natgillin/translations-raw huggingface dataset:
I kontrollerede undersøgelser viste 1 års behandling med lamivudin signifikant suppression af HBV- DNA- replikation [34- 57% af patienterne var under assay detektionsgrænserne, (Abbott Genostics solution hybridization assay, LLOD < 1, 6 pg/ ml)}, normaliseret ALAT- niveau (40- 72% af patienterne), induceret HBeAg- serokonversion (tab af HBeAg og HBeAb- detektion med HBV DNA tab [ved konventionel assay], 16- 18% af patienterne), forbedret histologi (38- 52% af patienterne havde ≥ 2 points fald i Knodell histologisk aktivitets index [HAI]), og reduceret fibroseudviklinger (hos 3- 17% af patienterne) og udvikling til cirrhosis.
Experience in patients with HBeAg positive CHB and compensated liver disease: in controlled studies, 1 year of lamivudine therapy significantly suppressed HBV DNA replication [34-57% of patients were below the assay detection limits (Abbott Genostics solution hybridization assay, LLOD < 1.6pg/ ml)}, normalised ALT level (40-72% of patients), induced HBeAg seroconversion (HBeAg loss and HBeAb detection with HBV DNA loss [by conventional assay], 16-18% of patients), improved histology (38-52% of patients had a ≥ 2 point decrease in the Knodell Histologic Activity Index [HAI]) and reduced progression of fibrosis (in 3-17% of patients) and progression to cirrhosis.
Fortsat lamivudinbehandling i yderligere 2 år hos patienter, som ikke opnåede HBeAg- serokonversion i de initiale 1 års kontrollerede studier, resulterede i yderligere forbedring i brofibrose.
Continued lamivudine treatment for an additional 2 years in patients who had failed to achieve HBeAg seroconversion in the initial 1 year controlled studies resulted in further improvement in bridging fibrosis.
Hos patienter med YMDD- variant HBV udviste 41/ 82 (50%) patienter forbedring af leverinflammation og 40/ 56 (71%) patienter uden YMDD- variant HBV udviste forbedring.
In patients with YMDD variant HBV, 41/ 82 (50%) patients had improvement in liver inflammation and 40/ 56 (71%) patients without YMDD variant HBV had improvement.
Forbedring i brofibrose viste sig hos 19/ 30 (63%) patienter uden YMDD- variant og hos 22/ 44 (50%) patienter med varianten.
Improvement in bridging fibrosis occurred in 19/ 30 (63%) patients without YMDD variant and 22/ 44 (50%) patients with the variant.
Fem procent (3/ 56) af patienterne uden YMDD- varianten og 13 procent (11/ 82) af patienterne med YMDD- varianten udviste forværring i leverinflammation sammenlignet med præ- behandling.
Five percent (3/ 56) of patients without the YMDD variant and 13% (11/ 82) of patients with YMDD variant showed worsening in liver inflammation compared to pre-treatment.
Udvikling af cirrhosis opstod hos 4/ 68 (6%) patienter med YMDD- variant, hvorimod ingen patienter uden varianten udviklede cirrhosis.
Progression to cirrhosis occurred in 4/ 68 (6%) patients with the YMDD variant, whereas no patients without the variant progressed to cirrhosis.
I et udvidet behandlingsstudie med asiatiske patienter (NUCB3018) var HBeAg- serokonversionsraten og ALAT- normaliseringsraten ved slutningen af den 5- årige behandlingsperiode henholdsvis 48% (28/ 58) og 47% (15/ 32).
In an extended treatment study in Asian patients (NUCB3018) the HBeAg seroconversion rate and ALT normalisation rate at the end of the 5 year treatment period was 48% (28/ 58) and 47% (15/ 32), respectively.
HBeAg- serokonversion var øget hos patienter med forhøjede ALAT - niveauer; 77% (20/ 26) patienter, med præ- behandling ALAT > 2 x ULN, serokonverterede.
HBeAg seroconversion was increased in patients with elevated ALT levels; 77% (20/ 26) of patients with pre-treatment ALT > 2 x ULN seroconverted.
Ved afslutningen af de 5 år havde alle patienter HBV DNA niveauer der var udetekterbare eller lavere end præ- behandlingsniveauer.
At the end of 5 years, all patients had HBV DNA levels that were undetectable or lower than pre-treatment levels.
Yderligere resultater fra studiet med YMDD- variantstatus er opsummeret i tabel 2.
Further results from the trial by YMDD variant status are summarised in Table 2.
