natgillin/translations-raw huggingface dataset:
REYATAZ/ RTV med tenofovir/ emtricitabin (fast dosis på 300 mg/ 200 mg tabletter én gang dagligt). b Lopinavir/ RTV med tenofovir/ emtricitabin (fast dosis på 300 mg/ 200 mg tabletter én gang dagligt). c ITT- analyse (Intent- to- treat), hvor manglende værdier anses som svigt. d Antal evaluerbare patienter.
REYATAZ/ RTV with tenofovir/ emtricitabine (fixed dose 300 mg/ 200 mg tablets once daily). b Lopinavir/ RTV with tenofovir/ emtricitabine (fixed dose 300 mg/ 200 mg tablets once daily). c Intent-to-treat analysis, with missing values considered as failures. d Number of patients evaluable.
4. 5 og 4. 8) og én NRTI, hos 347 (af 358 randomiserede) patienter med virologisk svigt ved to eller flere tidligere regimer indeholdende mindst én PI, NRTI og NNRTI.
In antiretroviral experienced patients Study 045 is a randomised, multicenter trial comparing REYATAZ (300 mg once daily) with ritonavir (100 mg once daily) to REYATAZ (400 mg once daily) with saquinavir soft gelatine capsules (1,200 mg once daily), and to lopinavir + ritonavir (400/ 100 mg fixed dose combination twice daily), each in combination with tenofovir (see sections 4.5 and 4.8) and one NRTI, in 347 (of 358 randomised) patients with virologic failure on two or more prior regimens containing at least one PI, NRTI, and NNRTI.
Femten ud af 120 (13%) patienter i REYATAZ + ritonavir- behandlingsarmen og 17 ud af 123 (14%) patienter i lopinavir + ritonavir - armen havde fire eller flere af PI- substitutionerne L10, M46, I54, V82, I84 og L90.
Fifteen of 120 (13%) patients in the REYATAZ + ritonavir treatment arm and 17 of 123 (14%) patients in the lopinavir + ritonavir arm had four or more of the PI substitutions L10, M46, I54, V82, I84, and L90.
Toogtredive procent af patienterne i undersøgelsen havde en viral stamme med færre end to NRTI- substitutioner.
Thirty-two percent of patients in the study had a viral strain with fewer than two NRTI substitutions.
Middel CD4- celletal ved baseline var 337 celler/ mm3 (område:
The mean baseline CD4 cell count was 337 cells/ mm3 (range:
14 til 1. 543 celler/ mm3) og middel plasma- HIV- 1 RNA- niveau ved baseline var 4, 4 log10 kopier/ ml (område:
14 to 1,543 cells/ mm3) and the mean baseline plasma HIV-1 RNA level was 4.4 log10 copies/ ml (range:
Forsøgspopulationen var moderat præ- behandlet.
The population included in this study was moderately pretreated.
Det primære endpoint var den tidsgennemsnitlige forskel i ændring fra baseline i HIV RNA gennem 48 uger.
The primary endpoint was the time-averaged difference in change from baseline in HIV RNA through 48 weeks.
Gennem 48 ugers behandling var faldet i HIV RNA- niveauer fra baseline (primært endpoint) 1, 93 log10 kopier/ ml for REYATAZ + ritonavir og 1, 87 log10 kopier/ ml for lopinavir + ritonavir.
Through 48 weeks of treatment, the decreases from baseline in HIV RNA levels (primary endpoint) were 1.93 log10 copies/ ml for REYATAZ + ritonavir and 1.87 log10 copies/ ml for lopinavir + ritonavir.
REYATAZ + ritonavir svarede til (ikke- inferiørt) lopinavir + ritonavir i denne effektmåling (tidsgennemsnitlig forskel på 0, 13, 97, 5% konfidensinterval [- 0, 12; 0, 39]).
REYATAZ + ritonavir was similar (non-inferior) to lopinavir + ritonavir on this efficacy measure (time-averaged difference of 0.13, 97.5% confidence interval [-0.12, 0.39]).
Der blev opnået samstemmede resultater ved en analysemetode, hvor sidste observation blev fremskrevet (tidsgennemsnitlig forskel på 0, 11; 97, 5% konfidensinterval [- 0, 15; 0c36]).
Consistent results were obtained with the last observation carried forward method of analysis (time-averaged difference of 0.11, 97.5% confidence interval [-0.15, 0.36]).
