natgillin/translations-raw huggingface dataset:
In TRIUMPH, study patients treated with Soliris had significantly reduced (p &lt; 0.001) haemolysis resulting in improvements in anaemia as indicated by increased haemoglobin stabilization and reduced need for RBC transfusions compared to placebo treated patients (see Table 3).
U ispitivanju TRIUMPH, bolesnici liječeni lijekom Soliris imali su značajno smanjenu (p &lt; 0,001) hemolizu, što je rezultiralo poboljšanjem anemije sudeći po povećanoj stabilnosti hemoglobina i smanjenoj potrebi za transfuzijom crvenih krvnih stanica u usporedbi s bolesnicima koji su primali placebo (vidjeti tablicu 3).
In two 12-week, placebo controlled studies (200109 and 200110), the addition of Incruse to fluticasone furoate/vilanterol (FF/VI) (92/22 micrograms) once daily in adult patients with a clinical diagnosis of COPD, resulted in statistically significant and clinically meaningful improvements in the primary endpoint of trough FEV1 at Day 85 compared to placebo plus FF/VI (124 mL (95% CI 93, 154, p &lt; 0.001) and 122 mL (95%CI 91, 152, p &lt; 0.001)).
U dva 12-tjedna, placebom kontrolirana ispitivanja (200109 i 200110), dodavanje lijeka Incruse kombinaciji flutikazonfuorat/vilanterol (FF/VI) (92/22 mikrograma) jedanput dnevno, u odraslih bolesnika s kliničkom dijagnozom KOPB-a, ishodilo je statistički značajnim i kliničkim bitnim poboljšanjima najnižih vrijednosti FEV1 (primarna mjera ishoda) nakon 85 dana u usporedbi s placebom uz FF/VI (124 ml (95% CI 93, 154, p &lt; 0,001) i 122 ml (95% CI 91, 152, p &lt; 0,001)).
In two randomised, double-blind studies with a total of 1,132 patients receiving moderately emetogenic chemotherapy that included cisplatin ≤50 mg/m2, carboplatin, cyclophosphamide ≤1,500 mg/m2 and doxorubicin &gt; 25 mg/m2, palonosetron 250 micrograms and 750 micrograms were compared with ondansetron 32 mg (half-life 4 hours) or dolasetron 100 mg (half-life 7.3 hours) administered intravenously on Day 1, without dexamethasone.
U dva randomizirana, dvostruko slijepa ispitivanja na ukupno 1132 bolesnika na umjereno emetogenoj kemoterapiji koja je uključivala cisplatin ≤50 mg/m2, karboplatin, ciklofosfamid 1500 mg/m2 i doksorubicin 25 mg/m2, uspoređivan je palonosetron 250 mikrograma i 750 mikrograma s ondansetronom 32 mg (poluvijek 4 sata) ili dolasetronom 100 mg (poluvijek 7,3 sata) primijenjeno intravenski na dan 1, bez deksametazona.
In two randomised, double-blind studies with a total of 1,132 patients receiving moderately emetogenic chemotherapy that included cisplatin ≤50 mg/m2, carboplatin, cyclophosphamide ≤1,500 mg/m2 and doxorubicin &gt; 25 mg/m2, palonosetron 250 micrograms and 750 micrograms were compared with ondansetron 32 mg (half-life 4 hours) or dolasetron 100 mg (half-life 7.3 hours) administered intravenously on Day 1, without dexamethasone.
U dva randomizirana, dvostruko slijepa ispitivanja na ukupno 1132 bolesnika na umjereno emetogenoj kemoterapiji koja je uključivala cisplatin ≤50 mg/m2, karboplatin, ciklofosfamid 1500 mg/m2 i doksorubicin 25 mg/m2, uspoređivan je palonozetron 250 mikrograma i 750 mikrograma s ondanzetronom 32 mg (poluvijek 4 sata) ili dolazetronom 100 mg (poluvijek 7,3 sata) primijenjeno intravenski na dan 1, bez deksametazona.
