natgillin/translations-raw huggingface dataset:
At week 12, the proportion of tocilizumab treated patients showing a minimally clinically important improvement in the Childhood Health Assessment Questionnaire – Disability Index (defined as an individual total score decrease of ≥ 0.13) was significantly higher than in placebo treated patients, 77% versus 19% (p &lt; 0.0001).
V 12. tednu je bil delež bolnikov, zdravljenih s tocilizumabom, pri katerih je bilo vsaj minimalno klinično pomembno izboljšanje glede na vprašalnik Childhood Health Assessment Questionaire- Disability Index (definirano kot individualno zmanjšanje celokupne ocene ≥ 0,13) signifikantno večji kot pri bolnikih, ki so prejemali placebo (77 % v primerjavi z 19 %) (p &lt; 0,0001).
At week 16, 47 placebo patients with &lt; 10% improvement from baseline in both swollen and tender joint counts were switched to infliximab induction (early escape).
V 16. tednu je 47 bolnikov na placebu z &lt; 10 % izboljšanjem stanja glede na začetek študije - tako glede števila oteklih kot bolečih sklepov - prešlo na uvedbo infliksimaba (zgodnji umik).
At week 24 the time-weighted average change from baseline in log10 plasma HIV-1 RNA levels (DAVG24) was -0.03 log10 copies/ml and -0.61 log10 copies/ml for the placebo and tenofovir disoproxil 245 mg (as fumarate) recipients (p &lt; 0.0001).
V 24. tednu je časovno vrednotena povprečna sprememba od začetne vrednosti izražena kot log10 plazemske koncentracije HIV-1 RNA (DAVG24) znašala -0,03 log10 kopij/ml pri bolnikih, ki so prejemali placebo in -0,61 log10 kopij/ml pri prejemnikih 245 mg dizoproksiltenofovirata (v obliki dizoproksiltenofovirijevega fumarata) (p &lt; 0,0001).
At week 24, a significant reduction in DAS28 from baseline of 3.1 was observed on subcutaneous and 1.7 on placebo arm, and for DAS28 &lt; 2.6, 32.0% was observed on subcutaneous and 4.0% on placebo arm.
V 24. tednu so opazili značilno znižanje DAS28 za 3,1 od izhodišča v subkutani skupini in 1,7 v skupini na placebu, DAS28 &lt; 2,6 pa so opazili pri 32 % v subkutani skupini in 4,0 % v skupini na placebu.
At week 24, the number of ASAS 20 responders was 15/78 (19%) in the placebo group, and 123/201 (61%) in the 5 mg/kg infliximab group (p &lt; 0.001).
V 24. tednu je število bolnikov z odzivom ASAS 20 znašalo 15 od 78 (19 %) v skupini za placebo in 123 od 201 (61 %) v skupini, ki je prejemala infliksimab v odmerku 5 mg/kg (p &lt; 0,001).
At Week 26, the mean percent change in LDL-C from baseline of LDL-C was -40% (p &lt; 0.001) in the Intent to Treat (ITT) population.
V 26. tednu je bil v populaciji, ki so jo nameravali zdraviti, povprečen odstotek spremembe holesterola LDL od izhodišča –40 % (p &lt; 0,001).
At week 26, Ultibro Breezhaler produced statistically significant improvement in peak FEV1 compared to placebo in the first 4 hours post dose (330 ml) (p &lt; 0.001).
Po 26 tednih zdravljenja je zdravilo Ultibro Breezhaler doseglo statistično značilno izboljšanje najvišjih vrednosti FEV1 v prvih 4 urah po odmerjanju (330 ml) (p &lt; 0,001).
At week 26, Ulunar Breezhaler produced statistically significant improvement in peak FEV1 compared to placebo in the first 4 hours post dose (330 ml) (p &lt; 0.001).
Po 26 tednih zdravljenja je zdravilo Ulunar Breezhaler doseglo statistično značilno izboljšanje najvišjih vrednosti FEV1 v prvih 4 urah po odmerjanju (330 ml) (p &lt; 0,001).
At week 26, Xoterna Breezhaler produced statistically significant improvement in peak FEV1 compared to placebo in the first 4 hours post dose (330 ml) (p &lt; 0.001).