Andelen af patienter med HIV RNA < 400 kopier/ ml i REYATAZ + ritonavir- armen og lopinavir + ritonavir- armen var henholdsvis 53% 54% ved ITT- analyse (intent- to- treat), hvor manglende værdier betragtedes som manglende effekt.
The proportions of patients with HIV RNA < 400 copies/ ml in the REYATAZ + ritonavir arm and the lopinavir + ritonavir arm were 53% and 54%, respectively, by intent-to-treat analysis, with missing values considered as failures.
Andelen af patienter med HIV RNA < 50 kopier/ ml i REYATAZ + ritonavir- armen
The proportions of patients with HIV RNA < 50 copies/ ml in the REYATAZ + ritonavir arm and the lopinavir + ritonavir arm were 36% and 42%, respectively.
Ved en AT- analyse (as- treated), hvor manglende værdier blev ekskluderet, var andelen af patienter med HIV RNA < 400 kopier/ ml (< 50 kopier/ ml) i REYATAZ + ritonavir- armen og lopinavir + ritonavir- armen henholdsvis 55% (40%) og 56% (46%).
By as-treated analysis, excluding missing values, the proportions of patients with HIV RNA < 400 copies/ ml (< 50 copies/ ml) in the REYATAZ + ritonavir arm and the lopinavir + ritonavir arm were 55% (40%) and 56% (46%), respectively.
Den gennemsnitlige stigning fra baseline i CD4- celletal var 110 celler/ mm3 og 121 celler/ mm3 i henholdsvis REYATAZ + ritonavir- armen og lopinavir + ritonavir- armen.
The mean increases from baseline in CD4 cell count were 110 cells/ mm3 and 121 cells/ mm3 in the REYATAZ + ritonavir and lopinavir + ritonavir arms, respectively.
Analyser af data ved 96 ugers behandlingstid påviste varigheden af den antivirale aktivitet.
Analyses of data through 96 weeks of treatment demonstrated durability of antiviral activity.
Gennemsnitlige HIV RNA- ændringer fra baseline i uge 96 (- 2, 29 log10 kopier/ ml for REYATAZ + ritonavir og - 2, 08 log10 kopier/ ml for lopinavir + ritonavir, med forskel i tidsgennemsnit på 0, 14 [- 0, 13, 0, 41], 97, 5% konfidensinterval, opfyldte kriterierne for ” ikke inferiøritet ” baseret på observerede tilfælde.
Mean HIV RNA changes from baseline at Week 96 (-2.29 log10 copies/ ml for REYATAZ + ritonavir and -2.08 log10 copies/ ml for lopinavir + ritonavir, time-averaged difference of 0.14, 97.5% confidence interval [-0.13, 0.41]) met criteria for non-inferiority based on observed cases.
Andelen af patienter med HIV RNA < 400 kopier/ ml (< 50 kopier/ ml) for REYATAZ + ritonavir var 43% (32%) og 46% (35%) for lopinavir + ritonavir.
17 lopinavir + ritonavir were 46% (35%).
Patienter som fuldendte behandling med respons efter 48 uger blev censureret.
Patients completing treatment while in response after 48 weeks were censored.
Ved AT- analyse, hvor manglende værdier blev ekskluderet, var andelen af patienter med HIV RNA < 400 kopier/ ml (< 50 kopier/ ml) for REYATAZ+ ritonavir 84% (72%) og for lopinavir + ritonavir 82% (72%).
By as-treated analysis, excluding missing values, the proportions of patients with HIV RNA < 400 copies/ ml (< 50 copies/ ml) for REYATAZ + ritonavir were 84% (72%) and for lopinavir + ritonavir were 82% (72%).
Det er vigtigt at bemærke, at 48% af det samlede antal patienter i undersøgelsen fortsatte efter 96- ugersanalysen.
It is important to note that at time of the 96-week analysis, 48% of patients overall remained on study.
Der blev gennem den 48 ugers behandlingstid foretaget to typer analyser baseret på genotypiske mutationer ved baseline.
Through 48 weeks of treatment, two types of analyses were performed based on baseline genotypic mutations.
Den første bestod i en vurdering af ændringen i HIV RNA fra baseline hos en subgruppe af patienter med < eller ≥4 af følgende mutationer (10, 20, 24, 32, 33, 36, 46, 48, 50, 54, 63, 71, 73, 82, 84 og 90).
10, 20, 24, 32, 33, 36, 46, 48, 50, 54, 63, 71, 73, 82, 84 and 90.
