrega.
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.
U dobrovoljaca s blagim do umjerenim oštećenjem funkcije bubrega (klirens kreatinina 30-80 ml/min) farmakokinetika vardenafila bila je slična onoj u kontrolnoj skupini s normalnom funkcijom bubrega.
In volunteers with mild to moderate renal impairment (creatinine clearance = 30-80 mL/min), the pharmacokinetics of sildenafil were not altered after receiving a 50 mg single oral dose.
U dobrovoljaca s blagim do umjerenim poremećajem funkcije bubrega (klirens kreatinina= 30-80 ml/min) nakon uzimanja jednokratne oralne doze od 50 mg nije bilo promjena u farmakokinetici sildenafila.
In volunteers with moderate hepatic impairment (Child Pugh B), exposure was 7.6-fold higher based on Cmax (90% CI 4.4 – 13.2) and 8.7-fold higher (90% CI 5.7 – 13.1) based on AUC, respectively, compared to healthy volunteers.
U dobrovoljaca s umjerenim oštećenjem funkcije jetre (Child Pugh B), izloženost je bila 7,6 puta veća na temelju Cmax (90% CI 4,4 – 13,2) odnosno 8,7 puta veća (90% CI 5,7 – 13,1) na temelju AUC u usporedbi sa zdravim dobrovoljcima.
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.
Kod dobrovoljaca s normalnom funkcijom bubrega ukupni klirens (Cltot) iznosi do 170 ml/min/1,73 m², ta dio ukupnog bubrežnog klirensa postiže se tubularnom sekrecijom.
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.
U dobrovoljaca s teškim oštećenjem bubrega (klirens kreatinina < 30 ml/min) klirens sildenafila je bio smanjen, što je rezultiralo srednjom vrijednošću povećanja AUC-a od 100%, a Cmax od 88% u usporedbi s dobrovoljcima bez oštećenja bubrega podudarnima s obzirom na dob.
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.
U dobrovoljaca s teškim oštećenjem bubrega (eGFR-MDRD 15 do 29 ml/min1/.73 m2), srednje vrijednosti Cmax i AUC bile su 92% odnosno 118% više.
In Waldenström’s macroglobulinaemia, Imbruvica was studied in one main study involving 63 patients who had previously received another treatment for their disease.
U slučaju Waldenströmove makroglobulinemije lijek Imbruvica ispitivan je u jednom glavnom ispitivanju koje je obuhvatilo 63 bolesnika koji su prethodno primili drugu terapiju za svoju bolest.
In wet AMD and in visual impairment due to DME, to macular oedema secondary to RVO or to CNV secondary to PM, the recommended dose for Lucentis is 0.5 mg given as a single intravitreal injection.
Kod vlažnog AMD-a te poremećaja vida nastalog zbog DME-a, makularnog edema posljedičnog RVO-u ili CNV-a posljedičnog PM-u, preporučena doza Lucentisa iznosi 0,5 mg u obliku jednokratne intravitrealne injekcije.
in whom an autonomic neuropathy is present,
u kojih je prisutna autonomna neuropatija
in whom an autonomic neuropathy is present,
u kojih je prisutna autonomna neuropatija,
in whom glycaemic control is markedly improved,
u kojih je regulacija glikemije izrazito poboljšana
in whom glycaemic control is markedly improved,
u kojih je regulacija glikemije izrazito poboljšana,
in whom hypoglycaemia develops gradually,
u kojih se hipoglikemija razvija postupno
in whom hypoglycaemia develops gradually,
u kojih se hipoglikemija razvija postupno,
In women 27- through 45 years of age, efficacy of Gardasil 9 for the 4 original types is expected based on (1) high efficacy of qHPV vaccine in women 16- through 45 years of age and (2) comparable immunogenicity of Gardasil 9 and qHPV vaccine in girls and women 9- through 26 years of age.