Resultater på effekten efter 5 år med YMDD- status (asiatisk undersøgelse) NUCB3018
Efficacy results 5 years by YMDD status (Asian Study) NUCB3018
Personer,% (nr.) YMDD- variant HBV status HBeAg- serokonversion
YMDD variant HBV status HBeAg seroconversion
- Alle patienter - Baseline ALAT ≤ 1 x ULN2 - Baseline ALAT > 2 x ULN
- All patients - Baseline ALT ≤ 1 x ULN2 - Baseline ALT > 2 x ULN
Udetekterbar HBV DNA
Undetectable HBV DNA
- Baseline3 - Uge 2604
Baseline 3
negativ positiv < baseline positiv > baseline
positive< baseline positive> baseline
8 (2/ 25) 92 (23/ 25) 0
(23/ 25) 100 0
0 100 (4/ 4) 0
(4/ 4)
ALAT- normalisering
ALT normalisation
- Baseline
- Baseline
normal over normal
normal
- Uge 260
Week 260
normal over normal < baseline over normal > baseline
normal above normal < baseline
1 Patienter kategoriseret som YMDD- variant var patienter med ≥ 5% YMDD- variant HBV på ethvert årligt tidspunkt under den 5- årige undersøgelsesperiode.
Patients designated as YMDD variant were those with ≥ 5% YMDD variant HBV at any annual time-point during the 5-year period.
Patienter kategoriseret som non- YMDD- varianter var patienter med > 95% wild- type HBV på alle årlige tidspunkter under den 5- årrige undersøgelsesperiode.
Patients categorised as non-YMDD variant were those with > 95% wild-type HBV at all annual time-points during the 5-year study period
3 Abbott Genostics solution hybridisation assay (LLOD < 1. 6 pg/ ml) 4 Chiron Quantiplex assay (LLOD 0. 7 Meq/ ml)
Upper limit of normal Abbott Genostics solution hybridisation assay (LLOD < 1.6 pg/ ml Chiron Quantiplex assay (LLOD 0.7 Meq/ ml)
Sammenlignende data i henhold til YMDD- status var også tilgængelige for histologisk vurdering, men kun i op til 3 år.
Comparative data according to YMDD status were also available for histological assessment but only up to three years.
Hos patienter med YMDD- variant HBV, udviste 18/ 39 (46%) forbedringer i nekroinflammatorisk aktivitet og 9/ 39 (23%) udviste forværring.
In patients with YMDD variant HBV, 18/ 39 (46%) had improvements in necroinflammatory activity and 9/ 39 (23%) had worsening.
Hos patienter uden varianten, udviste 20/ 27 (74%) forbedringer i nekroinflammatorisk aktivitet og 2/ 27 (7%) udviste forværring.
In patients without the variant, 20/ 27 (74%) had improvements in necroinflammatory activity and 2/ 27 (7%) had worsening.
Efter HBeAg- serokonversion er serologisk respons og klinisk bedring generelt vedvarende når behandling med lamivudin stoppes.
Following HBeAg seroconversion, serologic response and clinical remission are generally durable after stopping lamivudine.
I et længerevarende follow- up- studie med patienter, som tidligere havde serokonverteret og som var stoppet med lamivudin, opstod der sent virologisk tilbagefald hos 39% af personerne.
In a long-term follow-up study of patients who had previously seroconverted and discontinued lamivudine, late virological relapse occurred in 39% of the subjects.
Efter HBeAg - serokonversion bør patienterne derfor monitoreres periodisk for at afgøre om det serologiske og kliniske respons opretholdes.
Therefore, following HBeAg seroconversion, patients should be periodically monitored to determine that serologic and clinical responses are being maintained.
En sammenligning af post- behandling ALAT- stigninger mellem uge 52 og uge 68 hos patienter, som ophørte med lamivudin behandling i uge 52 og patienter, fra samme undersøgelser, som modtog placebo i hele behandlingsforløbet er vist i Tabel 3.
A comparison of post-treatment ALT elevations between weeks 52 and 68 in patients who discontinued lamivudine at week 52 and patients in the same studies who
Andelen af patienter som havde post- behandling ALAT- stigninger, i forbindelse med en stigning i billirubin niveauer, var lav og ensartet hos patienter der modtog enten lamivudin eller placebo.
The proportion of patients who had post-treatment ALT elevations in association with an increase in bilirubin levels was low and similar in patients receiving either lamivudine or placebo.
