natgillin/translations-raw huggingface dataset:
A minor increase in shift from none or trace to + was observed with the 20 mg dose.
Manjše č zvečanje z 0 ali v sledeh na + se je pojavilo pri tistih, ki so jemali 20- miligramske odmerke.
Skeletal muscle effects:
Vpliv na skeletno mišičje:
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.
Pri jemanju zdravila Crestor so pri bolnikih opazili učinke na skeletne mišice, npr. mialgijo, miopatijo in v redkih primerih tudi rabdomiolizo, pri vseh odmerkih, predvsem pa pri odmerkih > 20 mg.
If CK levels are elevated (> 5xULN), treatment should be discontinued (see Section 4.4 Special warnings and special precautions for use).
Vrednost CK se je v skladu z velikostjo odmerka zvečala pri bolnikih, ki so jemali rosuvastatin; v večini primerov je bilo zvečanje blago, asimptomatsko in prehodno. e je vrednost CK zvečana (> 5x ULN), je Č treba zdravljenje ustaviti (glejte poglavje 4. 4 Posebna opozorila in previdnostni ukrepi).
Liver Effects:
Vpliv na jetra:
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.
Serumska vrednost transaminaz se je pri majhnem številu bolnikov, ki so jemali rosuvastatin – tako kot pri uporabi drugih zaviralcev reduktaze HMG- CoA – v skladu z velikostjo odmerka zvečala; v večini primerov je bilo zvečanje blago, asimptomatsko in prehodno.
There is no specific treatment in the event of overdose.
Specifičnega zdravljenja v primeru prevelikega odmerjanja ni.
In the event of overdose, the patient should be treated symptomatically and supportive measures instituted as required.
Zdravljenje je simptomatsko; zagotoviti je treba delovanje vitalnih organov.
Liver function and CK levels should be monitored.
Spremljati je treba delovanje jeter in vrednosti CK.
Haemodialysis is unlikely to be of benefit.
Hemodializa verjetno ni učinkovita.
HMG-CoA reductase inhibitors
Farmakoterapevtska skupina: zaviralci reduktaze HMG- CoA
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.
13 Rosuvastatin je selektiven in kompetitiven zaviralec reduktaze HMG- CoA, encima, ki določa hitrost pretvorbe 3- hidroksi- 3- metilglutaril koencima A v mevalonat, ki je prekurzor holesterola.
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.
Rosuvastatin zvečuje število jetrnih receptorjev za LDL na površini celice in zveča prevzem in katabolizem LDL ter zavira nastajanje VLDL v jetrih in tako zmanjša skupno število delcev VLDL in LDL.
Pharmacodynamic effects Crestor reduces elevated LDL-cholesterol, total cholesterol and triglycerides and increases HDL- cholesterol.
Farmakodinamični učinki Crestor zmanjšuje zvečano koncentracijo holesterola LDL, skupnega holesterola in trigliceridov ter zvečuje vrednost holesterola HDL.
It also lowers ApoB, nonHDL-C, VLDL-C, VLDL-TG and increases ApoA-I (see Table 1).
Znižuje tudi raven ApoB, neHDL holesterola, holesterola VLDL, VLDL- TG in zvišuje raven ApoA- I (glejte preglednico 1).
Crestor also lowers the LDL-C/ HDL-C, total C/ HDL-C and nonHDL-C/ HDL-C and the ApoB/ ApoA-I ratios.
Prav tako zmanjšuje naslednja razmerja: holesterol LDL/ HDL, skupni holesterol/ holesterol HDL, holesterol neHDL / HDL ter ApoB / ApoA- I.
Table 1 Dose response in patients with primary hypercholesterolaemia (type IIa and IIb) (adjusted mean percent change from baseline)
Učinkovitost odmerka pri bolnikih s primarno hiperholesterolemijo (tipa IIa in IIb) (prilagojen povprečni odstotek spremembe glede na izhodiščno vrednost)
LDL- C
holesterol
Total- C
holesterol skupni holesterol
HDL- C
apoA- I
TG
LDL
nonHDL- C
holesterol
Apo B
HDL
ApoA-I
neHDL
-7
1
-7 -5 3
– 3
-3 -7 -3
– 7 – 3
5 10 20 40
5 10 20 40
17 17 17 18
17 17 17 18
-45 -52 -55 -63
– 45 – 52 – 55 – 63
-33 -36 -40 -46
– 33 – 36 – 40 – 46
13 14 8 10
13 14 8 10
-35 -10 -23 -28
– 35 – 10 – 23 – 28
-44 -48 -51 -60
– 44 – 48 – 51 – 60
-38 -42 -46 -54
– 38 – 42 – 46 – 54
4 4 5 0
4 4 5 0
A therapeutic effect is obtained within 1 week following treatment initiation and 90% of maximum response is achieved in 2 weeks.
Terapevtski učinek se pojavi prvi teden zdravljenja, 90% največjega učinka pa po dveh tednih.
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.