In two separate 12 week pivotal trials (Trials 1 and 2), ospemifene was associated with a statistically significant mean decrease from baseline in the percentage of parabasal cells and vaginal pH and a statistically significant mean increase from baseline in the percentage of superficial cells, compared with placebo (P &lt; 0.001 for each parameter) at weeks 4 and 12.
U dva odvojena ključna ispitivanja u trajanju od 12 tjedana (Ispitivanje 1 i 2), ospemifen je povezan sa statistički značajnim srednjim smanjenjem postotka parabazalnih stanica i vaginalnog pH u odnosu na početak ispitivanja, i statistički značajnim srednjim porastom postotka površinskih stanica u odnosu na početak ispitivanja, u usporedbi s placebo skupinom (P &lt; 0,001 za svaki parametar) u 4. i 12. tjednu.
In two years, the risk was 85% in the placebo group and 69% in the Extavia group (Hazard Ratio = 0.57, 95% confidence interval (0.46, 0.71), p &lt; 0.00001).
U dvije godine rizik je bio 85% u placebo skupini i 69% u skupini koja je primala Extaviju (omjer hazarda = 0,57, interval pouzdanosti 95% (0,46, 0,71), p &lt; 0,00001).
In very rare cases ( &lt; 0.01 %) the temporary infertility may last more than 18 months.
Privremena neplodnost može vrlo rijetko ( &lt; 0.01 %) trajati duže od 18 mjeseci.
In very rare cases ( &lt; 0.01%) there has been transitory increased sexual interest, increased testicle size and testicular pain immediately after implantation.
U veoma rijetkom broju slučajeva ( &lt; 0,01%) postojao je pojačani seksualni interes, povećan obujam testisa i bol u testisima neposredno po implantaciji.
In very rare cases ( &lt; 0.01%) there has been transitory increased sexual interest, increased testicle size and testicular pain immediately after implantation.
U vrlo rijetkim slučajevima ( &lt; 0.01%) primijećen je pojačan seksualni interes, povećanje veličine testis i pojava boli u testisima odmah nakon implantacije.
In very rare cases ( &lt; 0.01%), a transient behavioural change has been reported with development of aggression (see section 12 “Special warnings”).
U veoma rijetkim slučajevima ( &lt; 0,01%) dolazilo je do privremenih promjena u ponašanju uz razvitak agresije. (vidi dio 12 „Posebna upozorenja“)
In very rare cases ( &lt; 0.01%), a transient behavioural change has been reported with the development of aggression (see section 4.4).
Još rjeđe ( &lt; 0.01%) prijavljene su i promjene u ponašanju uz razvitak agresije. (vidi dio 4.4)
In very rare cases ( &lt; 0.01%), a transient behavioural change has been reported with the development of aggression (see section 4.4).
U veoma rijetkim slučajevima ( &lt; 0,01%) dolazilo je do privremenih promjena u ponašanju uz razvitak agresije. (vidi dio 4.4)
In very rare cases ( &lt; 1/100,000), hypersensitivity can be observed.
U vrlo rijetkim slučajevima ( &lt; 1/100 000) može se pojaviti preosjetljivost.
In very rare cases, the use of the veterinary medicinal product has been associated with hearing impairment, usually temporary, and primarily in geriatric dogs.
U vrlo malo slučajeva ( &lt; 0.01%) prilikom primjene ovog VMP primijećena je pojava oštećenja sluha, uglavnom privremeno i najčešće kod starih pasa.
In very rare cases, Type-I Hypersensitivity reactions (facial swelling, allergic pruritus) have been observed.
Također, u vrlo malo slučajeva ( &lt; 0.01%) primijećena je i reakcija preosjetljivosti tipa I ( znojenje lica, alergijski pruritis ).
In view of the potential impact of bisphosphonates, including zoledronic acid, on renal function, the lack of clinical safety data in patients with severe renal impairment (in clinical trials defined as serum creatinine ≥ 400 μmol/l or ≥ 4.5 mg/dl for patients with TIH and ≥ 265 μmol/l or ≥ 3.0 mg/dl for patients with cancer and bone metastases, respectively) at baseline and only limited pharmacokinetic data in patients with severe renal impairment at baseline (creatinine clearance &lt; 30 ml/min), the use of Zoledronic Acid Teva is not recommended in patients with severe renal impairment.