Post- behandling ALAT- stigninger i 2 placebo kontrollerede undersøgelser hos voksne.
Post-treatment ALT Elevations in 2 Placebo-Controlled Studies in Adults
Patienter med stigninger i ALAT / Patienter med observationer * Abnorm værdi ALAT ≥ 2 x baseline værdien ALAT ≥ 3 x baseline værdien † ALAT ≥ 2 x baseline værdien og absolut
ALT ≥ 2 x baseline value ALT ≥ 3 x baseline value† ALT ≥ 2 x baseline value and absolute ALT
Lamivudin 37/ 137 (27%) 29/ 137 (21%)
37/ 137 (27%) 29/ 137 (21%)
Placebo 22/ 116 (19%) 9/ 116 (8%)
22/ 116 (19%) 9/ 116 (8%)
ALAT > 500 IU/ I ALAT ≥ 2 x baseline værdien; og bilirubin
> 500 IU/ l ALT ≥ 2 x baseline value; and bilirubin > 2 x ULN
> 2 x ULN og ≥ 2 x baseline værdien * Hver patient kan være repræsenteret i en eller †
and ≥ 2 x baseline value *Each patient may be represented in one or more category. †
1/ 137 (0, 7%) flere kategorier.
1/ 137 (0.7%)
Sammenlignelig med 3. grads toksicitet i henhold til modificerede WHO kriterier.
Comparable to a Grade 3 toxicity in accordance with modified WHO criteria.
Initiale data indikerer, at effekten af lamivudin hos patienter med HBeAg- negativ CHB er ens med effekten hos patienter med HBeAg- positiv CHB, 71% af patienterne har HBV DNA suppression under detektionsgrænsen for assayet, 67% ALAT - normalisering og 38% med forbedring i HAI efter et års behandling.
Experience in patients with HBeAg negative CHB: initial data indicate the efficacy of lamivudine in patients with HBeAg negative CHB is similar to patients with HBeAg positive CHB, with 71% of patients having HBV DNA suppressed below the detection limit of the assay, 67% ALT normalisation and 38% with improvement in HAI after one year of treatment.
Når lamivudin blev seponeret, fik hovedparten af patienterne (70%) et tilbagevenden af virusreplikation.
When lamivudine was discontinued, the majority of patients (70%) had a return of viral replication.
Efter to års behandling i dette studie, opstod der ALAT- normalisering og udetekterbar HBV DNA hos henholdsvis 30/ 69 (43%) og 32/ 68 (47%) af patienterne, og forbedring af nekroinflammatorisk score hos 18/ 49 (37%) af patienterne.
After two years of treatment in this study, ALT normalisation and undetectable HBV DNA occurred in 30/ 69 (43%) and 32/ 68 (47%) patients respectively and improvement in necroinflammatory score in 18/ 49 (37%) patients.
Hos patienter uden YMDD- variant HBV, udviste 14/ 22 (64%) forbedring i nekroinflammatorisk score og 1/ 22 (5%) patienter udviste forværring sammenlignet med præ- behandling.
In patients without YMDD variant HBV, 14/ 22 (64%) showed improvement in necroinflammatory score and 1/ 22 (5%) patients worsened compared to pre-treatment.
Hos patienter med varianten, udviste 4/ 26 (15%) patienter forbedring i nekroinflammatorisk score og 8/ 26 (31%) patienter udviste forværring sammenlignet med præ- behandling.
In patients with the variant, 4/ 26 (15%) patients showed improvement in necroinflammatory score and 8/ 26 (31%) patients worsened compared to pre-treatment.
24% patienter efter 1 års behandling, og stiger til 67% efter 4 års behandling.
Frequency of emergence of YMDD variant HBV and impact on the treatment response: lamivudine monotherapy results in the selection of YMDD variant HBV in approximately 24% of patients following one year of therapy, increasing to 67% following 4 years of therapy.
Udvikling af YMDD- variant HBV er associeret med reduceret behandlingsrespons hos nogle patienter, som viser sig ved øgede HBV DNA niveauer og forhøjelse af ALAT fra tidligere terapiniveauer, progression af tegn og symptomer på hepatitis sygdom og/ eller forværring af hepatiske nekroinflammatoriske fund.
Development of YMDD variant HBV is associated with reduced treatment response in some patients, as evidenced by increased HBV DNA levels and ALT elevations from previous on-therapy levels, progression of signs and symptoms of hepatitis disease and/ or worsening of hepatic necroinflammatory findings.
