natgillin/translations-raw huggingface dataset:
In these clinical studies patients had active viral replication (HBV DNA ≥ 100,000 copies/ ml) and elevated ALT levels (≥ 1.2 x Upper Limit of Normal (ULN)).
8 V teh kliničnih študijah so imeli bolniki aktivno virološko replikacijo (HBV DNA ≥ 100. 000 kopij/ ml) in povišane vrednosti ALT (≥ 1, 2 krat zgornja referenčna vrednost (ULN, Upper Limit of Normal)).
Experience in patients with compensated liver disease:
Izkušnje pri bolnikih z kompenzirano boleznijo jeter:
In two placebo-controlled studies (total n=522) in HBeAg positive or in HBeAg negative chronic hepatitis B patients with compensated liver disease, significantly more patients (p < 0.001) in the 10 mg adefovir dipivoxil groups (53 and 64%, 8 respectively) had histological improvement from baseline at week 48 than in the placebo groups (25 and 33%).
V dveh s placebom kontroliranih študijah (skupno n=522) pri HBeAg pozitivnih oziroma HBeAg negativnih bolnikih s kroničnim hepatitisom B s kompenzirano boleznijo jeter, se je pri značilno več bolnikih (p < 0, 001) v skupini, ki je prejemala 10 mg adefovirdipivoksila (53% oziroma 64%) pokazalo histološko izboljšanje od začetne vrednosti v 48. tednu kot pri placebo skupini (25% oziroma 33%).
High baseline ALT levels (≥ 2 x ULN) and Knodell Histology Activity Index (HAI) scores (≥ 10) and low HBV DNA (< 7.6 log10 copies/ ml) were associated with greater histological improvement.
Večje histološko izboljšanje je bilo povezano z visokimi začetnimi vrednostmi ALT (≥ 2 krat zgornja referenčna vrednost - ULN), z visokimi vrednostmi Knodellovega indeksa histološke aktivnosti (HAI, Histology Activity Index) (≥ 10) in z nizkim HBV DNA (< 7, 6 log10 kopij/ ml).
Blinded, ranked assessments of both necro- inflammatory activity and fibrosis at baseline and week 48, demonstrated that patients treated with 10 mg adefovir dipivoxil had improved necro-inflammatory and fibrosis scores relative to placebo- treated patients.
Slepa, razvrščena ocena tako nekroinflamatorne aktivnosti kot fibroze na začetku in v 48. tednu je pokazala, da so imeli bolniki zdravljeni z 10 mg adefovirdipivoksila boljše nekroinflamatorne in fibrozne rezultate glede na bolnike, ki so prejemali placebo.
Assessment of the change in fibrosis after 48 weeks treatment using the Knodell scores confirms that patients treated with adefovir dipivoxil 10 mg had more regression and less progression of fibrosis than patients treated with placebo.
Ocena sprememb fibroze po 48 tednih zdravljenja glede na Knodellovo lestvico potrjuje, da je fibroza pri bolnikih zdravljenih z 10 mg adefovirdipivoksila bolj nazadovala in manj napredovala kot pri bolnikih zdravljenih s placebom.
In the two studies mentioned above, treatment with 10 mg adefovir dipivoxil was associated with significant reductions in serum HBV DNA (3.52 and 3.91 log10 copies/ ml, respectively, versus 0.55 and 1.35 log10 copies/ ml), increased proportion of patients with normalisation of ALT (48 and 72% versus 16 and 29%) or increased proportion of patients with serum HBV DNA below the limits of quantification (< 400 copies/ ml Roche Amplicor Monitor PCR assay) (21 and 51% versus 0%) when compared with placebo.
V obeh zgoraj omenjenih študijah je bilo zdravljenje z 10 mg adefovirdipivoksila v primerjavi s placebom združeno s pomembnim zmanjšanjem serumske HBV DNA (3, 52 in 3, 91 log10 kopij/ ml v primerjavi z 0, 55 in 1, 35 log10 kopij/ ml), z večjim deležem bolnikov z normalizacijo vrednosti ALT (48 in 72% v primerjavi s 16 in 29%) in s povečanim deležem bolnikov s serumsko HBV DNA pod mejo količinske zaznave (< 400 kopij/ ml po analizi Roche Amplicor Monitor PCR) (21 in 51% v primerjavi z 0%).