Po 26 tednih zdravljenja je zdravilo Xoterna Breezhaler doseglo statistično značilno izboljšanje najvišjih vrednosti FEV1 v prvih 4 urah po odmerjanju (330 ml) (p &lt; 0,001).
At week 48 the proportion of subjects with HIV RNA &lt; 50 copies/ml were 63 %, 80 % and 86 % for the ZDV/3TC/ABC, ZDV/3TC/EFV and ZDV/3TC/ABC/EFV arms, respectively.
V 48. tednu je HIV RNA &lt; 50 kopij/ml imelo 63 % oseb, ki so prejemale ZDV/3TC/ABC, 80 % oseb, ki so prejemale ZDV/3TC/EFV in 86 % oseb, ki so prejemale ZDV/3TC/ABC/EFV.
At week 48 the proportion of subjects with HIV RNA &lt; 50 copies/ml were 63%, 80% and 86% for the ZDV/3TC/ABC, ZDV/3TC/EFV and ZDV/3TC/ABC/EFV arms, respectively.
V 48. tednu je HIV RNA &lt; 50 kopij/ml imelo 63 % oseb, ki so prejemale ZDV/3TC/ABC, 80 % oseb, ki so prejemale ZDV/3TC/EFV in 86 % oseb, ki so prejemale ZDV/3TC/ABC/EFV.
At week 48, 12/30 (40%) subjects had HIV-1 RNA &lt; 50 copies/mL (ITT-E, Snapshot algorithm).
Po 48 tednih je imelo 12/30 (40 %) preiskovancev HIV-1 RNA &lt; 50 kopij/ml (ITT-E, algoritem Snapshot).
At week 48, 53.5% of all paediatric patients had a confirmed undetectable viral load &lt; 50 HIV-1 RNA copies/ml according to the TLOVR algorithm.
V 48. tednu je imelo 53,5% vseh bolnikov doseženo potrjeno nezaznavno virusno breme &lt; 50 HIV-1 RNK kopij/ml (glede na algoritem TLOVR).
At week 48, 53.5% of all paediatric patients had a confirmed undetectable viral load &lt; 50 HIV-1 RNA copies/ml according to the TLOVR algorithm.
V 48. tednu je imelo 53,5% vseh bolnikov doseženo potrjeno nezaznavno virusno breme &lt; 50 HIV-1 RNK kopij/ml.
At week 48, 83% of patients in the tenofovir disoproxil fumarate treatment group and 92% of patients in the stavudine or zidovudine treatment group had HIV-1 RNA concentrations &lt; 400 copies/ml.
V 48. tednu je 83% bolnikov v skupini, zdravljeni z dizoproksiltenofovirijevim fumaratom, in 92% bolnikov v skupini, zdravljeni s stavudinom ali zidovudinom, imelo koncentracije HIV-1 RNA &lt; 400 kopij/ml.
At week 48, 89% (283/317) of patients randomised to switch to Eviplera at baseline (Eviplera) had HIV-1 RNA &lt; 50 copies/mL, 3% (8/317) were considered virologic failures (HIV RNA ≥ 50 copies/mL), and 8% (26/317) did not have data available in the week 48 window.
V 48. tednu je imelo 89 % (283/317) bolnikov, randomiziranih za prehod na zdravilo Eviplera na začetku (Eviplera), HIV-1 RNA &lt; 50 kopij/ml, 3 % (8/317) so bili obravnavani kot virološki neuspehi (HIV RNA ≥ 50 kopij/ml) in za 8 % (26/317) v oknu 48. tedna ni bilo razpoložljivih podatkov.
At week 48, non-inferiority was shown with 68 % of patients in the group treated with nelfinavir and 69 % patients treated with fosamprenavir/ritonavir having plasma HIV-1 RNA &lt; 400 copies/ml whereas 53 % in the nelfinavir and 55 % in the fosamprenavir/ritonavir patients had HIV-1 RNA &lt; 50 copies/ml (intent-to-treat, rebound/discontinuation = failure).