Den anden bestod i en vurdering af ændringen i HIV RNA fra baseline hos en subgruppe af patienter med < eller ≥4 af følgende mere specifikke mutationer:
The second consisted in assessing the HIV RNA change from baseline in the subgroup of patients with < or ≥ of 4 of the following more specific set of mutations:
10, 46, 54, 82, 84 og 90.
10, 46, 54, 82, 84, 90.
I analysen udført hos patienter med ≥4 protease- genmutationer blandt de følgende mutationer 10, 20, 24, 32, 33, 36, 46, 48, 50, 54, 63, 71, 73, 82, 84 og 90, var resultatet statistisk signifikant til fordel for lopinavir + ritonavir- armen.
In the analysis performed for patients with ≥ 4 protease gene mutations among the following set of mutations 10, 20, 24, 32, 33, 36, 46, 48, 50, 54, 63, 71, 73, 82, 84 and 90, the results significantly favoured the lopinavir + ritonavir arm.
Der var for få patienter med ≥4 af de andre mere specifikke mutationer (dvs 10, 46, 54, 82, 84 og 90) til at kunne vurdere sammenligneligheden af REYATAZ + ritonavir og lopinavir + ritonavir- regimer, men reduceret virologisk aktivitet kan forventes hos patienter med denne resistensprofil.
10, 46, 54, 82, 84, 90) to assess the comparability of the REYATAZ + ritonavir and lopinavir + ritonavir regimens, but reduced virologic activity may be anticipated among patients with this resistance profile.
Farmakokinetik for atazanavir er evalueret hos raske, voksne frivillige og hos HIV- inficerede patienter; der er observeret væsentlige forskelle mellem de to grupper.
The pharmacokinetics of atazanavir were evaluated in healthy adult volunteers and in HIV-infected patients; significant differences were observed between the two groups.
Farmakokinetik for atazanavir udviser en ikke- lineær disposition.
The pharmacokinetics of atazanavir exhibit a non-linear disposition.
Hos raske forsøgspersoner var AUC for atazanavir ens for kapsler og for oralt pulver.
In healthy subjects, the AUC of atazanavir from the capsules and oral powder were similar.
2, 5 timer.
Absorption: in HIV-infected patients (n=33, combined studies), multiple dosing of REYATAZ 300 mg once daily with ritonavir 100 mg once daily with food produced a geometric mean (CV%) for atazanavir, Cmax of 4466 (42%) ng/ ml, with time to Cmax of approximately 2.5 hours.
Det geometriske gennemsnit (CV%) for atazanavir Cmin og AUC var henholdsvis 654 (76%) ng/ ml og 44185 (51%) ng• t/ ml.
The geometric mean (CV%) for atazanavir Cmin and AUC was 654 (76%) ng/ ml and 44185 (51%) ng• h/ ml, respectively.
Fødepåvirkning: samtidig indtag af REYATAZ og ritonavir og mad optimerer biotilgængeligheden af atazanavir.
Food effect: co-administration of REYATAZ and ritonavir with food optimizes the bioavailability of atazanavir.
Samtidig indtag af enkeltdosis REYATAZ 300 mg og ritonavir 100 mg og et let måltid medførte en stigning i AUC på 33% og en stigning i såvel Cmax som 24- timerskoncentrationen af atazanavir på 40% i forhold til i fastende tilstand.
Co-administration of a single 300-mg dose of REYATAZ and 100-mg dose of ritonavir with a light meal resulted in a 33% increase in the AUC and a 40% increase in both the Cmax and the 24-hour concentration of atazanavir relative to the fasting state.
Samtidig indtag af fedtrigt måltid påvirkede ikke AUC for atazanavir i forhold til i fastende tilstand, og Cmax lå inden for 11% i forhold til faste - værdierne.
Co-administration with a high-fat meal did not affect the AUC of atazanavir relative to fasting conditions and the Cmax was within 11% of fasting values.
33% på grund af forsinket absorption; middel- Tmax steg fra 2, 0 til 5, 0 timer.
The 24-hour concentration following a high fat meal was increased by approximately 33% due to delayed absorption; the median Tmax increased from 2.0 to 5.0 hours.
25% sammenlignet med i fastende tilstand.
Administration of REYATAZ with ritonavir with either a light or a high-fat meal decreased the coefficient of variation of AUC and Cmax by approximately 25% compared to the fasting state.
Atazanavir bindes med cirka 86% til humane serumproteiner over et koncentrationsinterval på 100 til 10. 000 ng/ ml.
Distribution: atazanavir was approximately 86% bound to human serum proteins over a concentration range of 100 to 10,000 ng/ ml.
