natgillin/translations-raw huggingface dataset:
Race Farmakokinetiske studier viser en øget eksponering hos Japanske og Kinesiske patienter sammenlignet med kaukasere (se afsnit 4. 2 Dosering og indgivelsesmåde og afsnit 5. 2 Farmakokinetiske egenskaber).
Race Pharmacokinetic studies show an increase in exposure in Japanese and Chinese subjects compared with Caucasians (see section 4.2 Posology and Method of administration and section 5.2 Pharmacokinetic properties)
Ciclosporin:
Cyclosporin:
Ved samtidig behandling med Crestor og ciclosporin var rosuvastatin’ s AUC værdier i gennemsnit 7 gange højere end hos raske frivillige (se afsnit 4. 3 Kontraindikationer).
During concomitant treatment with Crestor and cyclosporin, rosuvastatin AUC values were on average 7 times higher than those observed in healthy volunteers (see Section 4.3 Contraindications).
Samtidig administration påvirkede ikke ciclosporin’ s plasmakoncentration.
Concomitant administration did not affect plasma concentrations of cyclosporin.
Vitamin K antagonister:
Vitamin K antagonists:
Som med andre HMG- CoA reduktasehæmmere kan initiering af behandling eller dosis optitrering med Crestor hos patienter som samtidig behandles med vitamin K antagonister (f. eks. warfarin) resultere i en stigning i International Normaliseret Ratio (INR).
As with other HMG-CoA reductase inhibitors, the initiation of treatment or dosage up-titration of Crestor in patients treated concomitantly with vitamin K antagonists (e. g. warfarin) may result in an increase in International Normalised Ratio (INR).
Seponering eller nedtitrering af Crestor kan resultere i et fald i INR.
Discontinuation or down- titration of Crestor may result in a decrease in INR.
Gemfibrozil og andre lipidsænkende produkter:
Gemfibrozil and other lipid-lowering products:
Samtidig behandling med Crestor og gemfibrozil medførte en 2- foldig stigning i rosuvastatin’ s Cmax og AUC (se afsnit 4. 4 Særlige advarsler og forsigtighedsregler vedrørende brugen).
Concomitant use of Crestor and gemfibrozil resulted in a 2-fold increase in rosuvastatin C max and AUC (see Section 4.4 Special warnings and special precautions for use).
Gemfibrozil, fenofibrater, andre fibrater og lipid sænkende doser (> eller svarende til 1 g/ dag) af niacin (nikotinsyre) øger risikoen for myopati, når det gives sammen med HMG- CoA reduktasehæmmere, sandsynligvis fordi de kan give myopati, når de gives alene.
Gemfibrozil, fenofibrate, other fibrates and lipid lowering doses (> or equal to 1g/ day) of niacin (nicotinic acid) increase the risk of myopathy when given concomitantly with HMG-CoA reductase inhibitors, probably because they can produce myopathy when given alone.
Doser på 40 mg er kontraindiceret ved samtidig anvendelse af fibrater (se afsnit 4. 3 Kontraindikationer og afsnit 4. 4 Særlige advarsler og forsigtighedsregler vedrørende brugen).
The 40 mg dose is contraindicated with concomitant use of a fibrate (see Section 4.3 Contraindications and Section 4.4 Special warnings and special precautions for use).
50%.
The simultaneous dosing of Crestor with an antacid suspension containing aluminium and magnesium hydroxide resulted in a decrease in rosuvastatin plasma concentration of approximately 50%.
Erythromycin:
11 Erythromycin:
Samtidig anvendelse af Crestor og erythromycin medførte et fald på 20% i AUC (0- t) og i et fald på 30% i Cmax af rosuvastatin.
Concomitant use of Crestor and erythromycin resulted in a 20% decrease in AUC (0-t) and a 30% decrease in Cmax of rosuvastatin.
11 Peroral antikonception/ hormonsubstitutionsbehandling:
Oral contraceptive/ hormone replacement therapy (HRT):
Samtidig anvendelse af Crestor og et peroralt antikonceptivum medførte en stigning i ethinylestradiol’ s og norgestrel’ s AUC på henholdsvis 26% og 34%.