69 % bolnikov, zdravljenih s fosamprenavirjem/ritonavirjem, imelo koncentracijo HIV-1 RNK v plazmi &lt; 400 kopij/ml, kar je kazalo na enakost med skupinama, medtem ko je imelo 53 % bolnikov v skupini, zdravljeni z nelfinavirjem, in 55 % bolnikov v skupini, zdravljeni s fosamprenavirjem/ritonavirjem, HIV-1 RNK &lt; 50 kopij/ml (namen zdravljenja, ponoven pojav/ukinitev = neuspeh).
At week 48, non-inferiority was shown with 68 % of patients in the group treated with nelfinavir and 69 % patients treated with fosamprenavir/ritonavir having plasma HIV-1 RNA &lt; 400 copies/ml whereas 53 % in the nelfinavir and 55 % in the fosamprenavir/ritonavir patients had HIV-1 RNA &lt; 50 copies/ml (intent-to-treat, rebound/discontinuation = failure).
plazmi &lt; 400 kopij/ml, kar je kazalo na enakost med skupinama, medtem ko je imelo 53 % bolnikov v skupini, zdravljeni z nelfinavirjem, in 55 % bolnikov v skupini, zdravljeni s fosamprenavirjem/ritonavirjem, HIV-1 RNK &lt; 50 kopij/ml (namen zdravljenja, ponoven pojav/ukinitev = neuspeh).
At week 48, six adolescents in the tenofovir disoproxil fumarate group and one adolescent in the placebo group had significant lumbar spine BMD loss (defined as &gt; 4% loss).
V 48. tednu je šest mladostnikov v skupini z dizoproksiltenofovirijevim fumaratom in en mladostnik v skupini s placebom doživelo znatno izgubo MGK ledvene hrbtenice (opredeljeno kot izguba &gt; 4%).
At Week 52, 42.9% of patients who received Humira/methotrexate combination therapy achieved clinical remission (DAS28 (CRP) &lt; 2.6) compared to 20.6% of patients receiving methotrexate monotherapy and 23.4% of patients receiving Humira monotherapy.
Po 52. tednih je klinično remisijo (DAS28 (CRP) &lt; 2,6) doseglo 42,9 % bolnikov, ki so dobivali kombinirano terapijo z zdravilom Humira/metotreksatom, 20,6 % bolnikov, ki so dobivali metotreksat v monoterapiji, in 23,4 % bolnikov, ki so dobivali zdravilo Humira v monoterapiji.
At week 52, 42.9% of patients who received Trudexa/methotrexate combination therapy achieved clinical remission (DAS28 &lt; 2.6) compared to 20.6% of patients receiving methotrexate monotherapy and 23.4% of patients receiving Trudexa monotherapy.
Po 52. tednih je klinično remisijo (DAS28 &lt; 2,6) doseglo 42,9% bolnikov, ki so dobivali kombinirano terapijo s Trudexo/metotreksatom, 20,6% bolnikov, ki so dobivali metotreksat v monoterapiji, in 23,4% bolnikov, ki so dobivali Trudexo v monoterapiji.
At week 54, the figures were 55.8% (29/52) and 23.5% (12/51) in the q8 weeks and q12 weeks maintenance groups, respectively (p &lt; 0.001).
V 54. tednu so bili ti rezultati naslednji: 55,8 % (29/52) za skupino, ki je za vzdrževalno zdravljenje prejemala infuzije infliksimaba na vsakih 8 tednov, in 23,5 % (12/51) za skupino, ki jih je prejemala na vsakih 12 tednov (p &lt; 0,001).
At week 72, overall 88% (46/52) of patients in the tenofovir disoproxil fumarate treatment group and 0% (0/54) of patients in the placebo group had HBV DNA &lt; 400 copies/ml.
V 72. tednu je imelo skupaj 88% (46/52) bolnikov v skupini, zdravljeni z dizoproksiltenofovirijevim fumaratom in 0% (0/54) bolnikov v skupini, ki je prejemala placebo, koncentracijo HBV DNA &lt; 400 kopij/ml.
At Week 96, 88.4% (214/242 patients) maintained HIV-1 RNA &lt; 50 copies/mL after switching to E/C/F/TAF FDC tablet.