Atazanavir bindes til både alfa- 1- acid glykoprotein (AAG) og albumin i samme udstrækning (henholdsvis 89% og 86% ved 1. 000 ng/ ml).
Atazanavir binds to both alpha-1-acid glycoprotein (AAG) and albumin to a similar extent (89% and 86%, respectively, at 1,000 ng/ ml).
I en flerdosis - undersøgelse med HIV- inficerede patienter, der fik 400 mg atazanavir én gang dagligt med et let måltid i 12 uger, kunne atazanavir påvises i cerebrospinalvæsken og sæd.
In a multiple-dose study in HIV-infected patients dosed with 400 mg of atazanavir once daily with a light meal for 12 weeks, atazanavir was detected in the cerebrospinal fluid and semen.
Undersøgelser på mennesker og in vitro- undersøgelser med brug af humane levermikrosomer har vist, at atazanavir hovedsagelig metaboliseres til oxygenerede metabolitter af CYP3A4- isozymer.
Metabolism: studies in humans and in vitro studies using human liver microsomes have demonstrated that atazanavir is principally metabolised by CYP3A4 isozyme to oxygenated metabolites.
Yderligere mindre metaboliske pathways består af N- dealkylering og hydrolyse.
Additional minor metabolic pathways consist of N-dealkylation and hydrolysis.
Ingen af metabolitterne udviste in vitro- antiviral aktivitet.
Neither metabolite demonstrated in vitro antiviral activity.
Efter en enkelt dosis på 400 mg 14C- atazanavir, blev henholdsvis 79% og 13% af den totale radioaktivitet genfundet i fæces og urin.
18 Elimination: following a single 400-mg dose of 14C-atazanavir, 79% and 13% of the total radioactivity was recovered in the faeces and urine, respectively.
Gennemsnitlig halveringstid var, inden for atazanavirs dosisinterval, hos HIV- inficerede voksne patienter (n=33, kombinerede undersøgelser) 12 timer ved steady state efter en dosis på 300 mg dagligt med 100 mg ritonavir én gang dagligt med et let måltid.
In HIV-infected adult patients (n=33, combined studies) the mean half-life within a dosing interval for atazanavir was 12 hours at steady state following a dose of 300 mg daily with ritonavir 100 mg once daily with a light meal.
Hos raske forsøgspersoner var den renale udskillelse af uomdannet atazanavir cirka 7% af den administrerede dosis.
Impaired renal function: in healthy subjects, the renal elimination of unchanged atazanavir was approximately 7% of the administered dose.
4. 2); betydningen af nedsat nyrefunktion for udskillelsen af atazanavir forventes dog at være minimal.
There are no pharmacokinetic data available on patients with renal insufficiency (see section 4.2); however, the impact of renal impairment on atazanavir elimination is anticipated to be minimal.
Atazanavir metaboliseres og udskilles primært via leveren.
Impaired hepatic function: atazanavir is metabolised and eliminated primarily by the liver.
4. 2, 4. 3 og 4. 4).
Concentrations of atazanavir with or without ritonavir are expected to be increased in patients with moderately or severely impaired hepatic function (see sections 4.2, 4.3, and 4.4).
Der er gennemført farmakokinetisk undersøgelse af atazanavir på 59 raske mandlige og kvindelige forsøgspersoner (29 unge, 30 ældre).
Age/ Gender: a study of the pharmacokinetics of atazanavir was performed in 59 healthy male and female subjects (29 young, 30 elderly).
En befolkningsmæssig farmakokinetisk analyse af prøver fra fase II kliniske afprøvninger indikerede ingen racemæssig indvirkning på farmakokinetikken for atazanavir.
Race: a population pharmacokinetic analysis of samples from Phase II clinical trials indicated no effect of race on the pharmacokinetics of atazanavir.
Farmakokinetikken for atazanavir undersøges efter gentagne doser til pædiatriske patienter stratificeret efter alder.
Infants, toddlers, children, and adolescents: the pharmacokinetics of atazanavir is being studied after multiple doses in paediatric patients, stratified by age.
I toksicitetsundersøgelser med gentagne doser på mus, rotter og hunde var atazanavirrelaterede fund generelt begrænset til leveren og omfattede generelt minimale til milde forhøjelser af serum bilirubin og leverenzymer, hepatocellulær vacuolation og hypertrofi, og kun i hunmus hepatisk enkeltcellenekrose.
In repeat-dose toxicity studies, conducted in mice, rats, and dogs, atazanavir-related findings were generally confined to the liver and included generally minimal to mild increases in serum bilirubin and liver enzymes, hepatocellular vacuolation and hypertrophy, and, in female mice only, hepatic single-cell necrosis.
Serum- kolesterol og glukose var minimalt til let forhøjet hos rotter, men ikke hos mus eller hunde.
Serum cholesterol and glucose were minimally to mildly increased in rats but not in mice or dogs.
19 Den klonede, humane kardielle kaliumkanal, hERG, blev hæmmet med 15% i in vitro- undersøgelser ved en koncentration (30 μM) af atazanavir svarende til 30 gange den frie lægemiddelkoncentration ved Cmax hos mennesker.
During in vitro studies, cloned human cardiac potassium channel (hERG), was inhibited by 15% at a concentration (30 μ M) of atazanavir corresponding to 30-fold the free drug concentration at Cmax in humans.
Tilsvarende atazanavirkoncentrationer øgede den potentielle virkningsvarighed (ADP90) med 13% i en undersøgelse af Purkinjefibre hos kaniner.
Similar concentrations of atazanavir increased by 13% the action potential duration (APD90) in rabbit Purkinje fibres study.
Elektrokardiografiske forandringer (sinusbradykardi, forlængelse af PR - interval, forlængelse af QT - interval og forlængelse af QRS- kompleks) blev kun observeret i en indledende 2- ugers oral toksicitetsundersøgelse udført på hunde.
Electrocardiographic changes (sinus bradycardia, prolongation of PR interval, prolongation of QT interval, and prolongation of QRS complex) were observed only in an initial 2-week oral toxicity study performed in dogs.
Efterfølgende 9 måneders orale toksicitetsundersøgelser af hunde viste ingen lægemiddelrelaterede elektrokardiografiske forandringer.
Subsequent 9-month oral toxicity studies in dogs showed no drug-related electrocardiographic changes.
4. 4 og 4. 8).
Potential cardiac effects of this product in humans cannot be ruled out (see sections 4.4 and 4.8).
4. 9).
The potential for PR prolongation should be considered in cases of overdose (see section4.9).
I en undersøgelse af fertilitet og tidlig fosterudvikling hos rotter ændrede atazanavir brunstcyklus uden nogen effekt på parring eller fertilitet.
In a fertility and early embryonic development study in rats, atazanavir altered oestrus cycling with no effects on mating or fertility.
Der sås hos drægtige kaniner omfattende læsioner i mave og tarm hos døde eller moribunde hunner ved maternelle doser 2 og 4 gange den højeste dosis administreret i den endelige fosterudviklingsundersøgelse.
In pregnant rabbits, gross lesions of the stomach and intestines were observed in dead or moribund does at maternal doses 2 and 4 times the highest dose administered in the definitive embryo-development study.
I den præ - og postnatale udviklingsvurdering hos rotter, frembragte atazanavir en forbigående reduktion i legemsvægten hos afkommet ved en maternel toksisk dosis.
In the pre- and postnatal development assessment in rats, atazanavir
Atazanavir var negativ i Ames reverse- mutationsbestemmelse, men inducerede kromosomale afvigelser in vitro både ved fravær og tilstedeværelse af metabolisk aktivering.
Atazanavir was negative in an Ames reverse-mutation assay but did induce chromosomal aberrations in vitro in both the absence and presence of metabolic activation.
I in vivo- undersøgelser hos rotter inducerede atazanavir ikke mikronukleus i knoglemarv, DNA- beskadigelse i duodenum (comet assay) eller uplanlagt DNA- reparation i leveren ved plasma - og vævskoncentrationer, der overskrider dem, der var klastogene in vitro.
In in vivo studies in rats, atazanavir did not induce micronuclei in bone marrow, DNA damage in duodenum (comet assay), or unscheduled DNA repair in liver at plasma and tissue concentrations exceeding those that were clastogenic in vitro.
Der er i længerevarende undersøgelser af karcinogenecitet af atazanavir hos mus og rotter set en øget incidens af benigne hepatiske adenomer hos hunmus.
In long-term carcinogenicity studies of atazanavir in mice and rats, an increased incidence of benign hepatic adenomas was seen in female mice only.
Atazanavir øgede opaciteten af bovine corneae i en in vitro okulær irritationsundersøgelse, hvilket tyder på at det kan være en okulær irritant ved direkte kontakt med øjet.
Atazanavir increased opacity of bovine corneas in an in vitro ocular irritation study, indicating it may be an ocular irritant upon direct contact with the eye.