Concomitant use of Crestor and an oral contraceptive resulted in an increase in ethinyl oestradiol and norgestrel AUC of 26% and 34%, respectively.
På baggrund af data fra specifikke interaktionsstudier forventes der ingen klinisk relevante interaktioner med digoxin.
Based on data from specific interaction studies no clinically relevant interaction with digoxin is expected.
Cytochrom P450 enzymer:
Cytochrome P450 enzymes:
Resultater fra in vitro og in vivo studier viser, at rosuvastatin hverken inhiberer eller inducerer cytochrom P450 isoenzymer.
Results from in vitro and in vivo studies show that rosuvastatin is neither an inhibitor nor an inducer of cytochrome P450 isoenzymes.
Der er ikke observeret klinisk relevante interaktioner mellem rosuvastatin og enten fluconazol (en hæmmer af CYP2C9 og CYP3A4) eller ketoconazol (en hæmmer af CYP2A6 og CYP3A4).
No clinically relevant interactions have been observed between rosuvastatin and either fluconazole (an inhibitor of CYP2C9 and CYP3A4) or ketoconazole (an inhibitor of CYP2A6 and CYP3A4).
Samtidig administration af itraconazol (en hæmmer af CYP3A4) og rosuvastatin medførte en stigning på 28% i AUC for rosuvastatin.
Concomitant administration of itraconazole (an inhibitor of CYP3A4) and rosuvastatin resulted in a 28% increase in AUC of rosuvastatin.
Da kolesterol og andre produkter fra kolesterolbiosyntesen er essentielle for fosterets udvikling er den potentielle risiko ved hæmning af HMG- CoA reduktase større end fordelene ved behandling under graviditet.
Since cholesterol and other products of cholesterol biosynthesis are essential for the development of the foetus, the potential risk from inhibition of HMG-CoA reductase outweighs the advantage of treatment during pregnancy.
Dyrestudier giver begrænset bevis på reproduktionstoksicitet (se afsnit 5. 3 Prækliniske sikkerhedsdata).
Animal studies provide limited evidence of reproductive toxicity (see Section 5.3 Preclinical safety data).
Det vides ikke, om det udskilles i mælken hos mennesker (se afsnit 4. 3 Kontraindikationer).
(see Section 4.3 Contraindications).
Der er ikke foretaget undersøgelser af Crestor’ s indflydelse på evnen til at føre bil eller betjene maskiner.
Studies to determine the effect of Crestor on the ability to drive and use machines have not been conducted.
Crestor‘ s bivirkninger er generelt milde og forbigående.
The adverse events seen with Crestor are generally mild and transient.
I kontrollerede kliniske undersøgelser måtte færre end 4% af de patienter som fik Crestor udgå af undersøgelserne på grund af bivirkninger.
In controlled clinical trials, less than 4% of Crestor-treated patients were withdrawn due to adverse events.
Hyppigheden af bivirkningerne opdeles på følgende måde:
The frequencies of adverse events are ranked according to the following:
Almindelig (> 1/ 100, < 1/ 10); Usædvanlig (> 1/ 1000, < 1/ 100) Sjælden (> 1/ 10 000, < 1/ 1000).
Common (> 1/ 100 ,< 1/10); Uncommon (> 1/1 ,000, < 1/100); Rare (> 1/10,000, < 1/1000);
Overfølsomhedsreaktioner som f. eks. angioødem.
Immune system disorders Rare: hypersensitivity reactions including angioedema
Hovedpine, svimmelhed.
Nervous system disorders Common: headache, dizziness
12 Sygdomme i bevægeapparatet og bindevæv Almindelig:
12 Gastrointestinal disorders Common: constipation, nausea, abdominal pain
Myopati og rhabdomyolyse.