V 96. tednu je 88,4 % (214/242 bolnikov) ohranilo HIV-1 RNA &lt; 50 kopij/ml po prehodu na E/C/F/TAF v obliki tablete FDC.
At Week 96, 88.4% (214/242 patients) maintained HIV-1 RNA &lt; 50 copies/mL after switching to Genvoya.
V 96. tednu je 88,4 % (214/242 bolnikov) ohranilo HIV-1 RNA &lt; 50 kopij/ml po prehodu na zdravilo Genvoya.
At weeks 52 and 104, the majority of subjects ( &gt; 95%) had IOP values of within ± 5mmHg of the baseline value.
Po 52 in 104 tednih je imela večina preiskovancev ( &gt; 95 %) očesni tlak znotraj ± 5 mm Hg v primerjavi z izhodiščem.
Atripla is not recommended for patients with moderate or severe renal impairment (creatinine clearance (CrCl) &lt; 50 ml/min).
Uporabe zdravila Atripla pri bolnikih z zmerno ali hudo ledvično okvaro (kreatininski očistek (CrCl) &lt; 50 ml/min) ne priporočamo.
Atripla is not recommended for patients with moderate or severe renal impairment (creatinine clearance &lt; 50 ml/min)
Da zdravilo Atripla ni priporočljivo pri bolnikih z zmerno ali hudo ledvično okvaro (očistek kreatinina &lt; 50 ml/min)
Atripla is not recommended for patients with moderate or severe renal impairment (creatinine clearance &lt; 50 ml/min).
Uporaba zdravila Atripla pri bolnikih z zmerno ali hudo ledvično insuficienco (kreatininski očistek &lt; 50 ml/min) ni priporočljiva.
Atripla is not recommended for patients with moderate or severe renal impairment (creatinine clearance &lt; 50 ml/min).
Uporabe zdravila Atripla pri bolnikih z zmerno ali hudo ledvično okvaro ne priporočamo (očistek kreatinina &lt; 50 ml/min).
Available data demonstrate that there are no clinically meaningful differences between the safety profiles of patients with LDL-C levels &lt; 0.65 mmol/L and those with higher LDL-C, see section 4.8.
Podatki, ki so na voljo, kažejo, da ni klinično pomembnih razlik v varnostnih značilnostih pri bolnikih s koncentracijo LDL-H &lt; 0,65 mmol/l in bolnikih z višjim LDL-H (glejte poglavje 4.8).
Avanafil Increased plasma concentrations of avanafil (see sections 4.4 and 4.5)
Avanafil Zvišane plazemske koncentracije avanafila (glejte poglavji 4.4 in 4.5).
Avanafil Increased plasma concentrations of avanail (see sections 4.4 and 4.5)
Avanafil Zvišane plazemske koncentracije avanafila (glejte poglavji 4.4 in 4.5).
Avanafil is &gt; 100-fold more potent for PDE5 than PDE6, which is found in the retina and is responsible for phototransduction.
Avanafil je &gt; 100-krat močnejši za PDE5 kot za PDE6, ki ga najdemo v mrežnici in je odgovoren za prevajanje svetlobnih dražljajev.
Axitinib has not been studied in patients &lt; 18 years of age.
Uporabe aksitiniba pri bolnikih, mlajših od 18 let, niso raziskovali.
AZARGA has not been studied in patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) or in patients with hyperchloraemic acidosis (see section 4.3).
Zdravila AZARGA še niso preskušali pri bolnikih s hudo ledvično okvaro (očistek kreatinina &lt; 30 ml/min) ali pri tistih s hiperkloremično acidozo (glejte poglavje 4.3).
Azilsartan is highly bound to plasma proteins ( &gt; 99%), mainly serum albumin.
Azilsartan se močno veže na beljakovine v plazmi ( &gt; 99 %), v glavnem na serumski albumin.
AZOPT has not been studied in patients with severe renal impairment (creatinine clearance &lt; 30 ml/min) or in patients with hyperchloraemic acidosis.
Zdravila AZOPT še niso preskušali pri bolnikih s hudo ledvično okvaro (očistek kreatinina &lt; 30 ml/min) ali pri tistih s hiperkloremično acidozo.