S obzirom na mogući utjecaj bisfosfonata, uključujući i zoledronatnu kiselinu, na funkciju bubrega, nedostatak kliničkih podataka o sigurnosti primjene u bolesnika s teškim oštećenjem funkcije bubrega (u kliničkim ispitivanjima definiranim kao kreatinin u serumu ≥ 400 μmol/l ili ≥ 4,5 mg/dl u bolesnika s hiperkalcemijom izazvanom tumorom, odnosno ≥ 265 μmol/l ili ≥ 3,0 mg/dl u bolesnika s rakom i metastazama u kostima) na početku liječenja i ograničene farmakokinetičke podatke u bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min) na početku liječenja, ne preporučuje se primjena Zoledronatne kiseline Teva u bolesnika s teškim oštećenjem funkcije bubrega.
In view of the potential impact of zoledronic acid on renal function, the lack of clinical safety data in patients with severe renal impairment (in clinical trials defined as serum creatinine 400 µmol/l or 4.5 mg/dl for patients with TIH and 265 µmol/l or 3.0 mg/dl for patients with cancer and bone metastases, respectively) at baseline and only limited pharmacokinetic data in patients with severe renal impairment at baseline (creatinine clearance &lt; 30 ml/min), the use of zoledronic acid is not recommended in patients with severe renal impairment.
S obzirom na mogući utjecaj zoledronatne kiseline na funkciju bubrega, nedostatak kliničkih podataka o sigurnosti u bolesnika s teškim oštećenjem bubrega (u kliničkim ispitivanjima definiranim kao kreatinin u serumu ≥ 400 μmol/l ili ≥ 4,5 mg/dl u bolesnika s hiperkalcijemijom izazvanom tumorom odnosno ≥ 265 μmol/l ili ≥ 3,0 mg/dl u bolesnika s rakom i koštanim metastazama) na početku liječenja i ograničene farmakokinetičke podatke u bolesnika s teškim oštećenjem bubrega (klirens kreatinina &lt; 30 ml/min) na početku liječenja, ne preporučuje se primjena zoledronatne kiseline u bolesnika s teškim oštećenjem bubrega.
In view of the potential impact of zoledronic acid on renal function, the lack of clinical safety data in patients with severe renal impairment (in clinical trials defined as serum creatinine ≥ 400 micromol/l or ≥ 4.5 mg/dl for patients with TIH and ≥ 265 micromol/l or ≥ 3.0 mg/dl for patients with cancer and bone metastases, respectively) at baseline and only limited pharmacokinetic data in patients with severe renal impairment at baseline (creatinine clearance &lt; 30 ml/min), the use of Zoledronic acid Actavis is not recommended in patients with severe renal impairment.
S obzirom na mogući utjecaj zoledronatne kiseline na funkciju bubrega, nedostatak kliničkih podataka o sigurnosti primjene u bolesnika s teškim oštećenjem funkcije bubrega (u kliničkim ispitivanjima definiranim kao kreatinin u serumu ≥ 400 mikromola/l ili ≥ 4,5 mg/dl u bolesnika s hiperkalcemijom izazvanom tumorom, odnosno ≥ 265 mikromola/l ili ≥ 3,0 mg/dl u bolesnika s rakom i metastazama u kostima) na početku liječenja i samo ograničene farmakokinetičke podatke u bolesnika s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min) na početku liječenja, ne preporučuje se primjena Zoledronatne kiseline Actavis u bolesnika s teškim oštećenjem funkcije bubrega.
In vitro apixaban studies showed no inhibitory effect on the activity of CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2D6 or CYP3A4 (IC50 &gt; 45 M) and weak inhibitory effect on the activity of CYP2C19 (IC50 &gt; 20 M) at concentrations that are significantly greater than peak plasma concentrations observed in patients.
