natgillin/translations-raw huggingface dataset:
In HIV-infected patients with severe immune deficiency at the time of initiation of combination antiretroviral therapy (CART), an inflammatory reaction to asymptomatic or residual opportunistic infections may arise (see section 4.4).
Pri s HIV okuženih bolnikih s hudo imunsko pomanjkljivostjo lahko ob uvedbi kombiniranega protiretrovirusnega zdravljenja (CART - ˝combination antiretroviral therapy˝) nastane vnetna reakcija na asimptomatične ali rezidualne oportunistične okužbe (glejte poglavje 4. 4).
Laboratory test findings The laboratory abnormalities reported by the investigators as possibly, probably, or definitely related to CRIXIVAN in ≥ 10% of patients treated with CRIXIVAN alone or in combination were:
Vrednosti laboratorijskih testov Nenormalne vrednosti laboratorijskih testov, o katerih so raziskovalci poročali kot o možno, verjetno ali zagotovo povezanih z zdravilom pri ≥ 10% bolnikov, ki so jih zdravili z zdravilom CRIXIVAN samim ali v kombinaciji, so bile:
Very common (> 10%)
19 Zelo pogoste (> 10%)
Blood and lymphatic system disorders: increases in MCV, decreases in neutrophils.
Bolezni krvi in limfatičnega sistema: zvišanje MCV, zmanjšanja števila nevtrofilcev.
Renal and urinary disorders: haematuria, proteinuria, crystalluria; pyuria in paediatric patients 3 years of age and older.
Bolezni sečil: hematurija, proteinurija, kristalurija, piurija pri pediatričnih bolnikih, starih 3 leta ali več.
Hepato-biliary disorders: isolated asymptomatic hyperbilirubinaemia (total bilirubin ≥ 2.5 mg/ dl, 43 mcmol/ l), reported predominantly as elevated indirect bilirubin and rarely associated with elevations in ALT, AST, or alkaline phosphatase, has occurred in approximately 14% of patients treated with CRIXIVAN alone or in combination with other antiretroviral agents.
Do izolirane asimptomatične hiperbilirubinemije (koncentracija skupnega bilirubina ≥ 2, 5 mg/ dl, 43 μmol/ l), o kateri so večinoma poročali kot o zvišani koncentraciji indirektnega bilirubina in, ki je bila redko povezana s povečanjem vrednosti ALT, AST ali alkalne fosfataze, je prišlo pri približno 14% bolnikov, zdravljenih z zdravilom CRIXIVAN samim ali v kombinaciji z drugimi protiretrovirusnimi zdravili.
Most patients continued treatment with CRIXIVAN without dosage reduction and bilirubin values gradually declined toward baseline.
Večina bolnikov je nadaljevala z zdravljenjem z zdravilom CRIXIVAN, ne da bi jim zmanjšali odmerek, koncentracija bilirubina pa se je počasi zmanjšala proti osnovni vrednosti.
Hyperbilirubinaemia occurred more frequently at doses exceeding 2.4 g/ day compared to doses less than 2.4 g/ day.
Do hiperbilirubinemije je pogosteje prišlo pri odmerkih, višjih od 2, 4 g na dan, kot pa pri odmerkih, manjših od 2, 4 g na dan.
Increased ALT and AST.
Povečan ALT in AST.
In clinical trials with CRIXIVAN in paediatric patients 3 years of age and older, asymptomatic pyuria of unknown etiology was noted in 10.9% (6/ 55) of patients who received CRIXIVAN at the recommended dose of 500 mg/ m2 every 8 hours.
V kliničnih raziskavah z zdravilom CRIXIVAN pri pediatričnih bolnikih, starih 3 leta ali več, so asimptomatsko piurijo neznanega izvora opazili pri 10, 9% (6/ 55) bolnikov, ki so prejemali CRIXIVAN v priporočenih odmerkih 500 mg/ m2 vsakih 8 ur.
Some of these events were associated with mild elevation of serum creatinine.