Aztreonam is known to be excreted renally and therefore administration of Cayston in patients with renal impairment (serum creatinine &gt; 2 times upper limit of normal) should be undertaken with caution.
Znano je, da se aztreonam izloča preko ledvic, zato je treba pri bolnikih z okvarjenim delovanjem ledvic (kreatinin v serumu &gt; 2-kratna zgornja meja normale) zdravilo Cayston uporabljati previdno.
b 95% confidence interval about the median progression free survival time. c Based on Cox proportional hazards model comparing the hazard functions associated with treatment groups, stratified by age (≤75 vs &gt; 75),diseases population (refractory to both Lenalidomide and Bortezomib vs not refractory to both drugs), and prior number of anti myeloma therapy (=2 vs &gt; 2). d The p-value is based on a stratified log-rank test with the same stratification factors as the above Cox model.
b 95 % interval zaupanja pri mediani časa preživetja brez napredovanja. c Na podlagi modela sorazmernih ogroženosti po Coxu s primerjavo funkcij tveganja, povezanih z zdravljenimi skupinami, stratificiranimi po starosti (≤ 75 v primerjavi z &gt; 75), bolezni prebivalstva (neodzivni na lenalidomid in bortezomib v primerjavi z odzivnimi na obe zdravili) in predhodnim številom terapij proti plazmocitomu (= 2 v primerjavi z &gt; 2). d Vrednost p temelji na stratificiranem testu log-rank z enakimi stratifikacijskimi faktorji kot zgornji Coxov model.
b e.g. increased tendency to bruise, spontaneous haematoma, haemorrhagic diathesis c Identified in post-marketing experience d Frequencies derived from lab observations (Uric acid increases to &gt; upper limit of normal from baseline below or within reference range.
bnpr. večja nagnjenost k podplutbam, spontanim hematomom, hemoragični diatezi c Ugotovljeni med uporabo po prihodu zdravila na trg d Pogostnosti na podlagi laboratorijskih opažanj (Zvišanje sečne kisline na &gt; zgornjo normalno mejo od izhodiščne vrednosti pod referenčnim območjem ali znotraj njega.
b p &lt; 0.001 compared with etanercept
b p &lt; 0,001 v primerjavi z etanerceptom
b p &lt; 0.05 c nominally significant (p &lt; 0.05)
b p &lt; 0,05 p = NS
b p &lt; 0.05. c Not applicable. d p &lt; 0.001.
b p &lt; 0,05 c N/A: navedba ni smiselna d p &lt; 0,001
b p &lt; 0.05. c Not applicable. d p &lt; 0.001.
b p &lt; 0,05. c N/A: navedba ni smiselna d p &lt; 0,001.
b p &lt; 0.001.
kovariablami. b p &lt; 0.001.
b: n = number of responders/number of subjects with given genotype, and assigned treatment duration. c: Patients with genotype 3 low viral load ( &lt; 600,000 IU/mL) were to receive 24 weeks of treatment while those with genotype 3 and high viral load (≥ 600,000 IU/mL) were to receive 48 weeks of treatment.
b: n = število preiskovancev, ki so se odzvali na zdravljenje /število preiskovancev z danim genotipom virusa ter določeno dolžino zdravljenja c: Bolniki z genotipom 3 in majhnim virusnim bremenom ( &lt; 600.000 i.e./ml) so prejeli 24-tedensko zdravljenje, tisti z genotipom 3 in velikim virusnim bremenom (≥ 600.000 i.e./ml) so prejeli 48- tedensko zdravljenje.
b: n = number of responders/number of subjects with given genotype, and assigned treatment duration. c: Patients with genotype 3 low viral load ( &lt; 600,000 IU/ml) were to receive 24 weeks of treatment while those with genotype 3 and high viral load (≥ 600,000 IU/ml) were to receive 48 weeks of treatment.
b: n = število preiskovancev, ki so se odzvali na zdravljenje/število oseb z danim genotipom virusa ter določeno trajanje zdravljenja. c: Bolniki z genotipom 3 in majhnim virusnim bremenom ( &lt; 600.000 i.e./ml) so prejeli 24-tedensko zdravljenje, tisti z genotipom 3 in velikim virusnim bremenom (≥ 600.000 i.e./ml) so prejeli 48- tedensko zdravljenje.