Ispitivanja apiksabana in vitro pokazala su da on nema inhibicijski učinak na aktivnost CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2D6 i CYP3A4 (IC50 &gt; 45 µm) te da je slab inhibitor aktivnosti CYP2C19 (IC50 &gt; 20 µm) pri koncentracijama koje su značajno više od vršne koncentracije lijeka u plazmi zabilježene u bolesnika.
In vitro binding of axitinib to human plasma proteins is &gt; 99% with preferential binding to albumin and moderate binding to α1-acid glycoprotein.
Aksitinib se in vitro veže za proteine u ljudskoj plazmi u opsegu od &gt; 99%, prvenstveno za albumin te umjereno za α1-kiseli glikoprotein.
In vitro binding of emtricitabine to human plasma proteins is &lt; 4% and independent of concentrations over the range of 0.02 to 200 µg/ml.
In vitro vezivanje emtricitabina na proteine ljudske plazme je &lt; 4% i neovisno je o koncentracijama u rasponu od 0,02 do 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 to 200 µg/mL.
In vitro vezanje emtricitabina na humane plazmatske proteine bilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02 do 200 µg/mL.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 to 200 µg/mL.
In vitro vezanje emtricitabina za proteine ljudske plazme bilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02 do 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02 – 200 μg/ml.
Vezivanje emtricitabina za proteine u ljudskoj plazmi in vitro iznosilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02 do 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 µg/ml.
In vitro vezanje emtricitabina na humane proteine plazme bilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02 do 200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 µg/mL.
In vitro vezanje emtricitabina za humane proteine plazme bilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02-200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 µg/mL.
In vitro vezanje emtricitabina za proteine ljudske plazme bilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02-200 µg/ml.
In vitro binding of emtricitabine to human plasma proteins was &lt; 4% and independent of concentration over the range of 0.02-200 μg/mL.
In vitro vezanje emtricitabina za humane proteine plazme bilo je &lt; 4% i nije ovisilo o koncentraciji u rasponu od 0,02-200 µg/ml.
In vitro binding of tenofovir to human plasma or serum protein is &lt; 0.7% and 7.2%, respectively over the tenofovir concentration range 0.01 to 25 µg/ml.
In vitro vezivanje tenofovira na proteine ljudske plazme ili seruma je &lt; 0,7%, odnosno 7,2%, u rasponu koncentracija tenofovira od 0,01 do 25 µg/ml.
In vitro binding of tenofovir to human plasma proteins is &lt; 0.7% and is independent of concentration over the range of 0.01-25 µg/mL.
In vitro vezanje tenofovira za proteine ljudske plazme je &lt; 0,7% i ne ovisi o koncentraciji u rasponu od 0,01-25 µg/ml.
In vitro binding of tenofovir to human plasma proteins is &lt; 0.7% and is independent of concentration over the range of 0.01-25 μg/mL.
In vitro vezanje tenofovira za humane proteine plazme je &lt; 0,7% i ne ovisi o koncentraciji u rasponu od 0,01-25 µg/ml.
In vitro orlistat is &gt; 99 % bound to plasma proteins (lipoproteins and albumin were the major binding proteins).
Orlistat se in vitro &gt; 99 % veže za proteine plazme (lipoproteini i albumin najznačajniji su vezni proteini).
In vitro plasma protein binding in human plasma of fluticasone furoate and vilanterol was high, on average &gt; 99.6% and 93.9%, respectively.
Stupanj vezivanja flutikazonfuroata i vilanterola za proteine u ljudskoj plazmi in vitro bio je visok, prosječno &gt; 99,6% za flutikazonfuroat odnosno 93,9% za vilanterol.
In vitro selection of darunavir-resistant virus from wild type HIV-1 was lengthy ( &gt; 3 years).
In vitro selekcija virusa rezistentnog na darunavir iz divljeg tipa HIV-1 bila je dugotrajna ( &gt; 3 godine).