Nekaj teh dogodkov je bilo povezanih z rahlim povečanjem serumskega kreatinina.
The following additional laboratory abnormalities have been reported during post-marketing experience; they are derived from spontaneous reports for which precise incidences cannot be determined:
V času trženja so poročali o naslednjih dodatnih nenormalnih vrednostih laboratorijskih testov (izvirajo iz spontanih poročil, zato njihova pogostnost ne more biti določena):
Metabolic and nutritional disorders: increased serum triglycerides, increased serum cholesterol.
Presnovne in prehranske motnje: povišani serumski trigliceridi, povišan serumski holesterol.
Hepato-biliary disorders: liver function abnormalities.
Bolezni jeter, žolčnika in žolčevodov: nenormalnosti jetrne funkcije.
Musculoskeletal and connective tissue and bone disorders: increased CPK.
Bolezni mišično- skeletnega sistema in vezivnega tkiva: povečan CPK.
The most commonly reported symptoms were gastro-intestinal (e. g., nausea, vomiting, diarrhoea) and renal (e. g., nephrolithiasis, flank pain, haematuria).
Simptomi, o katerih so najpogosteje poročali, so bili prebavni (npr. navzea, bruhanje, driska) in ledvični (npr. ledvični kamni, bolečina v ledvenem predelu, hematurija).
It is not known whether indinavir is dialyzable by peritoneal or haemodialysis.
Ni znano ali se indinavir dializira s peritonealno dializo ali hemodializo.
Protease inhibitor, ATC code JO5AE02
Farmakoterapevtska skupina: zaviralec proteaze, Oznaka ATC JO5AE02.
Mechanism of action Indinavir inhibits recombinant HIV– 1 and HIV– 2 protease with an approximate tenfold selectivity for HIV– 1 over HIV– 2 proteinase.
Mehanizem delovanja Indinavir zavira rekombinantno HIV- 1 in HIV- 2 proteazo; za prvo je približno desetkrat bolj selektiven kot za drugo.
Microbiology Indinavir at concentrations of 50 to 100 nM mediated 95% inhibition (IC95) of viral spread (relative to an untreated virus– infected control) in human T– lymphoid cell cultures and primary human monocytes/ macrophages infected with HIV− 1 variants LAI, MN, RF, and a macrophage– tropic variant SF– 162, respectively.
Mikrobiologija Indinavir je v koncentracijah od 50 do 100 nM povzročil 95% inhibicijo (IC95) virusnega širjenja (relativno glede na z virusom okuženo nezdravljeno kontrolo) v kulturah človeških T- limfoidnih celic in primarnih človeških monocitih/ makrofagih, okuženih s HIV- 1 različicami LAI, MN, RF oz. makrofagotropično različico SF- 162.
Indinavir at concentrations of 25 to 100 nM mediated 95% inhibition of viral spread in cultures of mitogen– activated human peripheral blood mononuclear cells infected with diverse, primary clinical isolates of HIV− 1, including isolates resistant to zidovudine and non– nucleoside reverse transcriptase inhibitors (NNRTIs).
Indinavir je v koncentracijah od 25 do 100 nM povzročil 95% inhibicijo virusnega širjenja v kulturah z mitogenom aktiviranih človeških perifernih krvnih enojedrnih celic, okuženih z različnimi, primarno kliničnimi izolati HIV- 1, vključno z izolati,
Synergistic antiretroviral activity was observed when human T– lymphoid cells infected with the LAI variant of HIV– 1 were incubated with indinavir and either zidovudine, didanosine, or NNRTIs.
Človeške T- limfoidne celice, okužene z LAI različico HIV- 1, so inkubirali z indinavirjem v kombinaciji z zidovudinom, didanozinom ali NNRTI- ji in opazili sinergistično protiretrovirusno delovanje.
Drug resistance Loss of suppression of viral RNA levels occurred in some patients; however, CD4 cell counts were often sustained above pre– treatment levels.
Rezistenca na zdravilo Pri nekaterih bolnikih je prišlo do izgube supresije ravni virusne RNA, vendar pa je število CD4 celic pogosto ostalo višje, kot je bilo pred zdravljenjem.
At least eleven amino acid sites in the protease have been associated with indinavir resistance:
Odkrili so najmanj enajst aminokislinskih mest na proteazi, ki so povezana z rezistenco na indinavir:
L10, K20, L24, M46, I54, L63, I64, A71, V82, I84, and L90.
L10, K20, L24, M46, I54, L63, I64, A71, V82, I84 in L90.
For example, no single substitution or pair of substitutions was capable of engendering measurable (≥ four– fold) resistance to indinavir, and the level of resistance was dependent on the ways in which multiple substitutions were combined.
Stopnja rezistence je bila odvisna od kombinacije mnogovrstnih substitucij.
In general, however, higher levels of resistance resulted from the co– expression of greater numbers of substitutions at the eleven identified positions.
Na splošno je višjo stopnjo rezistence sprožila koekspresija večjega števila substitucij na enajstih ugotovljenih mestih.
Among patients experiencing viral RNA rebound during indinavir monotherapy at 800 mg q8h, substitutions at only three of these sites were observed in the majority of patients:
Med bolniki, ki so bili zdravljeni samo z 800 mg indinavirja vsakih 8 ur in je prišlo do ponovnega izbruha virusne RNA, so pri večini bolnikov substitucije opazili samo na treh mestih:
V82 (to A or F), M46 (to I or L), and L10 (to I or R).
V82 (na A ali F), M46 (na I ali L) in L10 (na I ali R).
It should be noted that the decrease in suppression of viral RNA levels was seen more frequently when therapy with indinavir was initiated at doses lower than the recommended oral dose of 2.4 g/ day.
Treba je opozoriti še na to, da je do zmanjšanja supresije ravni virusne RNA prišlo pogosteje, kadar so zdravljenje z indinavirjem začeli z odmerki, nižjimi od priporočenega peroralnega odmerka 2, 4 g na dan.
20 associated amino acid substitution to both indinavir (from 13/ 24 to 2/ 20 at therapy week 24) and to the nucleoside analogues (from 10/ 16 to 0/ 20 at therapy week 24).
V primerjalni raziskavi je kombinirano zdravljenje z nukleozidnimi analogi (trojno zdravljenje z zidovudinom in didanozinom) potrdilo zaščito pred selekcijo virusa, ki ima izraženo vsaj eno aminokislinsko substitucijo, povezano z rezistenco na indinavir (od 13/ 24 do 2/ 20 v 24. tednu zdravljenja) in na nukleozidne analoge (od 10/ 16 do 0/ 20 v 24. tednu zdravljenja).
Cross resistance HIV− 1 patient isolates with reduced susceptibility to indinavir expressed varying patterns and degrees of cross– resistance to a series of diverse HIV PIs, including ritonavir and saquinavir.
Navzkrižna rezistenca Izolati bolnikov, okuženih s HIV- 1, z zmanjšano občutljivostjo na indinavir, so kazali različne vzorce in stopnje navzkrižne rezistence na vrsto različnih zaviralcev HIV proteaze, vključno z ritonavirom in sakvinavirom.
Complete cross− resistance was noted between indinavir and ritonavir; however, cross− resistance to saquinavir varied among isolates.
Popolno navzkrižno rezistenco so ugotovili med indinavirjem in ritonavirom; stopnja navzkrižne rezistence s sakvinavirom pa se je med izolati spreminjala.
Adults Treatment with indinavir alone or in combination with other antiretroviral agents (i. e., nucleoside analogues) has so far been documented to reduce viral load and increase CD4 lymphocytes in patients with CD4 cell counts below 500 cells/ mm3.
Odrasli Doslej so ugotovili, da zdravljenje z indinavirjem samim ali v kombinaciji z drugimi protiretrovirusnimi zdravili (npr. nukleozidnimi analogi) zmanjša virusno obremenitev in poveča število CD4 limfocitov pri bolnikih s številom CD4 celic, manjšim od 500 celic/ mm3.
In one published study, 20 HIV-infected patients with undetectable plasma viral load (< 200 copies / ml) receiving indinavir 800 mg every 8 hours were switched in an open, cross-over design to indinavir/ ritonavir 400/ 100 mg every 12 hours.
V eni objavljeni študiji so 20- im bolnikom, okuženim s HIV- om in nedoločljivo količino virusa v plazmi (< 200 kopij/ ml), ki so prejemali indinavir 800 mg na vsakih 8 ur, odprto, navzkrižno začeli dajati indinavir/ ritonavir 400/ 100 mg na vsakih 12 ur.
Viral load remained < 200 copies/ mL for 48 weeks in all patients.
Količina virusov po 48- ih tednih je bila pri vseh bolnikih še vedno < 200 kopij/ ml.
Another published study evaluated the efficacy and safety of indinavir/ ritonavir 400/ 100 mg every 12 hours in 40 antiretroviral-naïve patients.
21 Druga objavljena študija je ocenila učinkovitost in varnost indinavirja/ ritonavirja 400/ 100 mg na vsakih 12 ur pri 40- ih bolnikih, ki še niso prejemali protiretrovirusnih zdravil.
Thirty subjects completed 48 weeks of treatment.
48- tedensko zdravljenje je zaključilo trideset preizkušancev.
At week 4, the indinavir Cmin was 500 ng/ mL with substantial trough variability (range 5 to 8100 ng/ mL).
V četrtem tednu je bil Cmin indinavirja 500 ng/ mL, pri čemer je najmanjša koncentracija pomembno nihala (razpon od 5 do 8100 ng/ ml).
By intent to treat analysis 65% of patients had HIV RNA < 400 copies/ mL and 50% had viral load < 50 copies/ mL; by on-treatment analysis 96% of patients had HIV RNA < 400 copies/ mL and 74% had viral load < 50 copies/ mL.
Pri analizi populacije, ki so jo nameravali zdraviti, je imelo 65% bolnikov HIV RNA < 400 kopij/ ml, 50% pa virusno breme < 50 kopij/ ml; pri analizi zdravljene populacije je imelo 96% bolnikov HIV RNA < 400 kopij/ ml, 74% pa virusno breme < 50 kopij/ ml.
In this open label non- randomized single arm study, patients were treated with stavudine and lamivudine plus indinavir/ ritonavir 400/ 100 mg every 12 hours.
V tej odprti nerandomizirani študiji z eno skupino so bolnike zdravili s stavudinom in lamivudinom v kombinaciji z indinavirjem/ ritonavirjem 400/ 100 mg na vsakih 12 ur.
In the intent to treat and on treatment analyses the proportion of patients with HIV RNA of < 50 copies/ mL was 68.8% and 88.7%, respectively, at week 96.
V analizi populacije, ki so jo nameravali zdraviti, je imelo HIV RNA < 50 kopij/ ml po 96. tednu 68, 8% bolnikov, v populaciji, ki se je zdravila, pa 88, 7% bolnikov.
Indinavir alone or in combination with nucleoside analogues (zidovudine/ stavudine and lamivudine) has been shown to delay clinical progression rate compared with nucleoside analogues and to provide a sustained effect on viral load and CD4 count.
Pokazalo se je, da indinavir sam ali v kombinaciji z nukleozidnimi analogi (zidovudin/ stavudin in lamivudin) v primerjavi z nukleozidnimi analogi povzroči zakasnitev stopnje kliničnega napredovanja bolezni ter zagotovi trajni učinek na virusno obremenitev in število CD4.
In zidovudine experienced patients, indinavir, zidovudine and lamivudine in combination compared with lamivudine added to zidovudine reduced the probability of AIDS defining illness or death (ADID) at 48 weeks from 13% to 7%.
Pri bolnikih zdravljenih z zidovudinom je kombinacija indinavirja, zidovudina in lamivudina v primerjavi z lamivudinom dodanim zidovudinu zmanjšala verjetnost določitve bolezni AIDS ali smrti (ADID) po 48 tednih s 13% na 7%.
Similarly, in antiretroviral naive patients, indinavir with and without zidovudine compared with zidovudine alone reduced the probability of ADID at 48 weeks from 15% with zidovudine alone to approximately 6% with indinavir alone or in combination with zidovudine.
Podobno je pri bolnikih, ki se še niso zdravili s protiretrovirusnimi zdravili, indinavir z ali brez zidovudina v primerjavi s samim zidovudinom zmanjšal verjetnost ADID po 48 tednih s 15% pri zidovudinu samem na približno 6% pri indinavirju samem ali v kombinaciji z zidovudinom.
Effects on viral load were consistently more pronounced in patients treated with indinavir in combination with nucleoside analogues, but the proportion of patients with serum viral RNA below the limit of quantification (500 copies/ ml) varied between studies, at week 24 from 40% to more than 80%.
Učinki na virusno obremenitev so bili pri bolnikih, zdravljenih z indinavirjem v kombinaciji z nukleozidnimi analogi, dosledno bolj izraziti, vendar je delež bolnikov s serumsko virusno RNA pod mejo določitve (500 kopij/ ml) med raziskavami v 24. tednu nihal od 40% do več kot 80%.
This proportion tends to remain stable over prolonged periods of follow– up.
Po daljšem obdobju spremljanja ta delež stremi k stalni vrednosti.
Within studies, this effect is sustained also after prolonged periods of follow– up.
Znotraj raziskav se ta učinek ohrani tudi po daljšem obdobju spremljanja.
Paediatric patients Two clinical trials in 41 paediatric patients (4 to 15 years of age) were designed to characterise the safety, antiretroviral activity, and pharmacokinetics of indinavir in combination with stavudine and
Pediatrični bolniki Da bi označili varnost, protiretrovirusno aktivnost in farmakokinetiko indinavirja v kombinaciji s stavudinom in lamivudinom pri pediatričnih bolnikih, so oblikovali dve klinični raziskavi, ki vključujeta 41 pediatričnih bolnikov (starih 4 do 15 let).
In one study, at week 24, the proportion of patients with plasma viral RNA below 400 copies/ ml was 60%; the mean increase in CD4 cell counts was 242 cells/ mm3; and the mean increase in percent CD4 cell counts was 4.2%.
V eni raziskavi je bil v 24. tednu delež bolnikov z vrednostjo virusne RNA v plazmi pod 400 kopij/ ml 60%, povprečno povečanje števila CD4 celic 242 celic/ mm3 ter povprečno povečanje odstotka števila CD4 celic 4, 2%.
In another study, at week 16, the proportion of patients with plasma viral RNA below 400 copies/ ml was 59%; the mean increase in CD4 cell counts was 73 cells/ mm3; and the mean increase in percent CD4 cell counts was 1.2%.
V 60. tednu je bil delež bolnikov z vrednostjo virusne RNA v plazmi pod 400 kopij/ ml 59%, povprečno povečanje števila CD4 celic 73 celic/ mm3 ter povprečno povečanje odstotka števila CD4 celic 1, 2%.
At week 24, the proportion of patients with plasma viral RNA below 400 copies/ ml was 60%.
V 24. tednu je bil delež bolnikov z vrednostjo virusne RNA v plazmi pod 400 kopij/ ml 60%.
Absorption Indinavir is rapidly absorbed in the fasted state with a time to peak plasma concentration of 0.8 hours ± 0.3 hours (mean ± S. D.).
Najvišjo plazemsko koncentracijo doseže po 0, 8 ure ± 0, 3 ure (povprečje ± S. D.).
A greater than dose– proportional increase in indinavir plasma concentrations was observed over the 200 – 800 mg dose range.
Pri odmerkih med 200 in 800 mg so opazili večje plazemske koncentracije, kot bi bilo to sorazmerno z odmerkom.
Between 800– mg and 1,000– mg dose levels, the deviation from dose– proportionality is less pronounced.
Ta odklon od sorazmerja plazemske koncentracije z odmerkom je pri odmerkih med 800 in 1000 mg manj izrazit.
As a result of the short half– life, 1.8 ± 0.4 hours, only a minimal increase in plasma concentrations occurred after multiple dosing.
Zaradi kratkega razpolovnega časa (1, 8 ± 0, 4 ure) je po večkratnem odmerjanju prišlo le do minimalnega porasta plazemske koncentracije.
The bioavailability of a single 800– mg dose of indinavir was approximately 65% (90% CI, 58 – 72%).
Biološka uporabnost enkratnega 800 mg odmerka indinavirja je bila približno 65% (90% CI – » confidential interval «, 58- 72%).
Following a dosage regimen of 800 mg every 8 hours, measured peak plasma concentrations (Cmax) after morning, afternoon and evening doses were 15,550 nM, 8,720 nM and 8,880 nM, respectively.
Po jemanju 800 mg odmerkov vsakih 8 ur so najvišje plazemske koncentracije (Cmax) znašale 15. 550 nM po jutranjem, 8. 720 nM po
At steady state following a dosage regimen of 800 mg every 8 hours, HIV– seropositive adult patients in one study achieved geometric means of:
V stanju dinamičnega ravnovesja po jemanju 800 mg odmerkov vsakih 8 ur so bile v raziskavi pri HIV- seropozitivnih bolnikih dosežene naslednje geometrične srednje vrednosti:
AUC0-8h of 27,813 nM*h (90% confidence interval = 22,185, 34,869), peak plasma concentrations 11,144 nM (90% confidence interval = 9,192, 13,512) and plasma concentrations at 8 hours post dose 211 nM (90% confidence interval = 163, 274).
AUC0- 8h 27. 813 nM* h (90% interval zaupanja = 22. 185, 34. 869), najvišje plazemske koncentracije 11. 144 nM (90% interval zaupanja = 9. 192, 13. 512) in plazemske koncentracije 8 ur po zaužitju zdravila 211 nM (90% interval zaupanja = 163, 274).
Food effect At steady state following a dosage regimen of 800 mg/ 100 mg of indinavir/ ritonavir every 12 hours with a low-fat meal, healthy volunteers in one study achieved geometric means:
Učinek hrane V raziskavi pri zdravih prostovoljcih so bile v stanju dinamičnega ravnovesja, po jemanju odmerkov 800 mg/ 100 mg indinavirja/ ritonavirja vsakih 12 ur z obroki z nizko vsebnostjo maščob, dosežene naslednje geometrične srednje vrednosti:
AUC0-12h 116,067 nM*h (90% confidence interval = 101,680, 132,490), peak plasma concentrations 19001 nM (90% confidence interval = 17,538, 20,588), and plasma concentrations at 12 hours post dose 2274 nM (90% confidence interval = 1,701, 3,042).
AUC0- 12h 116. 067 nM* h (90% interval zaupanja = 101. 680, 132. 490), najvišje plazemske koncentracije 19. 001 nM (90% interval zaupanja = 17. 538, 20. 588), in plazemske koncentracije 12 ur po zaužitju zdravila 2. 274 nM (90% interval zaupanja = 1. 701, 3. 042).
Pharmacokinetic analysis in one study was performed on nineteen of the patients, with a median (range) indinavir AUC 0-12hr, Cmax, and Cmin of 25421 nM*h (21489-36236 nM*h), 5758 nM (5056-6742 nM) and 239 (169-421 nM), respectively.
Analizo farmakokinetike v eni študiji so opravili pri 19- ih bolnikih, pri katerih je bila mediana (razpon) AUC0– 12 h indinavirja 25421 nM* h (21489– 36236 nM* h), Cmax 5758 nM (5056– 6742 nM) in Cmin 239 (169– 421 nM).
In HIV− infected paediatric patients, a dosage regimen of indinavir hard capsules, 500 mg/ m2 every 8 hours, produced AUC0– 8hr values of 27,412 nM*h, peak plasma concentrations of 12,182 nM, and plasma concentrations at 8 hours post dose of 122 nM.
Pri s HIV okuženih pediatričnih bolnikih so bile pri jemanju trdih kapsul indinavirja v odmerkih 500 mg/ m2 vsakih 8 ur AUC0- 8h vrednosti 27. 412 nM* h, najvišje plazemske koncentracije 12. 182 nM, plazemske koncentracije 8 ur po odmerku pa 122 nM.
The AUC and peak plasma concentrations were generally similar to those previously observed in HIV– infected adults receiving the recommended dose of 800 mg every 8 hours; it should be observed that the plasma concentrations 8 hours post dose were lower.
Plazemske koncentracije 8 ur po odmerku so bile nižje.
The mean indinavir plasma AUC0-8hr at week 30-32 of gestation (n=11) was 9,231 nM∗ hr, which is 74% (95% CI:
Povprečna plazemska AUC0- 8hr indinavirja je v 30. do 32. tednu gestacije (n=11) znašala 9231 nM* h, kar je 74% (95% CI:
50%, 86%) lower than that observed 6 weeks postpartum.
50%, 86%) manj kot 6 tednov po porodu.
The pharmacokinetics of
Šest preiskovank med temi 11 (55%) je imelo povprečno plazemsko koncentracijo indinavirja 8 ur po odmerku (cmin) nižjo od praga zanesljive kvantitativne določitve pri testu.
22 indinavir in these 11 patients at 6 weeks postpartum were generally similar to those observed in non-pregnant patients in another study (see section 4.6).
Farmakokinetika indinavirja pri teh 11 bolnicah je bila 6 tednov po porodu na splošno podobna kot pri ne nosečih bolnicah v drugi raziskavi (glejte poglavje 4. 6).
Administration of indinavir with a meal high in calories, fat, and protein resulted in a blunted and reduced absorption with an approximate 80% reduction in AUC and an 86% reduction in Cmax.
Pri jemanju indinavirja skupaj z visokokaloričnim obrokom hrane z veliko maščobami in beljakovinami je prišlo do upočasnjene in zmanjšane absorpcije z okrog 80% zmanjšanjem AUC in 86% zmanjšanjem Cmax.
Administration with light meals (e. g., dry toast with jam or fruit conserve, apple juice, and coffee with skimmed or fat– free milk and sugar or corn flakes, skimmed or fat– free milk and sugar) resulted in plasma concentrations comparable to the corresponding fasted values.
Pri jemanju skupaj z lahkim obrokom (npr. prepečenec z marmelado ali konzerviranim sadjem, jabolčni sok in kava s posnetim mlekom ali mlekom brez maščobe in sladkor; koruzni kosmiči, posneto mleko ali mleko brez maščobe in sladkor) so bile plazemske koncentracije primerljive s tistimi po zaužitju na tešče.
In HIV– infected paediatric patients, the pharmacokinetic parameters of indinavir in apple sauce were:
Pri s HIV okuženih pediatričnih bolnikih so bili farmakokinetični parametri indinavirja v jabolčnem soku naslednji:
AUC0– 8hr of 26,980 nM*h; peak plasma concentration of 13,711 nM; and plasma concentration at 8 hours post dose of 146 nM.
AUC0- 8h 26. 980 nM* h, najvišja plazemska koncentracija 13. 711 nM, plazemska koncentracija 8 ur po odmerku pa 146 nM.
Distribution Indinavir was not highly bound to human plasma proteins (39% unbound).
Porazdelitev Indinavir se ni močno vezal na plazemske beljakovine (39% nevezanega).