In the study in HBeAg positive patients, HBeAg seroconversion (12%) and HBeAg loss (24%) was observed significantly more frequently in patients receiving 10 mg adefovir dipivoxil than in patients receiving placebo (6% and 11%, respectively) after 48 weeks of treatment.
V študiji pri HBeAg pozitivnih bolnikih, ki so prejemali 10 mg adefovirdipivoksila napram placebu je bila značilno bolj pogosto opažena HBeAg serokonverzija (12% napram 6%) in izguba HBeAg (24% napram 11%) po 48 tednih zdravljenja.
In the HBeAg negative study patients on adefovir dipivoxil (0-48 weeks) were re-randomised in a blinded-manner to continue on adefovir dipivoxil or receive placebo for an additional 48 weeks.
V študiji s HBeAg negativnimi bolniki, ki so jemali adefovirdipivoksil (0- 48 tednov), so bolnike naključno slepo prerazporedili tako, da so nadaljnjih 48 tednov še naprej jemali adefovirdipivoksil ali pa prejemali placebo.
At week 96, patients continuing on adefovir dipivoxil 10 mg had sustained suppression of serum HBV with maintenance of the reduction seen at week 48.
V 96. tednu so imeli bolniki, ki so nadaljevali z jemanjem 10 mg adefovirdipivoksila, stalno supresijo serumskega HBV z ohranitvijo znižanja, kakršno je bilo vidno v 48. tednu.
In most patients who stopped treatment with adefovir dipivoxil, serum HBV DNA and ALT levels returned towards baseline.
Pri večini bolnikov, ki so prenehali z zdravljenjem z adefovirdipivoksilom, so se serumske vrednosti HBV DNA in ALT vrnile proti začetni vrednosti.
Treatment with adefovir dipivoxil resulted in improvement in the liver fibrosis from baseline to 96 weeks therapy when analysed using the Ishak score (median change:
Zdravljenje z adefovirdipivoksilom je pripeljalo do izboljšanja jetrne fibroze od začetne vrednosti v 96. tednu, merjeno z Ishakovo lestvico (mediana spremembe:
Patients who completed the first 96 weeks of the HBeAg negative study and received adefovir dipivoxil treatment during weeks 49 to 96, were offered the opportunity to receive open-label treatment with adefovir dipivoxil from study week 97 through to week 240.
Bolnikom, ki so zaključili prvih 96 tednov študije s HBeAg negativnimi bolniki in so prejemali zdravljenje z adefovirdipivoksilom med 49. in 96. tednom, so ponudili možnost prejemanja odprtega zdravljenja z adefovirdipivoksilom od 97. študijskega tedna do 240. tedna.
Serum HBV DNA levels remained undetectable and ALT levels normalised in approximately two thirds of patients following treatment with adefovir dipivoxil for up to 240 weeks.
Vrednosti serumske HBV DNA so ostale nezaznavne in vrednosti ALT so se normalizirale pri približno dveh tretjinah bolnikov po zdravljenju z adefovirdipivoksilom do 240. tedna.
Δ = -1).
Klinično in statistično pomembno izboljšanje fibroze je bilo opaženo pri spremembah na Ishakovi lestvici od začetka zdravljenja z adefovirdipivoksilom do konca študije (240. teden) (mediana spremembe: Δ= - 1).
By the end of the study, 7 of 12 patients (58%) with bridging fibrosis or cirrhosis at baseline, had an improved Ishak fibrosis score of ≥ 2 points.
Do konca študije je imelo 7 od 12 bolnikov (58%), ki so imeli na začetku premostitveno fibrozo ali cirozo, izboljšano fibrozno vrednost po Ishakovi lestvici za ≥ 2 točki.