In vitro studies evaluating the percent recovery of total dose delivered with nasogastric or gastrostomy tubes demonstrated the percent of dose recovered was &gt; 99% for doses &gt; 1 ml and 70% for a 0.5 ml dose.
In vitro ispitivanja za procjenu postotka povrata ukupne doze primijenjene putem nazogastrične sonde ili gastrostome pokazala su da je postotak povrata doze &gt; 99% za doze &gt; 1 ml, odnosno 70% za dozu od 0,5 ml.
In vitro studies evaluating the percent recovery of total dose delivered with nasogastric, nasojejunal or gastrostomy tubes demonstrated the percent of dose recovered was &gt; 99% for doses &gt; 1 ml and 70% for a 0.5 ml dose.
In vitro ispitivanja za procjenu postotka povrata ukupne doze primijenjene putem nazogastrične, nazojejunalne sonde ili gastrostome pokazala su postotak povrata doze &gt; 99% za doze &gt; 1 ml, odnosno 70% za dozu od 0,5 ml.
In vitro studies have shown that vardenafil is more potent on PDE5 than on other known phosphodiesterases ( &gt; 15-fold relative to PDE6, &gt; 130-fold relative to PDE1, &gt; 300-fold relative to PDE11, and &gt; 1000-fold relative to PDE2, PDE3, PDE4, PDE7, PDE8, PDE9 and PDE10).
In vitro ispitivanja pokazala su da vardenafil ima jači učinak na PDE5 nego na druge poznate fosfodiesteraze ( &gt; 15-struko u odnosu na PDE6, &gt; 130-struko u odnosu na PDE1, &gt; 300-struko u odnosu na PDE11 i &gt; 1000-struko u odnosu na PDE2, PDE3, PDE4, PDE7, PDE8, PDE9 i PDE10).
In vitro studies in human, dog, mouse and rat plasma showed a high plasma protein binding ( &gt; 99.5 %), mainly to albumin and α-1-acid glycoprotein.
In vitro ispitivanja u plazmi čovjeka, psa, miša i štakora pokazala su visoko vezanje na proteine u plazmi ( &gt; 99,5%) uglavnom na albumin i α-1 kiseli glikoprotein.
In vitro studies using human liver microsomes show no or little ( &lt; 25%) inhibition of cytochrome P450 isozymes 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 or 3A4 at zonisamide levels approximately two-fold or greater than clinically relevant unbound serum concentrations.
Ispitivanja in vitro na humanim mikrosomima jetre ne pokazuju ili pokazuju malu inhibiciju ( &lt; 25%) izoenzima 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 ili 3A4 citokroma P450 pri koncentracijama zonisamida koje su bile približno dva ili više puta veće od klinički važnih nevezanih koncentracija u serumu.
In vitro studies using human liver microsomes show no or little ( &lt; 25%) inhibition of cytochrome P450 isozymes 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 or 3A4 at zonisamide levels approximately two- fold or greater than clinically relevant unbound serum concentrations.
Ispitivanja in vitro na mikrosomima ljudske jetre ne pokazuju ili pokazuju malu inhibiciju ( &lt; 25%) izoenzima 1A2, 2A6, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1 ili 3A4 citokroma P450 pri koncentracijama zonisamida koje su bile približno dva ili više puta veće od klinički značajnih koncentracija slobodnog zonisamida u serumu.
In vitro, apremilast is a substrate, and a weak inhibitor of P-glycoprotein (IC50 &gt; 50µM), however clinically relevant drug interactions mediated via P-gp are not expected to occur.
In vitro, apremilast je supstrat i slabi inhibitor P-glikoproteina (IC50 &gt; 50µM), međutim, ne očekuje se da će doći do klinički važnih interakcija lijekova posredovanih putem P-gp-a.
In vitro, cytochrome P450 3A4 was demonstrated as the predominant ( &gt; 80%) isoform involved in the P450-mediated metabolism of lenvatinib.
In vitro, citokrom P450 3A4 pokazao se kao prevladavajući ( &gt; 80%) izooblik uključen u metabolizam lenvatiniba koji se odvija putem P450.