Skin and subcutaneous tissue disorders Uncommon: pruritus, rash and urticaria
Almene lidelser og reaktioner på indgivelsesstedet Almindelig:
Musculoskeletal, connective tissue and bone disorders Common: myalgia Rare: myopathy and rhabdomyolysis
Asteni.
General disorders Common: asthenia
Som med andre HMG- CoA reduktase hæmmere er der tendens til at bivirkninghyppigheden er dosisafhængig.
As with other HMG-CoA reductase inhibitors, the incidence of adverse drug reactions tends to be dose dependent.
Nyrepåvirkninger:
Renal Effects:
Der er observeret proteinuri (påvist ved sticktest og hovedsagelig tubulær af oprindelse) hos patienter behandlet med Crestor.
Proteinuria, detected by dipstick testing and mostly tubular in origin, has been observed in patients treated with Crestor.
3% af patienterne med 40 mg.
Shifts in urine protein from none or trace to ++ or more were seen in < 1% of patients at some time during treatment with 10 and 20 mg, and in approximately 3% of patients treated with 40 mg.
En mindre stigning i skift fra “ ingen ” eller “ spor ” til ” + ” blev observeret med dosis på 20 mg.
A minor increase in shift from none or trace to + was observed with the 20 mg dose.
I de fleste tilfælde reduceres eller forsvinder proteinuri spontant ved fortsat behandling og der er ikke vist, at det er tegn på akut eller progressiv nyresygdom.
In most cases, proteinuria decreases or disappears spontaneously on continued therapy, and has not been shown to be predictive of acute or progressive renal disease.
Skeletmuskulaturpåvirkninger:
Skeletal muscle effects:
Der er rapporteret om påvirkninger af skeletmuskulaturen, fx myalgi, myopati og sjældent rhabdomyolyse, hos individer behandlet med Crestor uafhængig af dosis, men specielt med doser > 20 mg.
Effects on skeletal muscle e. g. myalgia, myopathy and, rarely, rhabdomyolysis have been reported in Crestor-treated patients with all doses and in particular with doses > 20 mg.
Hvis CK niveauer er forhøjede (> 5xULN) bør behandlingen afbrydes (se afsnit 4. 4 Særlige advarsler og forsigtighedsregler vedrørende brugen).
If CK levels are elevated (> 5xULN), treatment should be discontinued (see Section 4.4 Special warnings and special precautions for use).
Leverpåvirkning:
Liver Effects:
Som med andre HMG- CoA reduktasehæmmere er der hos et lille antal patienter behandlet med rosuvastatin, set en dosis relateret stigning i transaminaser; de fleste tilfælde var milde, asymptomatiske og forbigående.
As with other HMG-CoA reductase inhibitors, a dose-related increase in transaminases has been observed in a small number of patients taking rosuvastatin; the majority of cases were mild, asymptomatic and transient.
HMG- CoA reduktasehæmmere
HMG-CoA reductase inhibitors
C10 A A07
C10A A07
Virkningsmekanisme Rosuvastatin er en selektiv og kompetitiv inhibitor af HMG- CoA reduktase, det hastighedsbegrænsende enzym som omdanner 3- hydroxy- 3- methylglutaryl coenzym A til mevalonat, et forstadie til kolesterol.
Mechanism of action Rosuvastatin is a selective and competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl coenzyme A to mevalonate, a precursor for cholesterol.
Farmakodynamiske virkninger
13 Rosuvastatin increases the number of hepatic LDL receptors on the cell-surface, enhancing uptake and catabolism of LDL and it inhibits the hepatic synthesis of VLDL, thereby reducing the total number of VLDL and LDL particles.
13 Crestor reducerer forhøjet LDL- kolesterol, total kolesterol og triglycerider og øger HDL kolesterol.
Pharmacodynamic effects Crestor reduces elevated LDL-cholesterol, total cholesterol and triglycerides and increases HDL- cholesterol.
Det sænker også ApoB, nonHDL- C, VLDL- C, VLDL- TG og øger ApoA- I (se tabel 1).