Five patients achieved and maintained HBsAg seroconversion (HBsAg negative/ HBsAb positive).
Pet bolnikov je doseglo in ohranilo HBsAg serokonverzijo (HBsAg negativni/ anti- HBs pozitivni).
Experience in patients pre- and post-liver transplantation with lamivudine-resistant HBV:
9 Izkušnje pri bolnikih pred in po transplantaciji jeter z na lamivudin odpornim HBV:
In a clinical study in 394 chronic hepatitis B patients with lamivudine-resistant HBV (pre-liver transplantation (n=186) and post-liver transplantation (n=208)), treatment with 10 mg adefovir dipivoxil resulted in a median reduction in serum HBV DNA of 4.1 and 4.2 log10 copies/ ml, respectively, at week 48.
V klinični študiji s 394 bolniki s kroničnim hepatitisom B z na lamivudin odpornim HBV (pred (n=186) in po transplantaciji jeter (n=208)) je zdravljenje z 10 mg adefovirdipivoksila privedlo do znižanja koncentracije serumske HBV DNA za 4, 1 log10 kopij/ ml (mediana vrednost) za bolnike pred oziroma za 4, 2 log10 kopij/ ml (mediana) za bolnike po transplantaciji jeter v 48. tednu.
In the pre-liver transplantation and post-liver transplantation cohorts 77 of 109 (71%) patients and 64 of 159 (40%) patients, respectively, achieved undetectable HBV DNA levels at week 48 (< 1,000 copies/ ml Roche Amplicor Monitor PCR assay).
V skupini bolnikov pred transplantacijo jeter je 77 od 109 bolnikov (71%) doseglo nezaznavne koncentracije HBV DNA v 48. tednu, v skupini bolnikov po transplantaciji jeter pa 64 od 159 bolnikov (40%) (< 1. 000 kopij/ ml po analizi Roche Amplicor Monitor PCR).
Treatment with 10 mg adefovir dipivoxil showed similar
Zdravljenje z 10 mg adefovirdipivoksila je pokazalo podobno učinkovitost ne glede na začetni vzorec polimeraznih mutacij HBV DNA rezistentnih na lamivudin.
9 efficacy regardless of the patterns of lamivudine-resistant HBV DNA polymerase mutations at baseline.
Izboljšanje ali stabilizacijo je prikazala lestvica po Child- Pugh- Turcotte.
Normalisation of ALT, albumin, bilirubin and prothrombin time was seen at week 48 in 51-85% of the patients.
V 48. tednu so bile opažene normalizacije vrednosti za ALT, albumin, bilirubin in protrombinski čas pri 51- 85% bolnikov.
In the pre-liver transplantation cohort, 25 of 33 (76%) patients achieved undetectable HBV DNA levels and 84% of patients had ALT normalisation at 96 weeks.
V skupini bolnikov pred transplantacijo jeter je 25 od 33 bolnikov (76%) doseglo nezaznavne koncentracije HBV DNA in 84% bolnikov je imelo normalizacijo vrednosti za ALT v 96. tednu.
In the post-liver transplantation cohort, 61 of 94 (65%) and 35 of 45 (78%) of patients achieved undetectable HBV DNA levels at 96 and 144 weeks, respectively, and 70% and 58% of patients had ALT normalisation at these study visits.
V skupni bolnikov po transplantaciji jeter je 61 od 94 bolnikov (65%) doseglo nezaznavne koncentracije HBV DNA v 96. tednu, 35 od 45 bolnikov (78%) pa v 144. tednu; 70% bolnikov je imelo pri študijskem obisku v 96. tednu normalizacijo vrednosti za ALT, 58% bolnikov pa v 144. tednu.
Experience in patients with compensated liver disease and lamivudine-resistant HBV:
Izkušnje pri bolnikih s kompenzirano boleznijo jeter in z na lamivudin odpornim HBV:
In a double-blind comparative study in chronic hepatitis B patients with lamivudine-resistant HBV (n=58), there was no median reduction in HBV DNA from baseline after 48 weeks of treatment with lamivudine.