b: n = number of responders/number of subjects with given genotype, and assigned treatment duration. c: Patients with genotype 3 low viral load ( &lt; 600,000 IU/mL) were to receive 24 weeks of treatment while those with genotype 3 and high viral load (≥ 600,000 IU/mL) were to receive 48 weeks of treatment.
b: n = število preiskovancev, ki so se odzvali na zdravljenje/število preiskovancev z danim genotipom virusa ter določeno dolžino zdravljenja c: Bolniki z genotipom 3 in majhnim virusnim bremenom ( &lt; 600.000 i.e./ml) so prejeli 24-tedensko zdravljenje, tisti z genotipom 3 in velikim virusnim bremenom (≥ 600.000 i.e./ml) so prejeli 48- tedensko zdravljenje.
b: n = number of responders/number of subjects with given genotype, and assigned treatment duration. c: Patients with genotype 3 low viral load ( &lt; 600,000 IU/ml) were to receive 24 weeks of treatment while those with genotype 3 and high viral load (≥ 600,000 IU/ml) were to receive 48 weeks of treatment.
b: n = število preizkušancev, ki so se odzvali na zdravljenje, in število preizkušancev z danim genotipom virusa ter določena dolžina zdravljenja. c: Bolniki z genotipom 3 in majhnim virusnim bremenom ( &lt; 600.000 i.e./ml) so prejeli 24-tedensko zdravljenje, tisti z genotipom 3 in velikim virusnim bremenom (≥ 600.000 i.e./ml) so prejeli 48- tedensko zdravljenje.
b: n = number of responders/number of subjects with given genotype, and assigned treatment duration. c: Patients with genotype 3 low viral load ( &lt; 600,000 IU/ml) were to receive 24 weeks of treatment while those with genotype 3 and high viral load (≥ 600,000 IU/ml) were to receive 48 weeks of treatment.
c: Bolniki z genotipom 3 in majhnim virusnim bremenom ( &lt; 600.000 i.e./ml) so prejeli 24-tedensko zdravljenje, tisti z genotipom 3 in velikim virusnim bremenom (≥ 600.000 i.e./ml) so prejeli 48- tedensko zdravljenje.
Babies and children aged 2 months to &lt; 3 years of age
Dojenčki in otroci, stari 2 meseca do &lt; 3 leta starosti
Background medicinal products included corticosteroids (76%; &gt; 7.5 mg/day 46%), immunosuppressives (56%), and anti-malarials (63%).
Med osnovnimi zdravili so bili kortikosteroidi (76 %, &gt; 7,5 mg/dan 46 %), imunosupresivi (56 %) in antimalariki (63 %).
Background medicinal products included corticosteroids (96%; &gt; 7.5 mg/day 69%), immunosuppressives (42%), and anti-malarials (67%).
Med osnovnimi zdravili so bili kortikosteroidi (96 %, &gt; 7,5 mg/dan 69 %), imunosupresivi (42 %) in antimalariki (67 %).
Baraclude is also indicated for the treatment of chronic HBV infection in nucleoside naive paediatric patients from 2 to &lt; 18 years of age with compensated liver disease who have evidence of active viral replication and persistently elevated serum ALT levels, or histological evidence of moderate to severe inflammation and/or fibrosis.
Zdravilo Baraclude je indicirano tudi za zdravljenje kronične okužbe s HBV pri z nukleozidi predhodno še nezdravljenih pediatričnih bolnikih, starih od 2 do &lt; 18 let, ki imajo kompenzirano bolezen jeter in znake aktivne replikacije virusa ter persistentno povečane vrednosti serumske ALT ali histološke znake zmernega do hudega vnetja in/ali fibroze.
Based mainly on PK/PD considerations, a 4-hour infusion time may be more suitable to maximize the percentage time during the dosing interval that the plasma concentration of doripenem exceeds the minimum inhibitory concentration (%T &gt; MIC), (see section 5.1).