Den optimale behandling af patienter med YMDD- variant HBV er endnu ikke fastlagt (se afsnit 4. 4).
The optimal therapeutic management of patients with YMDD variant HBV has not yet been established (see section 4.4).
I et dobbelt- blindt studie med CHB patienter med YMDD- variant HBV og kompenseret leversygdom (NUC20904) og med et reduceret virologisk og biokemisk respons over for lamivudin (n=95) resulterede addition af adefovir dipivoxil 10 mg en gang daglig til igangværende behandling med lamivudin 100 mg i 52 uger, i et gennemsnitligt fald i HBV DNA på 4. 6 log10 kopier/ ml sammenlignet med en gennemsnitlig stigning på 0, 3 log10 kopier/ ml hos patienter der modtog lamivudin monoterapi.
In a double-blind study in CHB patients with YMDD variant HBV and compensated liver disease (NUC20904), with a reduced virological and biochemical response to lamivudine (n=95), the addition of adefovir dipivoxil 10 mg once daily to ongoing lamivudine 100mg for 52 weeks resulted in a median decrease in HBV DNA of 4.6 log10 copies/ ml compared to a median increase of 0.3 log10 copies/ ml in those patients receiving lamivudine monotherapy.
Normalisering af ALAT- niveauer opstod hos 31% (14/ 45) patienter der modtog kombineret behandling versus 6% (3/ 47) der modtog lamivudin alene.
Normalisation of ALT levels occurred in 31% (14/ 45) of patients receiving combined therapy versus 6% (3/ 47) receiving lamivudine alone.
Fyrre patienter (HBeAg- negative eller HBeAg- positive) med enten dekompenseret leversygdom eller tilbagevendende HBV efter levertransplantation og YMDD- variant blev også indført i en åben arm af studiet.
Forty patients (HBeAg negative or HBeAg positive) with either decompensated liver disease or recurrent HBV following liver transplantation and YMDD variant were also enrolled into an open label arm of the study.
Addition af 10 mg adefovir dipivoxil en gang daglig til igangværende behandling med lamivudin 100 mg i 52 uger, resulterede i et gennemsnitligt fald i HBV DNA på 4. 6 log10 kopier/ ml.
Addition of 10 mg adefovir dipivoxil once daily to ongoing lamivudine 100mg for 52 weeks resulted in a median decrease in HBV DNA of 4.6 log10 copies/ ml.
Forbedring i leverfunktionen blev også set efter et års behandling.
Improvement in liver function was also seen after one year of therapy
Placebokontrollerede undersøgelser er betragtet som upassende hos patienter med dekompenseret leversygdom og er ikke gennemført.
9 Experience in patients with decompensated liver disease: placebo controlled studies have been regarded as inappropriate in patients with decompensated liver disease, and have not been undertaken.
Hvis behandling med lamivudin
In non-controlled studies, where lamivudine was administered prior to and during transplantation, effective HBV DNA suppression and ALT normalisation was demonstrated.
9 blev fortsat efter transplantationen, var der nedsat HBV- reinfektion af transplantatet, øget tab af HBsAg og på 1 år en overlevelsesrate på 76- 100%.
When lamivudine therapy was continued post transplantation there was reduced graft re-infection by HBV, increased HBsAg loss and on one-year survival rate of 76 – 100%.
Som forventet på grund af den samtidige immunosuppression er der en højere grad af fremkomst af YMDD- variant HBV efter 52 ugers behandling (36% - 64%) i gruppen af levertransplanterede end blandt immunkompetente CHB patienter (14% - 32%).
As anticipated due to the concomitant immunosuppression, the rate of emergence of YMDD variant HBV after 52 weeks treatment was higher (36% - 64%) in the liver transplant population than in the immunocompetent CHB patients (14% - 32%).
I et placebo- kontrolleret studie med 651 patienter, med klinisk kompenseret kronisk hepatitis B og histologisk bekræftet fibrose eller cirrhosis, reducerede lamivudin behandling (middelvarighed 32 måneder) signifikant hyppigheden af overordnet sygdomsprogression, (34/ 436, 7. 8% for lamivudin versus 38/ 215, 17. 7% for placebo, p=0. 001), demonstreret ved en signifikant reduktion i andelen af patienter der havde øget Child- Pugh scores (15/ 436, 3. 4% versus 19/ 215, 8. 8%, p=0. 023) eller udviklende hepatocellulær carcinoma (17/ 436, 3. 9% versus 16/ 215, 7. 4%, p=0. 047).