V dvojno slepi primerjalni študiji bolnikov s kroničnim hepatitisom B z na lamivudin odpornim HBV (n=58) ni prišlo do znižanja koncentracij (mediana) HBV DNA od začetne vrednosti po 48 tednih zdravljenja z lamivudinom.
Forty-eight weeks of treatment with adefovir dipivoxil 10 mg alone or in combination with lamivudine resulted in a similar significant decrease in median serum HBV DNA levels from baseline (4.04 log10 copies/ ml and 3.59 log10 copies/ ml, respectively).
Zdravljenje samo z 10 mg adefovirdipivoksila oziroma s kombinacijo 10 mg adefovirdipivoksila in lamivudina, pa je po 48 tednih privedlo do podobnega značilnega padca serumske koncentracije (mediana) HBV DNA od začetne vrednosti (4, 04 log10 kopij/ ml pri samo adefovirdipivoksilu oziroma 3, 59 log10 kopij/ ml pri kombinaciji).
Experience in patients with decompensated liver disease and lamivudine-resistant HBV:
Izkušnje pri bolnikih z dekompenzirano boleznijo jeter in z na lamivudin odpornim HBV:
In 40 HBeAg positive or HBeAg negative patients with lamivudine-resistant HBV and decompensated liver disease receiving treatment with 100 mg lamivudine, addition of 10 mg adefovir dipivoxil treatment for 52 weeks resulted in a median reduction in HBV DNA of 4.6 log10 copies/ ml.
Rezultati zdravljenja 40 HBeAg pozitivnih oziroma HBeAg negativnih bolnikov z na lamivudin odpornimi HBV in dekompenzirano boleznijo jeter, ki so prejemali 100 mg lamivudina in so bili dodatno 52 tednov zdravljeni z 10 mg adefovirdipivoksila, so pokazali mediano zmanjšanje vrednosti HBV DNA za 4, 6 log10 kopij/ ml.
Experience in patients with HIV co-infection and lamivudine-resistant HBV:
Izkušnje pri bolnikih s sočasno okužbo s HIV in na lamivudin odpornim HBV:
In an open-label investigator study in 35 chronic hepatitis B patients with lamivudine-resistant HBV and co-infected with HIV, continued treatment with 10 mg adefovir dipivoxil resulted in progressive reductions in serum HBV DNA levels and ALT levels throughout the course of treatment up to 144 weeks.
V odprti raziskovalni študiji pri 35 bolnikih s kroničnim hepatitisom B z na lamivudin odpornim HBV in sočasno okuženih s HIV je nadaljevanje zdravljenja z 10 mg adefovirdipivoksila privedlo do napredujočega zniževanja vrednosti serumske HBV DNA in ALT skozi celotno obdobje zdravljenja vse do 144 tednov.
In a second open-label, one-arm study, 10 mg adefovir dipivoxil and pegylated interferon alpha-2a were added to ongoing lamivudine therapy in 18 HIV/ HBV co-infected patients with lamivudine-resistant HBV.
V drugi odprti študiji z enim krakom so 10 mg adefovirdipivoksila in pegiliranega interferona alfa- 2a dodali potekajočemu zdravljenju z lamivudinom pri 18 bolnikih, sočasno okuženih z virusoma HIV/ HBV, z na lamivudin odpornim HBV.
Patients were all HBeAg positive and had median CD4 cell count of 441 cells/ mm3 (no patient had CD4 count < 200 cells/ mm3).
Vsi bolniki so bili pozitivni za HBeAg in so imeli srednje število celic CD4 441 celic/ mm3 (pri nobenem bolniku število celic CD4 ni bilo < 200 celic/ mm3).
However, on-treatment HBV DNA response was not maintained off-therapy since all the patients had a rebound in HBV DNA after adefovir dipivoxil and pegylated interferon alpha-2a discontinuation.
Vendar pa se odziv HBV DNA dosežen med zdravljenjem ni vzdrževal po prekinitvi zdravljenja, saj se je pri vseh bolnikih po prekinitvi adefovirdipivoksila in pegiliranega interferona alfa- 2a pojavil povratni odziv HBV DNA.
Due to the small sample size and the study design, in particular the lack of treatment arms with pegylated interferon alpha-2a monotherapy and with adefovir monotherapy, it is not possible to draw formal conclusions on the best therapeutic management of HIV co-infected patients with lamivudine-resistant HBV.
Zaradi majhnega vzorca in načrtovanja študije, predvsem zaradi pomanjkanja krakov zdravljenja, ki bi prejemali monoterapijo s pergiliranim interferonom alfa- 2a in monoterapijo z adefovirjem, ni mogoče formalno sklepati o najboljši terapevtski obravnavi bolnikov s HBV odpornim na lamivudin, sočasno okuženih s HIV.
Paediatric population:
10 Pediatrični populacija:
The efficacy and safety of a daily dose of 0.25 mg/ kg to 10 mg adefovir dipivoxil in children (aged from 2 to < 18 years) was examined in a double-blind, randomised, placebo-controlled study in 173 paediatric patients (115 on adefovir dipivoxil, 58 on placebo) who had HBeAg positive chronic hepatitis B, serum ALT levels ≥ 1.5 x upper limit of normal (ULN) and compensated liver disease.
Učinkovitost in varnost dnevnega odmerka 0, 25 mg/ kg do 10 mg adefovirdipivoksila pri otrocih (starih od 2 do < 18 let) so raziskali v dvojno slepi, randomizirani, s placebom kontrolirani študiji na 173 pediatričnih bolnikih (115 jih je prejemalo adefovirdipivoksil, 58 pa placebo), ki so imeli HBeAg pozitivni kronični hepatitis B, serumske vrednosti ALT ≥ 1, 5 krat zgornja referenčna vrednost (ULN) in kompenzirano bolezen jeter.
At week 48, in children aged 2 to 11 years old, no statistically significant difference was observed in the proportions of patients that achieved the primary endpoint of serum HBV DNA < 1,000 copies/ ml and normal ALT levels between the placebo arm and the adefovir dipivoxil arm.
V 48. tednu pri otrocih, starih od 2 do 11 let, niso opazili statistično pomembne razlike v deležu bolnikov, ki so dosegli primarni cilj serumske HBV DNA < 1. 000 kopij/ ml in normalne vrednosti ALT med skupino, ki je prejemala placebo in skupino, ki je prejemala adefovirdipivoksil.
In the adolescent population (n=83) (aged from 12 to < 18 years), significantly more patients treated with adefovir dipivoxil achieved the primary efficacy endpoint and obtained significant reductions in serum HBV DNA (23%) compared to placebo-treated patients (0%).
V populaciji mladostnikov (n=83) (starih od 12 do < 18 let) je pomembno več bolnikov, ki so prejemali adefovirdipivoksil, doseglo primarni cilj učinkovitosti in pomembno zmanjšanje serumske HBV DNA (23%) v primerjavi z bolniki, ki so prejemali placebo (0%).
However, the proportions of subjects who achieved HBeAg seroconversion at week 48 were similar (11%) between the placebo arm and the adefovir dipivoxil 10 mg arm in adolescent patients.
Vendar pa je bil pri mladostnikih delež bolnikov, pri katerih je prišlo do HBeAg serokonverzije v 48. tednu, podoben (11%) v skupini, ki je prejemala placebo in skupini, ki je prejemala 10 mg adefovirdipivoksila.
10 Overall, the safety profile of adefovir dipivoxil in children was consistent with the known safety profile in adult patients.
Varnostni profil adefovirdipivoksila pri otrocih je bil na splošno podoben znanemu varnostnemu profilu pri odraslih bolnikih.
However, a signal towards a higher rate of decreased appetite and/ or food intake was observed in the adefovir arm as compared to the placebo arm.
Vendar je bilo opaženo nakazovanje višje stopnje zmanjšanega teka in/ ali vnosa hrane v skupini, ki je prejemala adefovir, v primerjavi s skupino, ki je prejemala placebo.