Predvsem na osnovi FK/FD podatkov je pri bolnikih s tveganjem za okužbo z manj občutljivimi povzročitelji bolezni ali pri zelo hudih okužbah, 4-urno infundiranje lahko primernejše za povečanje odstotka časa med posameznimi odmerki, ko plazemska koncentracija doripenema presega minimalno inhibitorno koncentracijo (%T &gt; MIC), (glejte poglavje 5.1).
Based on a PopPK analysis, no clinically meaningful differences in the clearance of olaratumab were observed in patients with mild (total bilirubin within upper limit of normal [ULN] and AST &gt; ULN, or total bilirubin &gt; 1.0-1.5 times ULN and any AST level, n = 16), or moderate (total bilirubin &gt; 1.5-3.0 times ULN, n = 1) hepatic impairment compared to patients with normal hepatic function (total bilirubin and AST ≤ ULN, n = 126).
Analiza PopPK ni pokazala klinično pomembnih razlik med bolniki z blago (skupni bilirubin pod zgornjo mejo normale [ULN] in AST &gt; ULN ali skupni bilirubin &gt; 1,0–1,5-krat ULN in katera koli raven AST, n = 16) ali zmerno (skupni bilirubin &gt; 1,5–3,0-krat ULN, n = 1) okvaro jeter in bolniki z normalnim delovanjem jeter (skupni bilirubin in AST ≤ ULN, n = 126).
Based on a population pharmacokinetic analysis of 330 patients with mild renal impairment (CLcr 60 to less than 90 mL/min), 149 patients with moderate renal impairment (CLcr 30 to &lt; than 60 mL/min), 3 patients with severe renal impairment (CLcr 15 to &lt; than 30 mL/min) and 295 patients with normal renal function (≥90 mL/min), osimertinib exposures were similar.
Na podlagi populacijske farmakokinetične analize 330 bolnikov z blago okvaro ledvic (očistek kreatinina od 60 do manj kot 90 ml/min), 149 bolnikov z zmerno okvaro ledvic (očistek kreatinina od 30 do manj kot 60 ml/min), 3 bolnikov s hudo okvaro ledvic (očistek kreatinina od 15 do manj kot 30 ml/min) ter 295 oseb z normalnim delovanjem ledvic (≥ 90 ml/min) so bile izpostavljenosti osimertinibu podobne.
Based on a population pharmacokinetic analysis of 48 patients with mild hepatic impairment (total bilirubin ≤ULN and AST &gt; ULN or total bilirubin &gt; 1.0 to 1.5 times ULN and any AST) and
Po podatkih populacijske farmakokinetične analize pri 48 bolnikih z blago okvaro jeter (z vrednostjo celokupnega bilirubina ≤ ZMN in vrednostjo aspartat-aminotransferaze (AST) &gt; ZMN ali z vrednostjo celokupnega bilirubina &gt; 1,0 do 1,5-kratnika ZMN in kakršnokoli vrednostjo AST) in pri 254 bolnikih z normalnim delovanjem jeter (z vrednostjo celokupnega bilirubina ≤ ZMN in vrednostjo AST
Based on a population PK analysis, no dosage adjustments are necessary for patients with mild hepatic impairment (Total Bilirubin [TB] 1.0 x to 1.5 x upper limit of normal [ULN] or aspartate aminotransferase [AST] &gt; ULN).
Po podatkih populacijske farmakokinetične analize odmerkov ni treba prilagajati pri bolnikih z blago okvaro jeter (s koncentracijo celotnega bilirubina v razponu od 1,0 do 1,5-kratnika zgornje meje normalnih vrednosti [ZMN] oziroma s koncentracijo aspartat-aminotransferaze [AST] nad ZMN).
Based on a relationship observed in PLATO between maintenance ASA dose and relative efficacy of ticagrelor compared to clopidogrel, co-administration of Possia and high maintenance dose ASA ( &gt; 300 mg) is not recommended (see section 5.1).
Glede na razmerje med vzdrževalnim odmerkom ASA in relativno učinkovitostjo tikagrelorja v primerjavi s klopidogrelom, ugotovljeno v študiji PLATO, sočasna uporaba zdravila Possia in visokega vzdrževalnega odmerka ASA ( &gt; 300 mg) ni priporočljiva (glejte poglavje 5.1).