Kapslens indhold:
Capsule contents:
Crospovidon Lactosemonohydrat Magnesiumstearat
Crospovidone Lactose monohydrate Magnesium stearate
Kapslens skal:
Capsule shells:
Gelatine Indigocarmin (E132) Titaniumdioxid (E171)
Gelatine Indigocarmin (E132) Titanium dioxide (E171)
Blåt blæk indeholdende:
Blue ink containing:
Shellak Propylenglykol Ammoniumhydroxid Indigocarmin (E132)
Shellac Propylene glycol Ammonium hydroxide Indigocarmin (E132)
20 Hvid trykfarve indeholdende:
White ink containing:
Shellac Titaniumdioxid( E171) Ammoniumhydroxid Propylenglycol Simeticon
Shellac Titanium dioxide (E171) Ammonium hydroxide Propylene glycol Simethicone
6. 5 Emballagetype og pakningsstørrelser
20 6.5 Nature and contents of container
Hver æske indeholder en HDPE- beholder (high density polyethylen) med børnesikret polypropylenlåg.
Each carton contains one high-density polyethylene (HDPE) bottle closed with child-resistant polypropylene closure.
Hver karton indeholder 60 x 1 kapsel; 10 blisterkort med 6 x 1 kapsel hver i alu/ alu- perforeret enkelt- dosis- blisterpakning
Each carton contains 60 x 1 capsules; 10 blister cards of 6 x 1 capsules each in Alu/ Alu perforated unit dose blisters.
02 marts 2004 Dato for fornyelse af tilladelsen:
02 March 2004 Date of latest renewal:
{måned år}
{month year}
21 Yderligere information om dette lægemiddel er tilgængelig på Det europæiske Lægemiddelagenturs (EMEAs) hjemmeside http: // www. emea. europa. eu /.
Detailed information on this medicinal product is available on the website of the European Medicines Agency (EMEA) http: / /www. emea. europa. eu
Hver kapsel indeholder 150 mg atazanavir (som sulfat).
Each capsule contains 150 mg of atazanavir (as sulphate)
82, 18 mg lactose per kapsel.
82.18 mg of lactose per capsule.
Matblå og dueblå kapsler påtrykt ” BMS 150 mg ” på den ene halvdel og ” 3624 ” på den anden halvdel med hvidt og blåt blæk.
Hard capsule Opaque blue and powder blue capsule printed with white and blue inks, with "BMS 150 mg" on one half and with "3624" on the other half.
Til oral anvendelse.
22 Method of administration: for oral administration.
Der har været rapporter om øget blødning, inklusive spontane hudhæmatomer og hæmarthrose, hos type A og B hæmofile patienter, der havde fået behandling med proteasehæmmere.
23 There have been reports of increased bleeding, including spontaneous skin haematomas and haemarthroses, in type A and B haemophiliac patients treated with protease inhibitors.
24 fortsattes behandlingen med proteasehæmmere, eller behandlingen blev genoptaget hvis afbrudt.
In more than half of the reported cases, treatment with protease inhibitors was continued or reintroduced if treatment had been discontinued.
Relevante eksempler er cytomegalovirus retinitis, generaliserede og/ eller fokale mycobakterielle infektioner og pneumocystis carinii pneumoni.
24 Relevant examples are cytomegalovirus retinitis, generalised and/ or focal mycobacterial infections, and Pneumocystis carinii pneumonia.
Andre interaktioner Interaktioner mellem atazanavir/ ritonavir og proteasehæmmere, andre antiretrovirale midler end proteasehæmmere og andre ikke- antiretrovirale lægemidler angives i tabellerne neden for (stigninger er angivet med “ ↑ ”, fald med “ ↓ ”, ingen ændring med “ ↔ ”, to gange dagligt som “ BID ” og én gang dagligt som “ QD ”).
25 Other interactions Interactions between atazanavir/ ritonavir and protease inhibitors, antiretroviral agents other than protease inhibitors, and other non-antiretroviral medicinal products are listed in the tables below (increase is indicated as “↑”, decrease as “↓”, no change as “↔”, twice daily as “ BID” and once daily as “ QD”).
26 Det er vigtigt at nævne, at mange undersøgelser er udført med ikke- boosted atazanavir, hvilket ikke er det godkendte atazanavir- regime.
Of importance, many studies were conducted with unboosted atazanavir, which is not the approved regimen of atazanavir.
Samtidigt administrerede
27 Co-administered medicinal
29 Samtidigt administrerede
28 Co-administered medicinal
31
St.