natgillin/translations-raw huggingface dataset:
Farangytis, øget hoste
Pharyngitis, cough increased
Mavesmerter, kvalme, diarré, opkastning
Abdominal pain, nausea, diarrhoea, vomiting
Dyspepsi, anoreksi, lokal svælgirritation, flatulens, mundtørhed, ructus, mundsår
Dyspepsia, anorexia, local throat irritation, flatulence, dry mouth, eructation, mouth ulcer
Hepatitis og gulsot
Hepatitis and jaundice
Hududslæt, kløe, svedtendens, lipodystrofi
Rash, pruritus, sweating, lipodystrophy
Sygdomme i bevægeapparatet og bindevæv
Musculosketal and connective tissue disorders
Forhøjet CPK, myalgi
Increased CPK, myalgia
Myosit, rhabdomyolyse
Myositis, rhabdomyolysis
Sygdomme i nyre og urinveje Lidelser i det reproduktive system og brystsygdomme
Reproductive system and breast disorders
Ukendt hyppighed Ukendt hyppighed
Unknown frequency
Akut nyresvigt Menorrhagi
Menorrhagia
Feber, smerter, vægttab
Fever, pain weight loss
Forhøjet GGT, forhøjet CPK, forhøjede triglycerider, forhøjet SGPT, forhøjet SGOT, forhøjet amylase, forhøjet urinsyre, nedsat kalium, nedsat fri og total thyroxin
Increased GGT, increased CPK, increased triglycerides, increased SGPT, increased SGOT, increased amylase, increased uric acid, decreased potassium, decreased free and total thyroxin
Forhøjet glukose, nedsat total kalcium, forhøjet magnesium, forhøjet bilirubin, forhøjet alkalisk fosfatase
Increased glucose, decreased total calcium, increased magnesium, increased bilirubin, increased alkaline phosphatase
Bivirkninger, der er registreret med ukendt hyppighed, blev identificeret i forbindelse med postmarketing overvågning.
Events noted as having Unknown frequency were identified via post-marketing surveillance.
Stigning i hepatiske transaminaser udover 5 gange den øvre normalgrænse, klinisk hepatit og gulsot er set hos patienter som fik Norvir alene eller i kombination med andre retrovirale medikamenter.
Hepatic transaminase elevations exceeding five times the upper limit or normal, clinical hepatitis, and jaundice have occurred in patients receiving ritonavir alone or in combination with other antiretrovirals.
22 Antiretroviral kombinationsbehandling er blevet associeret med omfordelingen af kropsfedt (lypodystrophy) hos HIV- patienter, inklusiv forøgelse i intraabdominal – og visceral fedt, brysthyperthrofi og dorsocervical fedtaflejring (fedtnakke).
Combination antiretroviral therapy has been associated with redistribution of body fat (lipodystrophy) in HIV patients including the loss of peripheral and facial subcutaneous fat, increased intra-abdominal and visceral fat, breast hypertrophy and dorsocervical fat accumulation (buffalo hump).
Antiveral kombinationsbehandling er også blevet associeret med metaboliske abnormiteter som hypertriglycerid,, hyperkolerolæmi, insulinresistens, hyperglyceridæmi og hyperlactatæmi (se afsnit 4. 4.).
Combination antiretroviral therapy has been associated with metabolic abnormalities such as hypertriglyceridaemia, hypercholesterolaemia, insulin resistance, hyperglycaemia and hyperlactataemia (see section 4.4).
Hos HIV- inficerede patienter med svær immuninsufficiens kan der ved påbegyndelse af antiretroviral kombinationsbehandling (CART) opstå en inflammatorisk reaktion på asymptomatiske eller residuale opportunistiske infektioner (se afsnit 4. 4).
22 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).
Der er observeret tilfælde af pankreatit hos patienter i behandling med ritonavir, inkluderende de patienter, som udviklede hypertriglyceridæmi.
Pancreatitis has been observed in patients receiving ritonavir therapy, including those who developed hypertriglyceridemia.
I nogle tilfælde er der observeret fatale forløb.
In some cases fatalities have been observed.
Patienter med avanceret HIV sygdom kan have en risiko for forhøjede triglycerid værdier og pankreatit (se afsnit 4. 4).
Patients with advanced HIV disease may be at risk of elevated triglycerides and pancreatitis (see section 4.4).