It also lowers ApoB, nonHDL-C, VLDL-C, VLDL-TG and increases ApoA-I (see Table 1).
Crestor sænker også forholdene LDL- C/ HDL- C, total C/ HDL- C og nonHDL- C/ HDL- C samt ApoB/ ApoA- I.
Crestor also lowers the LDL-C/ HDL-C, total C/ HDL-C and nonHDL-C/ HDL-C and the ApoB/ ApoA-I ratios.
Dosisrespons hos patienter med primær hyperkolesterolæmi (type IIa og IIb) (justeret gennemsnitsændring fra baselinien i procent).
Table 1 Dose response in patients with primary hypercholesterolaemia (type IIa and IIb) (adjusted mean percent change from baseline)
Antal
N
LDL - C
LDL- C
Total - C
Total- C
HDL - C
HDL- C
TG
TG
nonHDL- C
nonHDL- C
ApoB
Apo B
ApoA - I
ApoA-I
- 7
-7
- 5 3 - 3 - 7
-5 3 -3 -7
3 - 7 - 5 3
3 -7 -5 3
- 3
-3
- 7 - 5 3
-7 -5 3
- 3 - 7 - 3
-3 -7 -3
5
5 10 20 40
17
17 17 17 18
- 52 - 55 - 63
-45 -52 -55 -63
- 36 - 40 - 46
-33 -36 -40 -46
14 8 10
13 14 8 10
- 10 - 23 - 28
-35 -10 -23 -28
- 48 - 51 - 60
-44 -48 -51 -60
- 42 - 46 - 54
-38 -42 -46 -54
4 5 0
4 4 5 0
Terapeutisk effekt opnås indenfor 1 uge efter behandlingens start og 90% af maksimum respons opnås på 2 uger.
A therapeutic effect is obtained within 1 week following treatment initiation and 90% of maximum response is achieved in 2 weeks.
Crestor er effektiv hos voksne med hyperkolesterolæmi med eller uden hypertriglyceridæmi uafhængig af race, køn og alder samt i specielle grupper som f. eks diabetikere eller patienter med familiær hyperkolesterolæmi.
Clinical efficacy Crestor is effective in adults with hypercholesterolaemia, with and without hypertriglyceridaemia, regardless of race, sex, or age and in special populations such as diabetics, or patients with familial hypercholesterolaemia.
80% af de patienter som blev behandlet med Crestor 10 mg nåede EAS målet for LDL- C niveaer (< 3 mmol/ l).
From pooled phase III data, Crestor has been shown to be effective at treating the majority of patients with type IIa and IIb hypercholesterolaemia (mean baseline LDL-C about 4.8 mmol/ l) to recognised European Atherosclerosis Society (EAS; 1998) guideline targets; about 80% of patients treated with 10 mg reached the EAS targets for LDL-C levels (< 3 mmol/ l).
I en stor undersøgelse af patienter med heterozygot familiær hyperkolesterolæmi fik 435 individer Crestor fra 20 mg til 80 mg i et force- titrerings design.
In a large study, 435 patients with heterozygous familial hypercholesterolaemia were given Crestor from 20 mg to 80 mg in a force-titration design.
Efter titrering til en daglig dosis på 40 mg (12 ugers behandling) var LDL- C reduceret med 53%.
Following titration to a daily dose of 40 mg (12 weeks of treatment), LDL-C was reduced by 53%.
33% af patienterne nåede EAS guideline målene for LDL- C niveauer (< 3 mmol/ l).
33% of patients reached EAS guidelines for LDL-C levels (< 3 mmol/ l).
I et force- titrerings open label studie blev 42 patienter med homozygot familiær hyperkolesterolæmi evalueret for deres respons på 20- 40 mg Crestor.
In a force-titration, open label trial, 42 patients with homozygous familial hypercholesterolaemia were evaluated for their response to Crestor 20 - 40 mg.
I den samlede population var middel LDL- C reduktionen på 22%.
In the overall population, the mean LDL-C reduction was 22%.