Experience in CHB patients with advanced fibrosis or cirrhosis: in a placebo-controlled study in 651 patients with clinically compensated chronic hepatitis B and histologically confirmed fibrosis or cirrhosis, lamivudine treatment (median duration 32 months) significantly reduced the rate of overall disease progression (34/ 436, 7.8% for lamivudine versus 38/ 215, 17.7% for placebo, p=0.001), demonstrated by a significant reduction in the proportion of patients having increased Child-Pugh scores (15/ 436, 3.4% versus 19/ 215, 8.8%, p=0.023) or developing hepatocellular carcinoma (17/ 436, 3.9% versus 16/ 215, 7.4%, p=0.047).
Hyppigheden af overordnet sygdomsprogression i lamivudingruppen var højere for personer med detekterbar YMDD- variant HBV DNA (23/ 209, 11%) sammenlignet med dem uden detekterbar YMDD- variant HBV (11/ 221, 5%).
The rate of overall disease progression in the lamivudine group was higher for subjects with detectable YMDD variant HBV DNA (23/ 209, 11%) compared to those without detectable YMDD variant HBV (11/ 221, 5%).
Sygdomsprogressionen hos YMDD- personerne i lamivudingruppen var dog lavere end sygdomsprogressionen i placebogruppen (henholdsvis 23/ 209, 11% versus 38/ 214, 18%).
However, disease progression in YMDD subjects in the lamivudine group was lower than the disease progression in the placebo group (23/ 209, 11% versus 38/ 214, 18% respectively).
Bekræftet HBeAg- serokonversion opstod hos 47% (118/ 252), af personer behandlet med lamivudin, og 93% (320/ 345) personer, der modtog lamivudin, blev HBV DNA negative, (VERSANT [version 1], bDNA assay, LLOD < 0, 7 MEq/ ml, under studiet.
Confirmed HBeAg seroconversion occurred in 47% (118/ 252) of subjects treated with lamivudine and 93% (320/ 345) of subjects receiving lamivudine became HBV DNA negative (VERSANT [version 1], bDNA assay, LLOD < 0.7 MEq/ ml) during the study.
Lamivudin er blevet givet til børn og unge med kompenseret CHB i en placebo kontrolleret undersøgelse af 286 patienter i alderen fra 2 til 17 år.
Experience in children and adolescents: lamivudine has been administered to children and adolescents with compensated CHB in a placebo controlled study of 286 patients aged 2 to 17 years.
Gruppen bestod primært af børn med minimal hepatitis B.
This population primarily consisted of children with minimal hepatitis B.
En dosering på 3 mg/ kg 1 gang daglig (op til maksimum 100 mg daglig) blev anvendt til børn mellem 2 og 11 år, mens en dosering på 100 mg 1 gang daglig blev givet til unge fra og med 12 år.
A dose of 3 mg/ kg once daily (up to a maximum of 100 mg daily) was used in children aged 2 to 11 years and a dose of 100 mg once daily in adolescents aged 12 years and above.
Forskellen i HBeAg - serokonversions hastighed (HBeAg og HBV DNA tab ved HbeAb- detektion) mellem placebo og lamivudin var ikke statistisk signifikant i denne population (forekomsten efter 1 år var 13% (12/ 95) for placebo versus 22% (42/ 191) for lamivudin; p=0, 057).
The difference in the HBeAg seroconversion rates (HBeAg and HBV DNA loss with HBeAb detection) between placebo and lamivudine was not statistically significant in this population (rates after one year were 13% (12/ 95) for placebo versus 22% (42/ 191) for lamivudine; p=0.057).
Forekomsten af YMDD- variant HBV var ens med den, der blev observeret hos voksne, fra 19% ved uge 52 op til 45% hos patienter i vedvarende behandling i 24 måneder.
The incidence of YMDD variant HBV was similar to that observed in adults, ranging from 19% at week 52 up to 45% in patients treated continuously for 24 months..
Ved terapeutiske dosisniveauer, dvs.
At therapeutic dose levels i. e.
1, 1- 1, 5 μg/ ml og Cmin- niveauer er 0, 015- 0, 020 μg/ ml.
100 mg once daily, Cmax is in the order of 1.1-1.5 µg/ ml and trough levels were 0.015-0.020 µg/ ml.
Indgift af lamivudin sammen med mad resulterer i en forsinket tmax og en lavere Cmax (nedsat med op til 47%).