Djelotvornost cjepiva Gardasil 9 za 4 izvorna tipa u žena u dobi od 27 do 45 godina očekuje se na temelju (1) visoke djelotvornosti cjepiva qHPV u žena u dobi od 16 do 45 godina i (2) usporedivosti imunogenosti cjepiva Gardasil 9 i cjepiva qHPV u djevojaka i žena u dobi od 9 do 26 godina.
In women aged 18 to 35, the Pearl Index was around 0.4 with Zoely and 0.8 with the comparator medicine in the first study, and around 1.2 with Zoely and 1.9 with the comparator medicine in the second study.
U žena u dobi od 18 do 35 godina, u prvom je ispitivanju Pearl indeks bio otprilike 0,4 za lijek Zoely i 0,8 za usporedni lijek, dok je u drugom ispitivanju bio 1,2 za lijek Zoely i 1,9 za usporedni lijek.
In women aged 50 to 54 who are not taking HRT, about 2 women in 2,000 will be diagnosed with ovarian cancer over a 5-year period.
U žena u dobi od 50 do 54 godine koje ne primaju hormonsku nadomjesnu terapiju (HNT), otprilike dvjema ženama od 2000 bit će dijagnosticiran rak jajnika u razdoblju od 5 godina.
In women in pre-term labour receiving atosiban by infusion (300 micrograms/min for 6 to 12 hours), steady state plasma concentrations were reached within one hour following the start of the infusion (mean 442 ± 73 ng/ml, range 298 to 533 ng/ml).
U žena s prijevremenim porodom koje su primale infuziju atosibana (300 mikrograma/min tijekom 6 do 12 sati), stanje dinamičke ravnoteže koncentracija u plazmi postignuto je unutar jednog sata nakon početka infuzije (srednja vrijednost 442 ± 73 ng/ml, raspon 298 do 533 ng/ml).
In women of child-bearing age, any existing pregnancy must be excluded with certainty by taking appropriate measures, e.g. a pregnancy test, prior to initiating therapy (see section 4.4).
U žena reproduktivne dobi mora se sa sigurnoću isključiti prisutnost trudnoće poduzimanjem odgovarajućih mjera, npr. testa na trudnoću, prije početka terapije (vidjeti dio 4.4).
In women receiving darunavir/ritonavir 600/100 mg twice daily during the second trimester of pregnancy, mean intra-individual values for total darunavir Cmax, AUC12h and Cmin were 28%, 24% and 17% lower, respectively, as compared with postpartum; during the third trimester of pregnancy, total darunavir Cmax, AUC12h and Cmin values were 19%, 17% lower and 2% higher, respectively, as compared with postpartum.
U žena koje su primale darunavir/ritonavir 600/100 mg dva puta na dan tijekom drugog tromjesečja trudnoće, srednje intra-individualne vrijednosti za ukupni darunavir Cmax, AUC12h u Cmin bile su 28%, 24% odnosno 17% niže, uspoređujući s postpartalnim razdobljem; tijekom trećeg tromjesečja trudnoće, ukupne vrijednosti za darunavir Cmax, AUC12h i Cmin bile su 19%, 17% niže, odnosno 2% više, uspoređujući s postpartalnim razdobljem.
In women receiving darunavir/ritonavir 800/100 mg once daily during the second trimester of pregnancy, mean intra-individual values for total darunavir Cmax, AUC12h and Cmin were 34%, 34% and 32% lower, respectively, as compared with postpartum; during the third trimester of pregnancy, total darunavir Cmax, AUC12h and Cmin values were 31%, 35% and 50% lower, respectively, as compared with postpartum.
U žena koje su primale darunavir/ritonavir 800/100 mg jedanput dnevno tijekom drugog tromjesečja trudnoće, srednje intra-individualne vrijednosti za ukupni darunavir Cmax, AUC12h u Cmin bile su Cmax, 34%, 34% odnosno 32% niže, uspoređujući s postpartalnim razdobljem; tijekom trećeg tromjesečja trudnoće, ukupne vrijednosti za darunavir Cmax, AUC12h i Cmin bile su 31%, 35% odnosno 50% niže, uspoređujući s postpartalnim razdobljem.