I kliniske undersøgelser med et begænset antal patienter har Crestor vist en additiv effekt i sænkning af triglycerider ved kombination med fenofibrat og i øgning af HDL- C niveaer i kombination med niacin (se afsnit 4. 4 Særlige advarsler og forsigtighedsregler vedrørende brugen).
In clinical studies with a limited number of patients, Crestor has been shown to have additive efficacy in lowering triglycerides when used in combination with fenofibrate and in increasing HDL-C levels when used in combination with niacin (see Section 4.4 Special warnings and special precautions for use).
Det er ikke påvist, at rosuvastatin forebygger følgekomplikationer forbundet med lipidabnormaliteter såsom koronar hjertesygdomme, da mortalites - og morbiditets undersøgelser med Crestor endnu ikke er færdiggjort.
Rosuvastatin has not been proven to prevent the associated complications of lipid abnormalities, such as coronary heart disease as mortality and morbidity studies with Crestor have not yet been completed.
5 timer efter peroral administration.
Maximum rosuvastatin plasma concentrations are achieved approximately 5 hours after oral administration.
20%.
The absolute bioavailability is approximately 20%.
Rosuvastatin optages hovedsagelig af leveren, det primære organ for kolesterolsyntese og LDL- C clearence.
Rosuvastatin is taken up extensively by the liver which is the primary site of cholesterol synthesis and LDL-C clearance.
134L.
The volume of distribution of rosuvastatin is approximately 134 L.
90% til plasmaproteiner, hovedsagelig til albumin.
Approximately 90% of rosuvastatin is bound to plasma proteins, mainly to albumin.
14 Metabolisme:
Metabolism:
10%).
Rosuvastatin undergoes limited metabolism (approximately 10%).
In vitro metabolisme undersøgelser med humane hepatocytter indikerer at rosuvastatin er et ringe substrat for cytochrom P450 baseret metabolisme.
In vitro metabolism studies using human hepatocytes indicate that rosuvastatin is a poor substrate for cytochrome P450- based metabolism.
De identificerede hovedmetabolitter er N- desmethyl og lakton metabolitterne.
The main metabolites identified are the N-desmethyl and lactone metabolites.
N- desmethyl metabolitten er ca. halvt så aktiv som rosuvastatin hvorimod laktonformen betragtes som klinisk inaktiv.
The N- desmethyl metabolite is approximately 50% less active than rosuvastatin whereas the lactone form is considered clinically inactive.
Rosuvastatin tegner sig for mere end 90% af den cirkulerende HMG- CoA reduktase aktivitet.
Rosuvastatin accounts for greater than 90% of the circulating HMG-CoA reductase inhibitor activity.
Elimination:
Excretion:
5% udskilles uomdannet i urinen.
Approximately 90% of the rosuvastatin dose is excreted unchanged in the faeces (consisting of absorbed and non-absorbed active substance) and the remaining part is excreted in urine.
Plasmaudskillelseshalveringstiden er ca.
Approximately 5% is excreted unchanged in urine.
19 timer.
The plasma elimination half-life is approximately 19 hours.
50 liter/ time (variationskoefficient 21, 7%).
The geometric mean plasma clearance is approximately 50 litres/ hour (coefficient of variation 21.7%).
Som med andre HMG- CoA reduktasehæmmere involverer rosuvastain’ s leveroptagelse membrantransporteren OATP- C.
As with other HMG-CoA reductase inhibitors, the hepatic uptake of rosuvastatin involves the membrane transporter OATP-C.
Denne transporter er vigtig for rosuvastatins ’ leverelimination.
This transporter is important in the hepatic elimination of rosuvastatin.
Rosuvastatin’ s systemiske eksponering stiger proportionelt med dosis.
Systemic exposure of rosuvastatin increases in proportion to dose.
Alder og køn:
Age and sex:
Alder og køn har ingen klinisk relevant effekt på rosuvastatin’ s farmakokinetik.
There was no clinically relevant effect of age or sex on the pharmacokinetics of rosuvastatin.
Farmakokinetiske studier viser en ca. fordoblet stigning i gennemsnits AUC sammenlignet med vestlige kaukasiere hos både Japanske patienter bosiddende i Japan og Kinesiske patienter bosiddende i Singapore.
Pharmacokinetic studies show an approximate 2-fold elevation in median AUC compared with western Caucasians in both Japanese subjects residing in Japan, and Chinese subjects living in Singapore.
I en undersøgelse hos individer med varierende grad af nyresinsufficiens, havde mild til moderat nyresygdom ingen indflydelse på rosuvastatin’ s eller N- desmethyl metabolittens plasmakoncentration.
In a study in subjects with varying degrees of renal impairment, mild to moderate renal disease had no influence on plasma concentration of rosuvastatin or the N-desmethyl metabolite.
Hos individer med svær nyreinsufficiens (CrCl < 30 ml/ min) sås en 3- foldig stigning i plasmakoncentration og en 9- foldig stigning i koncentrationen af N- desmethyl metabolitten sammenlignet med raske frivillige.
Subjects with severe impairment (CrCl < 30 ml/ min) had a 3-fold increase in plasma concentration and a 9-fold increase in the N-desmethyl metabolite concentration compared to healthy volunteers.
50% større sammenlignet med raske frivillige.
Steady-state plasma concentrations of rosuvastatin in subjects undergoing haemodialysis were approximately 50% greater compared to healthy volunteers.
I en undersøgelse hos individer med varierende grad af leverinsufficiens, sås intet tegn på en øget eksponering af rosuvastatin hos individer med Child- Pugh score på 7 eller derunder.
In a study with subjects with varying degrees of hepatic impairment there was no evidence of increased exposure to rosuvastatin in subjects with Child-Pugh scores of 7 or below.
Dog viste to individer med Child- Pugh score på 8 og 9 en stigning i systemisk eksponering som var mindst fordoblet sammenlignet med individer med lavere Child- Pugh score.
However, two subjects with Child-Pugh scores of 8 and 9 showed an increase in systemic exposure of at least 2-fold compared to subjects with lower Child-Pugh scores.
I en præ- og postnatal undersøgelse hos rotter sås reproduktionstoksicitet i form af reduktion i kuldstørrelser, kuldvægt og ungernes overlevelse.
In a rat pre- and postnatal study, reproductive toxicity was evident from reduced litter sizes, litter weight and pup
6.
15 survival.
FARMACEUTISKE OPLYSNINGER
These effects were observed at maternotoxic doses at systemic exposures several times above the therapeutic exposure level.
Tabletkerne
6.1 List of excipients
15 Lactose monohydrat Mikrokrystallinsk cellulose Calciumphosphat Crospovidon Magnesiumstearat
Tablet core Lactose monohydrate Microcrystalline cellulose Calcium phosphate Crospovidone Magnesium stearate
Tabletovertræk Lactosemonohydrat Hypromellose Glyceroltriacetat Titaniumdioxid (E 171) Gul jernoxid (E 172)
Tablet coat Lactose monohydrate Hypromellose Glycerol triacetate Titanium dioxide (E171) Ferric oxide, yellow (E172)
Blister af aluminium laminat/ aluminium folie 7, 14, 15, 20, 28, 30, 42, 50, 56, 60, 84, 98 og 100 tabletter samt HDPE beholder med 30 og 100 tabletter.
Blisters of aluminium laminate/ aluminium foil of 7, 14, 15, 20, 28, 30, 42, 50, 56, 60, 84, 98 and 100 tablets and HDPE bottles of 30 and 100 tablets.
< Se bilag I - Udfyldes nationalt >
< [See Annex I- to be completed nationally] >
< Udfyldes nationalt >
[To be completed nationally]
16 17
17
FORTEGNELSE OVER LÆGEMIDLERNES NAVNE, LÆGEMIDDELFORMER, STYRKER, INDGIVELSESVEJ, ANSØGERE, INDEHAVERE AF MARKEDSFØRINGSTILLADELSE I MEDLEMSSTATERNE
LIST OF THE NAMES, PHARMACEUTICAL FORM, STRENGTHS OF THE MEDICINAL PRODUCTS, ROUTE OF ADMINISTRATION, MARKETING AUTHORISATION HOLDERS IN THE MEMBER STATES Member State EU/ EEA
2 Medlemsstat EU/ EEA
4 Member State EU/ EEA
80 mg
Diovane 80 mg
Box 23490 Nicosia Cypern
Box 23490 Nicosia Cyprus
3 Medlemsstat EU/ EEA
5 Member State EU/ EEA
Novartis Healthcare A/ S Lyngbyvej 172 DK- 2100 København Ø
Novartis Healthcare A/ S Lyngbyvej 172 DK-2100 Kopenhagen Ø
4 Medlemsstat EU/ EEA
6 Member State EU/ EEA
2 and 4, rue Lionel Terray 92500 RUEIL- MALMAISON Frankrig
2 and 4, rue Lionel Terray 92500 RUEIL-MALMAISON France
5 Medlemsstat EU/ EEA
7 Member State EU/ EEA
Tareg 160
Tareg 160 mg
Diovan 40
Diovan 40 mg
40 mg
Cordinate 40 mg
80 mg
Cordinate 80 mg
6 Medlemsstat EU/ EEA
8 Member State EU/ EEA
7 Medlemsstat EU/ EEA
9 Member State EU/ EEA
Indehaver af markedsføringstilladelse GR- 144 51 Athens
Marketing Authorisation Holder GR-144 51 Athens
Hårde gelatinekapsler
Hard gelatine capsules
8 Medlemsstat EU/ EEA
10 Member State EU/ EEA
40 mg
Varexan 40 mg
Varexan
Varexan 80 mg
9 Medlemsstat EU/ EEA
11 Member State EU/ EEA
10 Medlemsstat EU/ EEA
12 Member State EU/ EEA
11 Medlemsstat EU/ EEA
13 Member State EU/ EEA
12 Medlemsstat EU/ EEA
14 Member State EU/ EEA
13 Medlemsstat EU/ EEA
15 Member State EU/ EEA
14 Medlemsstat EU/ EEA
16 Member State EU/ EEA
Prague Den Tjekkiske republik
Prague Czech Republic
15 Medlemsstat EU/ EEA
17 Member State EU/ EEA
16 Medlemsstat EU/ EEA
18 Member State EU/ EEA
17 Medlemsstat EU/ EEA
19 Member State EU/ EEA
18 Medlemsstat EU/ EEA
20 Member State EU/ EEA
19 Medlemsstat EU/ EEA
21 Member State EU/ EEA
20 BILAG II
22 ANNEX II
FAGLIGE KONKLUSIONER OG BEGRUNDELSER FOR ÆNDRING AF PRODUKTRESUME, ETIKETTERING OG INDLÆGSSEDDEL FREMLAGT AF EMEA
SCIENTIFIC CONCLUSIONS AND GROUNDS FOR AMENDMENT OF THE SUMMARIES OF PRODUCT CHARACTERISTICS, LABELLING AND PACKAGE LEAFLET PRESENTED BY THE EMEA
21 FAGLIGE KONKLUSIONER
23 SCIENTIFIC CONCLUSIONS
Diovan indeholder valsartan, en oral angiotensin II- receptorantagonist (AIIRA).
Diovan contains valsartan, an orally Angiotensin II Receptor Antagonist (AIIRA).
2, i direktiv 2001/ 83/ EF, med senere ændringer, da produktresuméet for ovennævnte lægemiddel ikke er det samme i alle EU- medlemsstater, Island og Norge.
Diovan was included in the list of products for Summary of Products Characteristics (SPC) harmonization, drawn up by the CMD(h), in accordance with Article 30(2) of Directive 2001/ 83/ EC, as amended, as the above-mentioned medicinal product does not have the same SPC across all EU Member States, Iceland and Norway.