Co-administration of lamivudine with food resulted in a delay of tmax and a lower Cmax (decreased by up to 47%).
Det gennemsnitlige fordelingsvolumen er 1, 3 l/ kg ifølge intravenøse undersøgelser.
From intravenous studies the mean volume of distribution is 1.3 l/ kg.
0, 12.
The mean lamivudine CSF/ serum concentration ratio 2-4 hours after oral administration was approximately 0.12.
Metabolisme:
10 Metabolism:
Sandsynligheden for metaboliske stofinteraktioner med lamivudin er lav på grund af begrænset (5 - 10%) levermetabolisme og lav plasmaproteinbinding.
The likelihood of metabolic substance interactions with lamivudine is low due to the small (5-10%) extent of hepatic metabolism and the low plasma protein binding.
0, 3 l/ h/ kg.
The mean systemic clearance of lamivudine is approximately 0.3 l/ h/ kg.
10 i urinen via glomerulær filtration og aktiv sekretion (via det organiske kationiske transportsystem).
The majority of lamivudine is excreted unchanged in the urine via glomerular filtration and active secretion (organic cationic transport system).
Renal clearance er ansvarlig for omkring 70% af eliminationen af lamivudin.
Renal clearance accounts for about 70% of lamivudine elimination.
Dosisreduktion er nødvendig til patienter med kreatininclearance under 50 ml/ minut (se afsnit 4. 2).
Dose reduction in patients with a creatinine clearance of < 50 ml/ min is necessary (see section 4.2).
Hos ældre patienter tyder den farmakokinetiske profil af lamivudin på, at normal ældning med ledsagende nedsættelse af nyrefunktionen ikke har nogen klinisk signifikant effekt på ekspositionen af lamivudin undtagen hos patienter med kreatininclearance under 50 ml/ min (se afsnit 4. 2).
In elderly patients the pharmacokinetic profile of lamivudine suggests that normal ageing with accompanying renal decline has no clinically significant effect on lamivudine exposure, except in patients with creatinine clearance of < 50 ml/ min (see section 4.2).
Ved de højeste doser fandtes mindre påvirkning af indikatorer for lever - og nyrefunktion samt af og til reduktioner af levervægt.
At the highest dosage levels, minor effects on indicators of liver and kidney function were seen together with occasional reduction in liver weights.
Reduktion i erytrocyt - og neutrofiltal blev identificeret som de virkninger, der mest sandsynligt var af klinisk relevans.
Reduction of erythrocytes and neutrophil counts were identified as the effects most likely to be of clinical relevance.
Lamivudin var ikke mutagent i bakterietests, men viste som mange andre nukleosidanaloger aktivitet i en in vitro cytogenprøve og i muse- lymfomprøven.
Lamivudine was not mutagenic in bacterial tests but, like many nucleoside analogues showed activity in an in vitro cytogenetic assay and the mouse lymphoma assay.
Lamivudin var ikke genotoksisk in vivo ved doser, der medførte plasmakoncentrationer omkring 60- 70 gange højere end de forventede kliniske plasmakoncentrationer.
Lamivudine was not genotoxic in vivo at doses that gave plasma concentrations around 60-70 times higher than the anticipated clinical plasma levels.
Hos gravide kaniner inducerer Lamivudin tidlig embryoletalitet ved doser sammenlignelige med dem opnået hos mennesker, men dette ses ikke hos rotter selv ved meget høje systemiske eksponeringer.
Lamivudine induces early embryolethality when administered to pregnant rabbits at exposure levels comparable to those achieved in man, but not in the rat even at very high systemic exposures.
Cellulose, mikrokrystallinsk Natriumstivelsesglycollat Magnesiumstearat
Microcrystalline Cellulose Sodium Starch Glycollate Magnesium Stearate
Hypromellose Titandioxid Macrogol 400 Polysorbat 80 Syntetisk gul og rød jernoxid
Hypromellose Titanium Dioxide Macrogol 400 Polysorbate 80 Synthetic yellow and red iron oxides
11 3 år.
3 years
Må ikke opbevares over 30º C.
Do not store above 30ºC.
Æsker med 28 eller 84 filmovertrukne tabletter i dobbeltfolie blisterpakning belagt med PVC.
Boxes containing 28 or 84 film-coated tablets in double foil blisters, laminated with polyvinyl chloride.
29. juli 1999 Dato for fornyelse af tilladelsen:
29 July 1999 Date of renewal of authorisation: