natgillin/translations-raw huggingface dataset:
Nevirapine exhibited antiviral activity in vitro against group M HIV-1 isolates from clades A, B, C, D, F, G, and H, and circulating recombinant forms (CRF), CRF01_AE, CRF02_AG and CRF12_BF (median EC50 value of 63 nM).
Nevirapin je in vitro učinkoval protivirusno proti izolatom iz skupine M HIV- 1 genotipskih skupin A, B, C, D, F, G in H in rekombinantnim oblikam v obtoku (CRF), CRF01_ AE, CRF02_ AG in CRF12_ BF (srednja vrednost EC50 je bila 63 nM).
Nevirapine had no antiviral activity in vitro against isolates from group O HIV-1 and HIV-2.
Nevirapin in vitro protivirusno ni učinkoval na izolate iz skupin O HIV- 1 in HIV- 2.
Nevirapine in combination with efavirenz exhibited a strong antagonistic anti-HIV-1 activity in vitro (see section 4.5) and was additive to antagonistic with the protease inhibitor ritonavir or the fusion inhibitor enfuvirtide. Nevirapine exhibited additive to synergistic anti-HIV-1 activity in combination with the protease inhibitors amprenavir, atazanavir, indinavir, lopinavir, nelfinavir, saquinavir and tipranavir, and the NRTIs abacavir, didanosine, emtricitabine, lamivudine, stavudine, tenofovir and zidovudine.
V kombinaciji z zaviralci proteaze amprenavirjem, atazanavirjem, indinavirjem, lopinavirjem, nelfinavirjem, sakvinavirjem in tipranavirjem ter zaviralci nukleozidne reverzne transkriptaze (NRTI) abakavirjem, didanozinom, emtricitabinom, lamivudinom, stavudinom, tenofovirjem in zidovudinom je deloval na HIV- 1 aditivno do sinergistično.
The anti-HIV-1 activity of nevirapine was antagonized by the anti-HBV drug adefovir and by the anti-HCV drug ribavirin in vitro.
Na učinek nevirapina proti HIV- 1 sta in vitro delovala antagonistično adefovir, zdravilo proti virusu hepatitisa B (HBV), in ribavirin, zdravilo proti virusu hepatitisa C.
Resistance HIV isolates with reduced susceptibility (100 to 250-fold) to nevirapine emerge in vitro.
Odpornost In vitro se pojavljajo izolati HIV z zmanjšano občutljivostjo (100 - do 250- krat) za nevirapin.
Phenotypic and genotypic changes occur in HIV isolates from patients treated with VIRAMUNE or VIRAMUNE + zidovudine over one to 12 weeks.
Fenotipske in genotipske spremembe se pojavljajo pri izolatih HIV, odvzetih bolnikom, ki se zdravijo z VIRAMUNOM ali VIRAMUNOM in zidovudinom od enega do 12 tednov.
By week 8 of VIRAMUNE monotherapy, 100% of the patients tested had HIV isolates with a > 100-fold decrease in susceptibility to nevirapine, regardless of dose.
Do 8. tedna zdravljenja s samim VIRAMUNOM je imelo 100% preiskanih bolnikov izolate HIV z več kot 100- krat zmanjšano občutljivostjo za nevirapin ne glede na odmerek.
VIRAMUNE + zidovudine combination therapy did not alter the emergence rate of nevirapine- resistant virus.
Kombinirano zdravljenje z VIRAMUNOM m in zidovudinom ni spremenilo stopnje pojavljanja proti nevirapinu odpornega virusa.
Genotypic and phenotypic resistance was examined for patients receiving VIRAMUNE in triple and double therapy drug combination therapy, and in the non-VIRAMUNE comparative group from the INCAS study.
Genotipsko in fenotipsko odpornost so raziskovali pri bolnikih, ki so prejemali VIRAMUNE v sklopu zdravljenja s trojno in dvojno kombinacijo zdravil, ter v primerjalni skupini, ki ni prejemala VIRAMUNA, v raziskavi INCAS.
Antiretroviral naive subjects with CD4 cells counts of 200-600/ mm3 were treated with either VIRAMUNE + zidovudine (n = 46), zidovudine + didanosine (n = 51) or VIRAMUNE + zidovudine + didanosine (n = 51) and followed for 52 weeks or longer on therapy.
Zdravljenje so spremljali 52 tednov ali dlje.
Virologic evaluations were performed at baseline, six months and 12 months.
Virološke preiskave so izvajali na začetku raziskave ter po šestih in 12 mesecih.
The phenotypic resistance test performed required a minimum of 1000 copies/ ml HIV RNA in order to be able to amplify the virus.
Za uporabljeni test fenotipske odpornosti so potrebovali najmanj 1000 kopij/ ml HIV RNA, da bi lahko povečali število virusov.
Of the three study groups, 16, 19 and 28 patients respectively had evaluable baseline isolates and subsequently remained in the study for at least 24 weeks.
V treh skupinah je imelo 16, 19 in 28 bolnikov ocenljive začetne izolate in so v raziskavi sodelovali najmanj 24 tednov.
At baseline, there were five cases of phenotypic resistance to nevirapine; the IC50 values were 5 to 6.5-fold increased in three and > 100 fold in two.
Na začetku je bilo pet primerov fenotipske odpornosti proti nevirapinu; vrednosti IC50 so bile 5 - do 6, 5- krat povečane pri treh in > 100- krat pri dveh.
At 24 weeks, all available isolates recoverable from patients receiving nevirapine were resistant to this agent, while 18/ 21 (86%) patients carried such isolates at 30-60 weeks.
Po 24 tednih so bili vsi izolati, ki so jih lahko odvzeli pri bolnikih, kateri so prejemali nevirapin, odporni proti temu zdravilu, medtem ko je 18/ 21 (86%) bolnikov imelo takšne izolate po 30 do 60 tednih.
In 16 subjects viral suppression was below the limits of detection (< 20 copies/ ml = 14, < 400 copies/ ml = 2).
Pri 16 osebah je bila supresija virusa pod mejo merljivosti (< 20 kopij/ ml = 14, < 400 kopij/ ml = 2).
Assuming that suppression below < 20 copies/ ml implies nevirapine susceptibility of the virus, 45% (17/ 38) of patients had virus measured or imputed to be susceptible to nevirapine.
Če predpostavimo, da supresija na < 20 kopij/ ml pomeni občutljivost virusa za nevirapin, je bil virus pri 45% bolnikov (17/ 38) občutljiv za nevirapin.
All 11 subjects receiving VIRAMUNE + zidovudine who were tested for phenotypic resistance were resistant to nevirapine by six months.
Vseh 11 oseb, ki so prejemale VIRAMUNE in zidovudin, in pri katerih so izvedli preizkus fenotipske odpornosti, je bilo po šestih mesecih odpornih proti nevirapinu.
Over the entire period of observation, one case of didanosine resistance was seen.
Ves čas opazovalnega obdobja so zasledili en primer odpornosti proti didanozinu.
Zidovudine resistance emerged as more frequent after 30 – 60 weeks, especially in patients receiving double combination therapy.
Odpornost proti zidovudinu se je pogosteje pojavljala po 30 do 60 tednih, zlasti pri bolnikih, ki so prejemali kombinacijo dveh zdravil.
Based on the increase in IC50, zidovudine resistance appeared lower in the VIRAMUNE + zidovudine + didanosine group than the other treatment groups.
Glede na povečanje IC50 je bilo videti, da je bila odpornost proti zidovudinu v skupini, ki je prejemala VIRAMUNE + zidovudin + didanozin, manjša kot v drugih skupinah.
With respect to nevirapine resistance, all isolates that were sequenced carried at least one mutation associated with resistance, the most common single changes being K103N and Y181C.
Najpogostnejši posamični spremembi sta bili K103N in Y181C.
Combinations of mutations were found in nine of the 12 patients observed.
Kombinacije mutacij so odkrili pri devetih od 12 bolnikov.
These data from INCAS illustrate that the use of highly active drug therapies is associated with a delay in the development of antiretroviral drug resistance.
Navedeni podatki iz raziskave INCAS kažejo, da je uporaba visoko aktivnih zdravil povezana z odlogom razvoja odpornosti proti protivirusnemu zdravilu.
The clinical relevance of phenotypic and genotypic changes associated with VIRAMUNE therapy has not been established.
Kliničnega pomena fenotipskih in genotipskih sprememb, povezanih z zdravljenjem z VIRAMUNOM, niso ugotovili.
17 In addition to the data presented above, there exists a risk of rapid emergence of resistance to NNRTIs in case of virological failure.
Poleg zgoraj navedenega je prisotno tudi tveganje hitrega pojava odpornosti proti nenukleozidnim zaviralcem reverzne transkriptaze, če je zdravljenje virološko neuspešno.
Cross-resistance Rapid emergence of HIV strains which are cross-resistant to NNRTIs has been observed in vitro.
16 In vitro so ugotovili hiter pojav sevov HIV, ki so navzkrižno odporni proti nenukleozidnim zaviralcem reverzne transkriptaze.
Data on cross-resistance between the NNRTI nevirapine and NRTIs are very limited.
Na voljo je zelo malo podatkov o navzkrižni odpornosti med nenukleozidnim zaviralcem reverzne transkriptaze nevirapinom in nukleozidnimi zaviralci reverzne transkriptaze.
In four patients, zidovudine-resistant isolates tested in vitro retained susceptibility to nevirapine and in six patients, nevirapine-resistant isolates were susceptible to zidovudine and didanosine.
Pri štirih bolnikih so proti zidovudinu odporni izolati, ki so jih testirali in vitro, ohranili občutljivost za nevirapin, pri šestih bolnikih pa so bili proti nevirapinu odporni izolati občutljivi za zidovudin in didanozin.
Cross-resistance between nevirapine and HIV PIs is unlikely because the enzyme targets involved are different.
Navzkrižna odpornost med nevirapinom in zaviralci proteaze HIV ni verjetna, ker sta ciljna encima različna.
Cross-resistance among the currently registered NNRTIs is broad.
Med doslej registriranimi nenukleozidnimi zaviralci reverzne transkriptaze je navzkrižna odpornost velika.
Some genotypic resistance data indicate that in most patients failing NNRTI, viral strains express cross-resistance to the other NNRTIs.
Nekateri podatki o genotipski odpornosti kažejo, da so pri večini bolnikov, pri katerih so nenukleozidni zaviralci reverzne transkriptaze neuspešni, virusni sevi navzkrižno odporni proti drugim nenukleozidnim zaviralcem reverzne transkriptaze.
The currently available data do not support sequential use of NNRTIs.
Dosegljivi podatki ne podpirajo zaporedne uporabe nenukleozidnih zaviralcev reverzne transkriptaze.
Pharmacodynamic Effects VIRAMUNE has been evaluated in both treatment naive and treatment experienced patients.
Farmakodinamični učinki VIRAMUNE so ocenjevali pri že zdravljenih kot nezdravljenih bolnikih.
Results from a trial (ACTG 241) evaluated triple therapy with VIRAMUNE, zidovudine and didanosine compared to zidovudine + didanosine, in 398 HIV-1 infected patients (mean baseline 153 CD4+ cells/ mm3; plasma HIV1 RNA 4.59 log10 copies/ ml), who had received at least 6 months of NRTI therapy prior to enrolment (median 115 weeks).
V eni od raziskav (ACTG 241) so ocenjevali zdravljenje s kombinacijo treh zdravil (VIRAMUNOM, zidovudinom in didanozinom) v primerjavi s kombinacijo dveh (zidovudinom in didanozinom) pri 398 s HIV- 1 okuženih bolnikih (srednja začetna raven 153 CD4+ celic/ mm3; HIV- 1 RNA v plazmi 4, 59 log10 kopij/ ml), ki so se pred sprejemom v raziskavo najmanj 6 mesecev zdravili z nukleozidnimi zaviralci reverzne transkriptaze (srednja vrednost 115 tednov).
These heavily experienced patients demonstrated a significant improvement of the triple therapy group over the double therapy group for one year in both viral RNA and CD4+ cell counts.
Izboljšanje je trajalo eno leto.
A durable response for at least one year was documented in a trial (INCAS) for the triple therapy arm with VIRAMUNE, zidovudine and didanosine compared to zidovudine + didanosine or VIRAMUNE + zidovudine in 151 HIV-1 infected, treatment naive patients with CD4+ cell counts of 200- 600 cells/ mm3 (mean 376 cells/ mm3) and a mean baseline plasma HIV-1 RNA concentration of 4.41 log10 copies/ ml (25,704 copies/ ml).
Dlje časa trajajoči odziv na zdravljenje (najmanj eno leto) so zabeležili v raziskavi (INCAS) pri zdravljenju s trojno kombinacijo (VIRAMUNOM, zidovudinom in didanozinom) v primerjavi s kombinacijo zidovudina in didanozina ali VIRAMUNA in zidovudina, pri 151 s HIV- 1 okuženih, še ne zdravljenih bolnikih s številom celic CD4+ 200 do 600 celic/ mm3 (srednja vrednost 376 celic/ mm3) in srednjo plazemsko koncentracijo HIV- 1 RNA 4, 41 log10 kopij/ ml (25. 704 kopij/ ml).
Treatment doses were VIRAMUNE, 200 mg daily for two weeks, followed by 200 mg twice daily, or placebo; zidovudine, 200 mg three times daily; didanosine, 125 or 200 mg twice daily (depending on the weight).
200 mg VIRAMUNA na dan dva tedna, nato 200 mg 2- krat na dan, ali placebo; 200 mg zidovudina 3- krat na dan; 125 ali 200 mg didanozina 2- krat na dan (odvisno od telesne mase).
Two studies evaluated the efficacy of VIRAMUNE to prevent vertical transmission of HIV-1 infection.
Učinkovitost VIRAMUNA proti vertikalnemu prenosu okužbe s HIV- 1 so ocenili v dveh raziskavah.
Mothers received only study antiretroviral therapy during these trials.
Matere so v njih prejemale samo preskušano zdravilo.
In the HIVNET 012 study in Kampala (Uganda) mother-infant pairs were randomised to receive oral VIRAMUNE (mother:
V raziskavi HIVNET 012 iz Kampale (Uganda) so matere in njihove dojenčke naključno razvrstili v dve skupini.
200 mg at the onset of labour; infant:
200 mg na začetku poroda; dojenček:
2 mg/ kg within 72 hours of birth), or an ultra-short oral zidovudine regimen (mother:
2 mg/ kg v 72 urah po rojstvu), druga pa ultrakratko zdravljenje z zidovudinom (mati:
600 mg at the onset of labour and 300 mg every 3 hours until delivery; infant:
600 mg na začetku poroda in 300 mg vsake 3 ure do poroda; dojenček:
4 mg/ kg twice daily for 7 days).
4 mg/ kg 2- krat na dan 7 dni).
The cumulative HIV-1 infant infection rate at 14-16 weeks was 13.1% (n = 310) in the VIRAMUNE group, versus 25.1% (n = 308 in the ultra-short zidovudine group (p = 0.00063).
Skupna stopnja okuženosti dojenčkov s HIV- 1 je bila po 14 do 16 tednih 13, 1% (n = 310) v skupini z VIRAMUNOM in 25, 1% (n = 308) v skupini z ultrakratkim zdravljenjem z zidovudinom (p = 0, 00063).
In the SAINT study conducted in South Africa, mother-infant pairs were randomised to receive oral VIRAMUNE (mother:
Prva je prejela peroralni VIRAMUNE (mati:
200 mg during labor and 200 mg 24 to 48 hours postdelivery; infant:
200 mg med porodom in 200 mg 24 do 48 ur po porodu; dojenček:
6 mg 24 to 48 hours postdelivery); or a short oral zidovudine plus lamivudine regimen (mother: zidovudine 600 mg, then 300 mg every 3 hours during labour, followed by 300 mg b. i. d. for 7 days postdelivery plus lamivudine 150 mg b. i. d. during labour and for 7 days postdelivery; infant: zidovudine 12 mg b. i. d. plus lamivudine 6 mg b. i. d. for 7 days [if infant weight < 2 kg, zidovudine 4 mg/ kg b. i. d. plus lamivudine 2 mg/ kg b. i. d. for 7 days]).
600 mg zidovudina, nato 300 mg vsake tri ure med porodom, nato 300 mg 2- krat na dan 7 dni po porodu + 150 mg lamivudina 2- krat na dan med porodom in 7 dni po porodu; dojenček:
There was no significant difference in HIV-1 transmission rates through 6 to 8 weeks between the VIRAMUNE group (5.7%, n = 652) and the zidovudine plus lamivudine group (3.6%, n = 649).
4 mg/ kg zidovudina 2- krat na dan + 2 mg/ kg lamivudina 2- krat na dan 7 dni)).
There was greater risk of HIV-1 transmission to babies whose mothers received their VIRAMUNE or their zidovudine plus lamivudine doses less than 2 hours before delivery.
V obdobju 6 do 8 tednov ni bilo pomembne razlike glede na stopnjo prenosa HIV- 1 med prvo skupino, ki je prejemala VIRAMUNE (5, 7%, n = 652) in drugo, ki je prejemala zidovudin in lamivudin (3, 6%, n = 649).
In the SAINT study 68% of nevirapine-exposed mothers had resistant strains at
Tveganje prenosa HIV- 1 je bilo večje pri dojenčkih, katerih matere so prejele odmerke
18 approximately 4 weeks after delivery.
V raziskavi SAINT je imelo 68% mater, ki so prejele nevirapin, odporne seve približno 4 tedne po porodu.
The clinical relevance of these data in European populations has not been established.
Klinični pomen teh podatkov za evropske populacije ni raziskan.
Furthermore, in the case VIRAMUNE is used as single dose to prevent vertical transmission of HIV-1 infection, the risk of hepatotoxicity in mother and child cannot be excluded.
Poleg tega po dajanju samo enega odmerka VIRAMUNA za preprečitev vertikalnega prenosa okužbe s HIV- 1 pri materi in otroku ni možno izključiti tveganja toksičnih učinkov na jetra.
A blinded randomized clinical trial in women already taking antiretroviral therapy throughout pregnancy (PACTG 316) demonstrated no further reduction of vertical HIV-1 transmission when the mother and the child received a single VIRAMUNE dose during labour and after birth respectively.
V slepi randomizirani klinični raziskavi z naključno izbranimi ženskami, ki so prejemale protivirusno zdravljenje vso nosečnost (PACTG 316), se vertikalni prenos okužbe s HIV- 1 ni nadalje zmanjšal, če sta mati in otrok prejela enkratni odmerek VIRAMUNA med porodom oz. po rojstvu.
HIV-1 transmission rates were similarly low in both treatment groups (1.3% in the VIRAMUNE group, 1.4% in the placebo group).
Stopnja prenosa HIV- 1 je bila podobno majhna v obeh skupinah (1, 3% v skupini z VIRAMUNOM in 1, 4% v skupini s placebom).
The vertical transmission decreased neither in women with HIV-1 RNA below the limit of quantification nor in women with HIV-1 RNA above the limit of quantification prior to partus.
Vertikalni prenos se ni zmanjšal niti pri ženskah s HIV- 1 RNA pod mejo količinske določljivosti niti pri ženskah s HIV- 1 RNA nad to mejo pred porodom.
Of the 95 women who received intrapartum VIRAMUNE, 15% developed nevirapine resistance mutations at 6 weeks post partus.
Med 95 ženskami, ki so VIRAMUNE prejele med porodom, so se 6 tednov po porodu pri 15% razvile odporne mutacije proti nevirapinu.
VIRAMUNE tablets and oral suspension have been shown to be comparably bioavailable and interchangeable at doses up to 200 mg.
Tablete in peroralna suspenzija VIRAMUNE imata primerljivo biološko uporabnost in sta v odmerkih do 200 mg zamenljiva.
Nevirapine is readily absorbed (> 90%) after oral administration in healthy volunteers and in adults with HIV-1 infection.
Absorpcija: nevirapin se po peroralnem dajanju pri zdravih prostovoljcih in odraslih s HIV- 1 okuženih osebah hitro in z lahkoto absorbira (> 90%).
Absolute bioavailability in 12 healthy adults following single-dose administration was 93 ± 9% (mean SD) for a 50 mg tablet and 91 ± 8% for an oral solution.
Absolutna biološka uporabnost je bila pri 12 zdravih odraslih po enkratnem odmerku 93 ± 9% (srednja SD) za tableto po 50 mg in 91 ± 8% za peroralno raztopino.
Peak plasma nevirapine concentrations of 2 ± 0.4 µg/ ml (7.5 µM) were attained by 4 hours following a single 200 mg dose.
7, 5 µM) so izmerili 4 ure po dajanju enkratnega odmerka po 200 mg.
Following multiple doses, nevirapine peak concentrations appear to increase linearly in the dose range of 200 to 400 mg/ day.
Kaže, da se po večkratnih odmerkih nevirapinove največje koncentracije v razponu 200 do 400 mg/ dan večajo linearno.
Data reported in the literature from 20 HIV infected patients suggest a steady state Cmax of 5.74 µg/ ml (5.00-7.44) and Cmin of 3.73 µg/ ml (3.20-5.08) with an AUC of 109.0 h*µg/ ml (96.0-143.5) in patients taking 200 mg of nevirapine bid.
Podatki iz literature za 20 s HIV okuženih bolnikov kažejo, da je Cmax v ravnovesnem stanju 5, 74 µg/ ml (5, 00 do 7, 44), Cmin 3, 73 µg/ ml (3, 20 do 5, 08) in AUC 109, 0 h* µg/ ml (96, 0 do 143, 5) pri bolnikih, ki jemljejo po 200 mg nevirapina 2- krat na dan.
Long-term efficacy appears to be most likely in patients whose nevirapine trough levels exceed 3.5 µg/ ml.
Dolgoročna učinkovitost je najverjetnejša pri bolnikih, pri katerih so najmanjše ravni nevirapina nad 3, 5 µg/ ml.
Nevirapine is lipophilic and is essentially nonionized at physiologic pH.
Distribucija: nevirapin je lipofilen in pri fiziološki vrednosti pH pretežno neioniziran.
Following intravenous administration to healthy adults, the volume of distribution (Vdss) of nevirapine was 1.21 ± 0.09 l/ kg, suggesting that nevirapine is widely distributed in humans.
Po intravenskem vnosu zdravim odraslim je bil volumen porazdelitve (Vdss) nevirapina 1, 21 ± 0, 09 l/ kg, kar kaže, da se pri človeku obsežno porazdeli.
Nevirapine is about 60% bound to plasma proteins in the plasma concentration range of 1-10 µg/ ml.
Približno 60% nevirapina se pri razponu plazemskih koncentracij 1 do 10 µg/ ml veže na beljakovine v plazmi.
Nevirapine concentrations in human cerebrospinal fluid (n = 6) were 45% (± 5%) of the concentrations in plasma; this ratio is approximately equal to the fraction not bound to plasma protein.
V cerebrospinalni tekočini pri človeku (n = 6) so bile nevirapinove koncentracije 45% (± 5%) glede na plazemske; to razmerje je približno enako frakciji, ki se ne veže na beljakovine v plazmi.
In vivo studies in humans and in vitro studies with human liver microsomes have shown that nevirapine is extensively biotransformed via cytochrome P450 (oxidative) metabolism to several hydroxylated metabolites.
Biotransformacija in izločanje: raziskave in vivo pri človeku ter raziskave in vitro s človeškimi jetrnimi mikrosomi so pokazale, da se nevirapin obsežno presnavlja prek citokroma P450 (oksidacijsko) v več hidroksiliranih presnovkov.