Der er rapporteret om tilfælde af osteonekrose, især hos patienter med generelt anerkendte risikofaktorer, fremskreden HIV- sygdom eller langvarig kombinationsbehandling med antiretroviral lægemidler (CART).
Cases of osteonecrosis have been reported, particularly in patients with generally acknowledged risk factors, advanced HIV disease or long-term exposure to combination antiretroviral therapy (CART).
4. 4)
The frequency of this is unknown (see section 4.4).
I et klinisk forsøg tog en patient ritonavir i en dosis på 1500 mg/ dag i to dage og meldte om paræstesi, der svandt efter at dosis blev sat ned.
One patient in clinical trials took ritonavir 1500 mg/day for two days and reported paraesthesia, which resolved after the dose was decreased.
ATC kode:
Pharmaco-therapeutic group: antiviral for systemic use, ATC code:
JO5A EO3.
J05A E03
Farmakokinetisk forstærkning via ritonavir er baseret på ritonavirs stærkt hæmmende virkning på CYP3A- medieret metabolisme.
Pharmacokinetic enhancement by ritonavir is based on ritonavir’s activity as a potent inhibitor of CYP3A- mediated metabolism.
4. 5 samt til produktresuméet for den konkrete samtidigt indgivne proteasehæmmer.
For additional information on the effect of ritonavir on co-administered protease inhibitor metabolism, see section 4.5 and refer to the Summary of Product Characteristics of the particular co-administered PIs.
23 Ritonavir er et peroralt aktivt, peptidomimetisk stof, der hæmmer HIV- 1 og HIV- 2 aspartyl protease.
Ritonavir is an orally active peptidomimetic inhibitor of the HIV-1 and HIV-2 aspartyl proteases.
Denne hæmning af HIV proteasen bevirker at enzymet bliver ude af stand til at danne gag- pol polyprotein- precursor hvorved der dannes HIV partikler med umoden morfologi, der er ude af stand til at starte en ny omgang infektion.
Inhibition of HIV protease renders the enzyme incapable of processing the gag-pol polyprotein precursor which leads to the production of HIV particles with immature morphology that are unable to initiate new rounds of infection.
Ritonavir har selektiv affinitet for HIV protease og virker kun i ringe udstrækning hæmmende på humane aspartyl proteaser.
Ritonavir has selective affinity for the HIV protease and has little inhibitory activity against human aspartyl proteases.
Ritonavir var den første proteasehæmmer (godkendt i 1996), hvis virkning blev påvist i et forsøg med kliniske effektmål.
Ritonavir was the first protease inhibitor (approved in 1996) for which efficacy was proven in a study with clinical endpoints.
4. 2).
However, due to ritonavir’s metabolic inhibitory properties its use as a 23 pharmacokinetic enhancer of other protease inhibitors is the prevalent use of ritonavir in clinical practice (see section 4.2).
Effekter på elektrokardiogram
Effects on the Electrocardiogram
QTcF- intervallet blev evalueret i et randomiseret, placebo og aktiv (moxifloxacin 400 mg en gang daglig) kontrolleret overkrydsnings- forsøg hos 45 raske voksne, med 10 målinger over 12 timer på dag 3.
QTcF interval was evaluated in a randomised, placebo and active (moxifloxacin 400 mg once daily) controlled crossover study in 45 healthy adults, with 10 measurements over 12 hours on Day 3.
De maksimale gennemsnitlige (95% øvre konfidensgrænse) forskelle i QTcF fra placebo var 5, 5 (7, 6) for 400 mg ritonavir to gange daglig.
The maximum mean (95% upper confidence bound) difference in QTcF from placebo was 5.5 (7.6) for 400 mg twice daily ritonavir.
Eksposition af ritonavir dag 3 var tilnærmelsesvis 1, 5 gange højere end den, som blev set med dosen 600 mg to gange daglig ved steady state.
The Day 3 ritonavir exposure was approximately 1.5 fold higher than that observed with the 600 mg twice daily dose at steady state.
Ingen individer oplevede en øgning i QTcF på ≥ 60 msek fra baseline eller et QTcF- interval, som oversteg den potentielt kliniske relevante grænse på 500 msek.
No subject experienced an increase in QTcF of ≥ 60 msec from baseline or a QTcF interval exceeding the potentially clinically relevant threshold of 500 msec.
På dag 3 blev også set beskeden forlængelse af PR- intervallet hos individer, som fik ritonavir i det samme forsøg.