At week 48 and 96, mean changes from baseline in weight and BMI Z scores tended to decrease in adefovir dipivoxil-treated patients.
Pri bolnikih, zdravljenih z adefovirdipivoksilom so se v 48. in 96. tednu povprečne spremembe od začetnih z- vrednosti telesne mase in indeksa telesne mase, nagibale k zmanjšanju.
No long-term safety data or long-term resistance data are available with adefovir dipivoxil in children.
Za adefovirdipivoksil podatki o dolgoročni varnosti ali dolgoročni odpornosti pri otrocih niso na voljo.
The clinical data available are insufficient to draw definitive conclusions on the benefit/ risk ratio of the adefovir treatment in children with chronic hepatitis B (see section 4.2).
Klinični podatki, ki so na voljo, ne zadostujejo za dokončne sklepe o razmerju koristi in tveganja zdravljenja z adefovirjem pri otrocih s kroničnim hepatitisom B (glejte poglavje 4. 2).
Clinical resistance in patients receiving adefovir dipivoxil as monotherapy and in combination with lamivudine:
Klinična odpornost pri bolnikih, ki prejemajo adefovirdipivoksil kot monoterapijo in v kombinaciji z lamivudinom:
In several clinical studies (HBeAg positive, HBeAg negative, pre- and post-liver transplantation with lamivudine-resistant HBV and lamivudine-resistant HBV co-infected with HIV patients), genotypic analyses were conducted on HBV isolates from 379 of a total of 629 patients, treated with adefovir dipivoxil for 48 weeks.
V več kliničnih študijah (HBeAg pozitivni, HBeAg negativni bolniki, bolniki pred in po transplantaciji jeter z na lamivudin odpornim HBV in bolniki z na lamivudin odpornim HBV, sočasno okuženi s HIV) so bile izpeljane genotipske analize na izolatih HBV pri 379 bolnikih od skupno 629 bolnikov, ki so bili 48 tednov zdravljeni z adefovirdipivoksilom.
No HBV DNA polymerase mutations associated with resistance to adefovir were identified when patients were genotyped at baseline and at week 48.
Pri genotipiziranju bolnikov na začetku in v 48. tednu ni bilo identificiranih nobenih HBV DNA- polimeraznih mutacij povezanih z rezistenco proti adefovirju.
After 96, 144, 192 and 240 weeks of treatment with adefovir dipivoxil, resistance surveillance was performed for 293, 221, 116 and 64 patients, respectively.
Po 96 tednih zdravljenja z adefovirdipivoksilom je bila opravljena kontrola odpornosti pri 293 bolnikih, po 144 tednih pri 221 bolnikih, po 192 tednih pri 116 bolnikih in po 240 tednih pri 64 bolnikih.
Two novel conserved site mutations were identified in the HBV polymerase gene (rtN236T and rtA181V), which conferred clinical resistance to adefovir dipivoxil.
Na genu HBV- polimeraze, na konzervativnem mestu, sta bili identificirani dve novi mutaciji (rtN236T in rtA181V), ki sta povzročili klinično odpornost proti adefovirdipivoksilu.
The cumulative probabilities of developing these adefovir-associated resistance mutations in all patients treated with adefovir dipivoxil were 0% at 48 weeks and approximately 2%, 7%, 14% and 25% after 96, 144, 192 and 240 weeks, respectively.
Kumulativne verjetnosti razvoja teh mutacij za rezistenco povezanih z adefovirjem so bile pri vseh bolnikih zdravljenih z adefovirdipivoksilom 0% v 48. tednu in približno 2% po 96 tednih, 7% po 144 tednih, 14% po 192 tednih in 25% po 240 tednih.
Clinical resistance in monotherapy studies in nucleoside naïve patients:
Klinična odpornost v študijah monoterapije pri bolnikih, ki še niso bili zdravljeni z nukleozidi:
In patients receiving adefovir dipivoxil monotherapy (HBeAg negative study) the cumulative probability of developing adefovir-associated resistance mutations was 0%, 3%, 11%, 18% and 29% at 48, 96, 144, 192 and 240 weeks respectively.
Pri bolnikih, ki so prejemali adefovirdipivoksil kot monoterapijo (študija s HBeAg negativnimi bolniki), je bila kumulativna verjetnost razvoja mutacij za rezistenco, povezanih z adefovirjem 0% v 48. tednu, 3% v 96. tednu, 11% v 144. tednu, 18% v 192. tednu in 29% v 240. tednu.
In addition, the long-term (4 to 5 years) development of resistance to adefovir dipivoxil was significantly lower in patients who had serum HBV DNA below the limit of quantification (< 1,000 copies/ ml) at week 48 as compared to patients with serum HBV DNA above 1,000 copies/ ml at week 48.
Poleg tega je bil dolgoročni (4 do 5 let) razvoj rezistence proti adefovirdipivoksilu značilno nižji pri bolnikih, ki so imeli serumsko HBV DNA pod mejo količinske zaznave (< 1. 000 kopij/ ml) v 48. tednu, v primerjavi z bolniki s serumsko HBV DNA nad 1. 000 kopij/ ml v 48. tednu.
In HBeAg positive patients, the incidence of adefovir-associated resistance mutations was 3% (2/ 65), 17% (11/ 65) and 20% (13/ 65) after a median duration exposure of 135, 189 and 235 weeks respectively.
Pri HBeAg pozitivnih bolnikih je bila incidenca mutacij za rezistenco, povezanih z adefovirjem, 3% (2/ 65) po medianem trajanju izpostavljenosti, 17% (11/ 65) po 189 tednih in 20% (13/ 65) po 235 tednih.
Clinical resistance in studies where adefovir dipivoxil was added to ongoing lamivudine in patients with lamivudine-resistance:
Klinična odpornost v študijah, v katerih je bil adefovirdipivoksil dodan k tekočemu zdravljenju z lamivudinom pri bolnikih z rezistenco proti lamivudinu:
In an open-label study of pre- and post-liver transplantation patients with clinical evidence of lamivudine-resistant HBV, no adefovir-associated resistance mutations were observed at week 48.
V odprti študiji pri bolnikih pred in po transplantaciji jeter s kliničnimi dokazi za obstoj na lamivudin odpornega HBV v 48. tednu niso bile opažene mutacije za rezistenco, povezane z adefovirjem.
With up to 3 years of exposure, no patients receiving both adefovir dipivoxil and lamivudine developed resistance to adefovir dipivoxil.
Pri izpostavljenosti do 3 let ni noben bolnik, ki je prejemal adefovirdipivoksil in lamivudin, razvil rezistence proti adefovirdipivoksilu.
However, 4 patients who discontinued lamivudine treatment developed the rtN236T mutation while receiving adefovir dipivoxil monotherapy and all experienced serum HBV rebound.
Vendar pa so 4 bolniki, ki so prekinili zdravljenje z lamivudinom, razvili mutacijo rtN236T med monoterapijo z adefovirdipivoksilom in vsi so izkusili rebound vrednosti serumske HBV.
The currently available data both in vitro and in patients suggest that HBV expressing the adefovir- associated resistance mutation rtN236T is susceptible to lamivudine.
11 Podatki, ki so trenutno na voljo tako in vitro kot pri bolnikih, kažejo, da je HBV z mutacijo rtN236T, povezano z rezistenco proti adefovirju, občutljiv za lamivudin.
Preliminary clinical data suggest the adefovir-associated resistance mutation rtA181V may confer a reduced susceptibility to lamivudine, and the lamivudine-associated mutation rtA181T may confer a reduced susceptibility to adefovir dipivoxil.
Preliminarni klinični podatki kažejo, da mutacija rtA181V, povezana z rezistenco proti adefovirju, lahko povzroči zmanjšano občutljivost za lamivudin, in da mutacija rtA181T, povezana z lamivudinom, lahko povzroči zmanjšano občutljivost za adefovirdipivoksil.