In a mass balance/ excretion study in eight healthy male volunteers dosed to steady state with nevirapine 200 mg given twice daily followed by a single 50 mg dose of 14C-nevirapine, approximately 91.4 ± 10.5% of the radiolabelled dose was recovered, with urine (81.3 ± 11.1%) representing the primary route of excretion compared to faeces (10.1 ± 1.5%).
V raziskavi o masni bilanci in izločanju pri osmih zdravih prostovoljcih, ki so do stanja dinamičnega ravnovesja prejemali odmerke nevirapina po 200 mg 2- krat na dan, nato enkratni odmerek po 50 mg 14C- nevirapina, se je izločilo približno 91, 4 ± 10, 5% radioaktivno označenega odmerka, pri čemer je bila glavna pot izločanja s sečem (81, 3 ± 11, 1%) v primerjavi z blatom (10, 1 ± 1, 5%).
Greater than 80% of the radioactivity in urine was made up of glucuronide conjugates of hydroxylated metabolites.
Več kot 80% radioaktivne snovi v seču so sestavljali glukuronidni konjugati hidroksiliranih presnovkov.
Only a small fraction (< 5%) of the radioactivity in urine (representing < 3% of the total dose) was made up of parent compound; therefore, renal excretion plays a minor role in elimination of the parent compound.
Torej ima zločanje skozi ledvice le manjši pomen pri izločanju matične spojine.
The
Za farmakokinetiko samoindukcije je značilno približno 1, 5 - do 2- kratno povečanje navideznega očistka peroralnega nevirapina, ko zdravljenje z začetnim enkratnim odmerkom nadaljujemo dva do štiri tedne
19 pharmacokinetics of autoinduction are characterised by an approximately 1.5 to 2 fold increase in the apparent oral clearance of nevirapine as treatment continues from a single dose to two-to-four weeks of dosing with 200-400 mg/ day.
18 z odmerki po 200 do 400 mg na dan.
Autoinduction also results in a corresponding decrease in the terminal phase half-life of nevirapine in plasma from approximately 45 hours (single dose) to approximately 25-30 hours following multiple dosing with 200-400 mg/ day.
Posledica samoindukcije je tudi ustrezno skrajšanje razpolovnega časa nevirapina v plazmi v končni fazi od približno 45 ur (enkratni odmerek) do približno 25 do 30 ur po večkratnem dajanju odmerkov po 200 do 400 mg na dan.
Renal dysfunction:
Motnje ledvične funkcije:
The single-dose pharmacokinetics of nevirapine have been compared in 23 subjects with either mild (50 ≤ CLcr < 80 ml/ min), moderate (30 ≤ CLcr < 50 ml/ min) or severe renal dysfunction (CLcr< 30 ml/min), renal impairment or end-stage renal disease (ESRD) requiring dialysis, and 8 subjects with normal renal function (CLcr> 80 ml/ min).
Farmakokinetiko nevirapina so po enkratnem odmerku primerjali pri 23 bolnikih z blago (50 ≤ CLcr < 80 ml/ min), zmerno (30 ≤ CLcr < 50 ml/ min) ali hudo motnjo ledvične funkcije (CLcr < 30 ml/ min), ledvično okvaro ali ledvično boleznijo v končni fazi, ki je zahtevala dializo, ter pri 8 osebah z normalno ledvično funkcijo (CLcr > 80 ml/ min).
However, subjects with ESRD requiring dialysis exhibited a 43.5% reduction in nevirapine AUC over a one-week exposure period.
Pri bolnikih s končno fazo ledvične bolezni, ki so se morali zdraviti z dializo, pa se je AUC nevirapina v enem tednu jemanja zmanjšala za 43, 5%.
The results suggest that supplementing VIRAMUNE therapy with an additional 200 mg dose of VIRAMUNE following each dialysis treatment would help offset the effects of dialysis on nevirapine clearance.
Rezultati kažejo, da lahko z dodatnim odmerkom po 200 mg VIRAMUNA po vsaki dializi uravnamo njen učinek na očistek nevirapina.