Modest prolongation of the PR interval was also noted in subjects receiving ritonavir in the same study on Day 3.
De gennemsnitlige ændringer i PR- interval fra baseline strækker sig fra 11, 0 til 24, 0 msek i et interval på 12 timer efter dosen.
The mean changes from baseline in PR interval ranged from 11.0 to 24.0 msec in the 12 hour interval post dose.
Det maksimale PR- interval var 252 msek, og der blev ikke observeret nogen anden eller tredie grads hjerte- blokade (se punkt 4. 4).
Maximum PR interval was 252 msec and no second or third degree heart block was observed (see section 4.4).
Ritonavir- resistente isolater af HIV- 1 er udvalgt in vitro og isoleret fra patienter i behandling med terapeutiske doser af ritonavir.
Ritonavir-resistant isolates of HIV-1 have been selected in vitro and isolated from patients treated with therapeutic doses of ritonavir.
Reduktion af ritonavirs antiretrovirale aktivitet er primært knyttet til proteasemutationerne V82A/ F/ T/ S og I84V.
Reduction in the antiretroviral activity of ritonavir is primarily associated with the protease mutations V82A/F/T/S and I84V.
Akkumulation af andre mutationer i proteasegenet (bl. a. ved positionerne 20, 33, 36, 46, 54, 71 og 90) kan også bidrage til resistens over for ritonavir.
Accumulation of other mutations in the protease gene (including at positions 20, 33, 36, 46, 54, 71, and 90) can also contribute to ritonavir resistance.
CD4 celletælling og viralt RNA, blev vurderet i flere forsøg, hvori der indgik HIV- 1 smittede patienter.
The effects of ritonavir (alone or combined with other antiretroviral agents) on biological markers of disease activity such as CD4 cell count and viral RNA were evaluated in several studies involving HIV-1 infected patients.
Følgende forsøg er de vigtigste:
The following studies are the most important.
Til voksne
Adult Use
Et kontrolleret forsøg afsluttet i 1996 med ritonavir som supplerende behandling hos HIV- 1 patienter efter intensiv forudgående behandling med nukleoside analoger og CD4 celletal ≤ 100 celler/ μl viste et fald i dødeligheden og AIDS definerende begivenheder.
A controlled study completed in 1996 with ritonavir as add-on therapy in HIV-1 infected patients extensively pre-treated with nucleoside analogues and baseline CD4 cell counts ≤ 100 cells/μl showed a reduction in mortality and AIDS defining events.
Den gennemsnitlige ændring fra basis i løbet af 16 uger for HIV RNA niveauerne var - 0, 79 log10 (maksimalt gennemsnitlige fald:
The mean average change from baseline over 16 weeks for HIV RNA levels was -0.79 log10 (maximum mean decrease:
1, 29 log10) i ritonavirgruppen sammenlignet med - 0, 01 log10 i kontrolgruppen.
1.29 log10) in the ritonavir group versus-0.01 log10 in the control group.
De oftest anvendte nukleosider i dette forsøg var zidovudin, stavudin, didanosin og zalcitabin.
The most frequently used nucleosides in this study were zidovudine, stavudine, didanosine and zalcitabine.
I et forsøg afsluttet i 1996 med patienter med mindre fremskredet HIV- 1 (CD4 200- 500 celler/ μl) uden forudgående antiretroviral behandling, medførte ritonavir sammen med zidovudin eller alene nedsat viralbelastning i plasma og forøget CD4 tal.
In a study completed in 1996 recruiting less advanced HIV-1 infected patients (CD4 200-500 cells/μl) without previous antiretroviral therapy, ritonavir in combination with zidovudine or alone reduced viral load in plasma and increased CD4 count.
Gennemsnitsændringen fra basis i løbet af 48 uger 24 for HIV RNA var - 0, 88 log10 for ritonavirgruppen i forhold til - 0, 66 log10 for den gruppe, der fik ritonavir+zidovudin og sammenlignet med - 0, 42 log10 for zidovudingruppen.
The mean average change from baseline over 48 weeks for HIV RNA levels was -0.88 log10 in the ritonavir group versus -0.66 log10 in the ritonavir + zidovudine group versus -0.42 log10 in the zidovudine group.
Fortsat indgift af ritonavir bør vurderes med undersøgelse for virusbelastning på grund af muligheden for udvikling af resistens, som beskrevet i 4. 1 Indikationer.
The continuation of ritonavir therapy should be evaluated by viral load because of the possibility of the emergence of resistance as described under section 4.1 Therapeutic indications.