In vitro, dolutegravir demonstrated no direct, or weak inhibition (IC50 &gt; 50 μM) of the enzymes cytochrome P450 (CYP)1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6 CYP3A, uridine diphosphate glucuronosyl transferase (UGT)1A1 or UGT2B7, or the transporters Pgp, BCRP, BSEP, OATP1B1, OATP1B3, OCT1, MATE2-K, MRP2 or MRP4.
In vitro dolutegravir nije pokazao ni izravnu ni slabu inhibiciju (IC50 &gt; 50 μM) enzima citokroma P450 (CYP)1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A, uridin difosfat glukuronoziltransferaze (UGT)1A1 ili UGT2B7 niti prijenosnika P-gp, BCRP, BSEP, OATP1B1, OATP1B3, OCT1, MATE2-K, MRP2 ili MRP4.
In vitro, lurasidone demonstrated no direct, or weak inhibition (direct or time-dependent) (IC50 &gt; 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 &gt; 5,9 μM) citokrom P450 enzima (CYP)1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19,
In vitro, orlistat is &gt; 99% bound to plasma proteins (lipoproteins and albumin were the major binding proteins).
In vitro se više od 99 % veže na proteine plazme (glavni vezujući proteini bili su lipoprotein i albumin).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase ( &lt; 10 %).
In vitro, taj metabolit pokazuje minimalnu inhibiciju acetilkolinesteraze ( &lt; 10 %).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase ( &lt; 10%).
In vitro ovaj metabolit pokazuje minimalnu inhibiciju acetilkolinesteraze ( &lt; 10%).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase ( &lt; 10%).
In vitro, taj metabolit pokazuje minimalnu inhibiciju acetilkolinesteraze ( &lt; 10%).
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 &gt; 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 &gt; 400 kopija/mL u 48., 96. ili 144. tjednu ili u vrijeme prijevremenog prekida uzimanja ispitivanog lijeka.
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 &gt; 4 fold reduced susceptibility to enfuvirtide compared with the corresponding pre-treatment samples.
Rezistencija na enfuvirtid in vivo: U kliničkim ispitivanjima faze III, HIV rekombinante koje su sadržavale gene env iz uzoraka HIV-RNK uzetih od 187 bolesnika do 24. tjedna pokazale su &gt; 4 puta smanjenu osjetljivost na enfuvirtid u usporedbi s odgovarajućim uzorcima uzetima prije liječenja.
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 &gt; 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 &gt; 400 kopija/ml u 48., 96. ili 144. tjednu ili u trenutku prijevremenog prekida uzimanja ispitivanog lijeka.
In volunteers with severe renal impairment (creatinine clearance &lt; 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 &lt; 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 (creatinine clearance &lt; 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 poremećajem bubrega (klirens kreatinina &lt; 30 ml/min), klirens sildenafila bio je snižen, što je rezultiralo srednjim porastom AUC i Cmax od 100%, odnosno 88% u usporedbi s dobrovoljcima odgovarajućim po dobi bez oštećenja bubrega.
In volunteers with severe renal impairment (creatinine clearance &lt; 30 ml/min) the mean AUC was increased by 21% and the mean Cmax decreased by 23%, compared to volunteers with no renal impairment.
U dobrovoljaca s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min) srednja vrijednost AUC-a bila je povećana za 21%, a srednja vrijednost Cmax smanjena za 23% u usporedbi s dobrovoljcima bez oštećenja bubrežne funkcije.
In volunteers with severe renal impairment (creatinine clearance &lt; 30 ml/min) the mean AUC was increased by 21% and the mean Cmax decreased by 23%, compared to volunteers with no renal impairment.
U dobrovoljaca s teškim oštećenjem funkcije bubrega (klirens kreatinina &lt; 30 ml/min) srednja vrijednost AUC-a bila je povećana za 21%, a srednja vrijednost Cmax smanjena za 23% u usporedbi s dobrovoljcima bez oštećenja funkcije bubrega.