Pædiatrisk anvendelse I et åbent forsøg afsluttet i 1998 med HIV- smittede, klinisk stabile børn ses en signifikant forskel (p=0, 03) i de påviselige RNA- niveauer efter en 48 ugers triple- behandling (ritonavir + zidovudine + lamivudine).
24 In an open label trial completed in 1998 in HIV infected, clinically stable children there was a significant difference (p = 0.03) in the detectable RNA levels in favour of a triple regimen (ritonavir, zidovudine and lamivudine) following 48 weeks treatment.
I et forsøg afsluttet i 2003 fik 50 HIV- 1- inficerede børn i alderen 4 uger til 2 år, der ikke tidligere havde fået proteasehæmmer og lamivudin, 350 eller 450 mg/ m2 ritonavir hver 12. time sammen med 160 mg/ m2 zidovudin hver 8. time og 4 mg/ kg lamivudin hver 12. time.
In a study completed in 2003, 50 HIV-1 infected, protease inhibitor and lamivudine naïve children age 4 weeks to 2 years received ritonavir 350 or 450 mg/m2 every 12 hours co-administered with zidovudine 160 mg/m2 every 8 hours and lamivudine 4 mg/kg every 12 hours.
I intent- to- treat analyser opnåede 72% og 36% af patienterne reduktion i plasma HIV- 1 RNA på < 400 kopier/ ml i henholdsvis uge 16 og 104.
In intent to treat analyses, 72% and 36% of patients achieved reduction in plasma HIV-1 RNA of ≤ 400 copies/ml at Week 16 and 104, respectively.
Ritonavirs farmakokinetik ved flergangsdosering er blevet undersøgt i ikke- fastende HIV- positive voksne frivillige forsøgspersoner.
The pharmacokinetics of ritonavir during multiple dose regimens were studied in non-fasting HIV-infected adult volunteers.
Ved flergangsdosering er ritonavir- akkumuleringen en smule mindre end forventet ud fra en enkelt dosis på grund af en tids - og dosisafhængig øgning i den tilsyneladende clearance (Cl/ F).
Upon multiple dosing, ritonavir accumulation is slightly less than predicted from a single dose due to a time and dose-related increase in apparent clearance (Cl/F).
Nyreclearance udgjorde i gennemsnit mindre end 0, 1 l/ t og var relativt konstant i doseringsintervallet.
Renal clearance averaged less than 0.1 l/h and was relatively constant throughout the dosage range.
600 mg to
100
gang daglig
mg once daily
gange daglig1
Cmax (µg/ml)
gang daglig
0.84 ± 0.39
gange daglig
4.5 ± 1.3
gange daglig
11.2 ± 3.6
Cmax (μg/ ml) Ctrough (μg/ ml) AUC12 eller 24 (μg• t/ ml)
Ctrough (µg/ml)
0, 84 ± 0, 39 0, 08 ± 0. 04 6, 6 ± 2, 4
0.16 ± 0.10
0, 89 0, 22 6, 2
6.6 ± 2.4
3, 4 ± 1, 3 0, 16 ± 0, 10 20, 0 ± 5, 6
20.0 ± 5.6
4, 5 ± 1, 3 0, 6 ± 0, 2 21, 92 ± 6, 48
21.92 ± 6.48
11, 2 ± 3, 6 3, 7 ± 2, 6 77, 5 ± 31, 5
77.5 ± 31.5
~5 ~5
~5 ~5
Cl/ F (l/ t) 1
Cl/F (L/h) 1
Værdier udtrykt som geometriske middelværdier.
Values expressed as geometric means.
Virkning af føde på oral absorption:
Effects of food on oral absorption:
Indtagelse af ritonavir sammen med føde resulterer i højere ritonavireksponering end indtagelse i fastende tilstand.
Ingestion of ritonavir with food results in higher ritonavir exposure than ingestion in the fasted state.
20- 40 l efter en enkelt 600 mg dosis.
The apparent volume of distribution (VB/F) of ritonavir is approximately 20 - 40 l after a single 600 mg dose.
98- 99% og er konstant inden for koncentrationsområdet 1, 0 – 100 μg/ ml.
The protein binding of ritonavir in human plasma is approximately 98 - 99% and is constant over the concentration range of 1.0 – 100 μg /ml.
Ritonavir binder sig både til humant alfa 1- syre glykoprotein (AAG) og humant serumalbumin (HSA) med sammenlignelig affinitet.
Ritonavir binds to both human alpha 1-acid glycoprotein (AAG) and human serum albumin (HSA) with comparable affinities.
25 Vævsdistributionsforsøg med 14C- mærket ritonavir i rotter har vist, at lever, binyrer, pankreas, nyrer og thyreoidea indeholdt den højeste koncentration af ritonavir.
Tissue distribution studies with 14C-labelled ritonavir in rats showed the liver, adrenals, pancreas, kidneys and thyroid to have the highest concentrations of ritonavir.
1 målt i rotters lymfekirtler viser, at ritonavir fordeler sig i lymfevæv.
Tissue to plasma ratios of approximately 1 measured in rat lymph nodes suggests that ritonavir distributes into lymphatic tissues.
Det er konstateret, at ritonavir i stor udstrækning metaboliseres af det hepatiske cytokrom P450 - system, især af isoenzym CYP3A4- familien og i mindre udstrækning af CYP2D6- isoformen.
Ritonavir was noted to be extensively metabolised by the hepatic cytochrome P450 system, primarily by the CYP3A isozyme family and to a lesser extent by the CYP2D6 isoform.
Dyreforsøg samt in vitro- forsøg med humane hepatiske mikrosomer har vist, at ritonavir hovedsagelig metaboliseres oxidativt.
Animal studies as well as in vitro experiments with human hepatic microsomes indicated that ritonavir primarily underwent oxidative metabolism.
Isopropylthiazol oxidationsmetabolitten (M- 2) er den vigtigste metabolit og har en antiviral aktivitet, der ligner moderstoffets.
The isopropylthiazole 25 oxidation metabolite (M-2) is the major metabolite and has antiviral activity similar to that of parent drug.
3% af moderstoffets AUC.
However, the AUC of the M-2 metabolite was approximately 3% of the AUC of parent drug.
4. 5).
Low doses of ritonavir have shown profound effects on the pharmacokinetics of other protease inhibitors (and other products metabolised by CYP3A4) and other protease inhibitors may influence the pharmacokinetics of ritonavir (see section 4.5).
86% af radiomærkningen blev genfundet i fæces, hvoraf en del anses for at være uabsorberet ritonavir.
Human studies with radiolabelled ritonavir demonstrated that the elimination of ritonavir was primarily via the hepatobiliary system; approximately 86% of radiolabel was recovered from stool, part of which is expected to be unabsorbed ritonavir.
I disse forsøg fandtes udskillelse via nyrerne ikke at være en vigtig vej til udskillelse af ritonavir.
In these studies renal elimination was not found to be a major route of elimination of ritonavir.
Dette var i overensstemmelse med observationerne i dyreforsøg.
This was consistent with the observations in animal studies.
Ritonavir plasma- eksponering hos patienter på 50 – 70 år doseret med 100 mg i kombination med lopinavir eller i højere doser ved fravær af andre protease- hæmmere, er sammenlignelig med, hvad der observeres hos yngre voksne.
Ritonavir plasma exposures in patients 50 – 70 years of age when dosed 100 mg in combination with lopinavir or at higher doses in the absence of other protease inhibitors is similar to that observed in younger adults.
Efter gentagen dosering af ritonavir til raske frivillige forsøgspersoner (500 mg to gange daglig) og forsøgspersoner med mild til moderat nedsat leverfunktion (Child- Pugh klasse A og B, 400 mg to gange daglig) var eksponeringen af ritonavir efter normalisering af dosis ikke signifikant forskellig for de to grupper.
Patients with impaired liver function: after multiple dosing of ritonavir to healthy volunteers (500 mg twice daily) and subjects with mild to moderate hepatic impairment (Child Pugh Class A and B, 400 mg twice daily) exposure to ritonavir after dose normalisation was not significantly different between the two groups.
Patienter med svækket nyrefunktion:
Patients with impaired renal function:
Pædiatriske patienter:
Paediatric Patients:
Ritonavirs steady- state farmakokinetiske parametre er blevet undersøgt hos HIV- inficerede børn over 2 år, som fik doser fra 250 mg/ m² to gange daglig til 400 mg/ m² to gange daglig.
Ritonavir steady-state pharmacokinetic parameters were evaluated in HIV infected children above 2 years of age receiving doses ranging from 250 mg/m² twice daily to 400 mg/m² twice daily.
De opnåede koncentrationer af ritonavir efter 350 til 400 mg/ m² to gange daglig hos pædiatriske patienter var sammenlignelige med de koncentrationer, der blev opnået hos voksne, som fik 600 mg (ca.
Ritonavir concentrations obtained after 350 to 400 mg/m² twice daily in paediatric patients were comparable to those obtained in adults receiving 600 mg (approximately 330 mg/m²) twice daily.
1, 5 til 1, 7 gange hurtigere hos pædiatriske patienter over 2 år end hos voksne forsøgspersoner.
Across dose groups, ritonavir oral clearance (CL/F/m2) was approximately 1.5 to 1.7 times faster in paediatric patients above 2 years of age than in adult subjects.
Ritonavirs steady- state farmakokinetiske parametre blev undersøgt hos HIV- inficerede børn under 2 år, som fik doser fra 350 til 450 mg/ m² to gange daglig.
Ritonavir steady-state pharmacokinetic parameters were evaluated in HIV infected children less than 2 years of age receiving doses ranging from 350 to 450 mg/m² twice daily.
De opnåede koncentrationer af ritonavir i dette forsøg var meget variable og noget lavere end de koncentrationer, der blev opnået hos voksne, som fik 600 mg (ca.
Ritonavir concentrations in this study were highly variable and somewhat lower than those obtained in adults receiving 600 mg (approximately 330 mg/m²) twice daily.
På tværs af dosisgrupper var oral clearance (CL/ F/ m2) af ritonavir faldt med alder med middelværdier på 9, 0 l/ t/ m2 hos børn på under 3 måneder, 7, 8 l/ t/ m2 hos børn på mellem 3 og 6 måneder og 4, 4 l/ t/ m2 hos børn på mellem 6 og 24 måneder.
Across dose groups, ritonavir oral clearance (CL/F/m2) declined with age with median values of 9.0 L/h/m2 in children less than 3 months of age, 7.8 L/h/m2 in children between 3 and 6 months of age and 4.4 L/h/m2 in children between 6 and 24 months of age.
26 fagocyterende elementer og ledsagedes af en stigning i leverenzymer.
Hepatic changes involved hepatocellular, biliary and phagocytic elements and were accompanied by increases in hepatic enzymes.
Kliniske undersøgelser viste imidlertid ingen klinisk betydningsfulde øjenforandringer hos mennesker på grund af medikamentet.
However, clinical trials revealed no evidence of drug-induced ocular changes in humans.
Alle thyreoidea - forandringer var reversible efter ophør med indtagelse af medikamentet.
All thyroid changes were reversible upon discontinuation of ritonavir.
Toksisk påvirkning af rotters udvikling (fosterdødelighed, nedsat fostervægt, forsinket knogledannelse og ændringer i de indre organer, herunder forsinket testis retention) fandtes hovedsaglig ved en maternelt toksisk dosis.
26 Developmental toxicity observed in rats (embryolethality, decreased foetal body weight and ossification delays and visceral changes, including delayed testicular descent) occurred mainly at a maternally toxic dosage.
Ritonavir er ikke fundet at være mutagent eller klastogent i en serie af in vitro og in vivo målinger, herunder Ames bakterielle tilbagemutationsmåling ved hjælp af S. typhimurium og E. coli, muselymfomtesten, musemikronukleustesten og måling af kromosomændringer i humane lymfocytter.
Ritonavir was not found to be mutagenic or clastogenic in a battery of in vitro and in vivo assays including the Ames bacterial reverse mutation assay using S. typhimurium and E. coli, the mouse lymphoma assay, the mouse micronucleus test and chromosomal aberration assays in human lymphocytes.
Langtids karcinogenecitetsundersøgelser i mus og rotter viste et potentiale for tumorer specifik for disse dyrearter, men dette anses ikke for at være relevant for mennesker.
Long term carcinogenicity studies of ritonavir in mice and rats revealed tumourigenic potential specific for these species, but are regarded as of no relevance for humans.
Norvir oral opløsning indeholder: alkohol, renset vand, polyoxyl 35 ricinusolie, propylenglykol, vandfri citronsyre, saccharinnatrium, pebermynteolie, flødekaramelaroma, Sunset yellow E110
Norvir oral solution contains: alcohol, purified water, polyoxyl 35 castor oil, propylene glycol, anhydrous citric acid, saccharin sodium, peppermint oil, creamy caramel flavour, sunset yellow E110