Klinična učinkovitost Crestor je učinkovit pri zdravljenju odraslih s hiperholesterolemijo s hipertrigliceridemijo ali brez nje, ne glede na raso, spol ali starost in pri posebnih populacijah, na primer sladkornih bolnikih ali pri bolnikih z družinsko hiperholesterolemijo.
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).
Po združenih podatkih raziskave III. faze je bilo zdravljenje s Crestorjem na podlagi smernic European Atherosclerosis Society (EAS; 1998) učinkovito pri večini bolnikov s hiperholesterolemijo tipa IIa in IIb (srednja izhodiščna vrednost holesterola LDL približno 4, 8 mmol/ l); okoli 80% bolnikov, ki so jemali po 10 mg zdravila, je po EAS doseglo ciljno vrednost za holesterol LDL (< 3 mmol/ l).
Following titration to a daily dose of 40 mg (12 weeks of treatment), LDL-C was reduced by 53%.
Po titriranju dnevnega odmerka na 40 mg (12 tednov zdravljenja) se je vrednost holesterola LDL zmanjšala za 53%.
33% of patients reached EAS guidelines for LDL-C levels (< 3 mmol/ l).
33% bolnikov je doseglo ciljno vrednost holesterola LDL (< 3 mmol/ l), kakor jo določajo smernice EAS.
In a force-titration, open label trial, 42 patients with homozygous familial hypercholesterolaemia were evaluated for their response to Crestor 20 - 40 mg.
V odprti raziskavi z določanjem odmerka na podlagi forsiranega titriranja so pri 42 bolnikih s homozigotno družinsko hiperholesterolemijo ocenjevali njihov odziv na zdravljenje z 20 - do 40 - miligramskimi odmerki Crestorja.
In the overall population, the mean LDL-C reduction was 22%.
Srednja vrednost holesterola LDL se je v celotni populaciji zmanjšala za 22%.
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).
V kliničnih raziskavah z omejenim številom bolnikov je Crestor med kombiniranim zdravljenjem s fenofibratom dodatno prispeval k učinkovitemu zmanjšanju vrednosti trigliceridov, v kombinaciji z niacinom pa k zvišanju ravni holesterola HDL (glejte poglavje 4. 4 Posebna opozorila in previdnostni ukrepi).
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.
14 Dokazov o preventivnem delovanju rosuvastatina na zaplete zaradi nenormalnih vrednosti lipidov, npr. koronarno srčno bolezen, ni, kajti raziskave o umrljivosti in zbolevnosti še niso končane.
Maximum rosuvastatin plasma concentrations are achieved approximately 5 hours after oral administration.
Plazemska koncentracija rosuvastatina je največja ez približno pet ur po peroralnem č zaužitju zdravila.
The absolute bioavailability is approximately 20%.
Absolutna biološka uporabnost je približno 20%.
Rosuvastatin is taken up extensively by the liver which is the primary site of cholesterol synthesis and LDL-C clearance.
Rosuvastatin se obsežno privzame v jetra, v katerih tudi nastaja največ holesterola in očistka holesterola LDL.
The volume of distribution of rosuvastatin is approximately 134 L.
Porazdelitveni volumen rosuvastatina je približno 134 l.
Approximately 90% of rosuvastatin is bound to plasma proteins, mainly to albumin.
Na plazemske beljakovine se ga veže približno 90%, v glavnem na albumin.
Rosuvastatin undergoes limited metabolism (approximately 10%).
Presnova rosuvastatina je majhna (približno 10%).
In vitro metabolism studies using human hepatocytes indicate that rosuvastatin is a poor substrate for cytochrome P450- based metabolism.
V raziskavah o presnovi in vitro so na loveških jetrnih parenhimskih celicah ugotovili, da je rosuvastatin slab substrat za presnovo s pomočjo č citokroma P450.
CYP2C9 was the principal isoenzyme involved, with 2C19, 3A4 and 2D6 involved to a lesser extent.
Glavni izoencim, ki sodeluje, je CYP2C9, drugi, manj pomembni, pa so 2C19, 3A4 in 2D6.
The main metabolites identified are the N-desmethyl and lactone metabolites.
Glavna presnovka sta N- demetilni in laktonski.
The N- desmethyl metabolite is approximately 50% less active than rosuvastatin whereas the lactone form is considered clinically inactive.
N- demetilni presnovek je približno 50% manj aktiven kot rosuvastatin, laktonski pa je klinično neaktiven.
Rosuvastatin accounts for greater than 90% of the circulating HMG-CoA reductase inhibitor activity.
Rosuvastatin je sam odgovoren za več kot 90% aktivnosti v krvi krožečega zaviralca reduktaze HMG- CoA.
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.
Z blatom (bodisi absorbirana bodisi neabsorbirana učinkovina) se v nespremenjeni obliki izloči okoli 90% odmerka rosuvastatina, preostanek pa se izloči s sečem.
Approximately 5% is excreted unchanged in urine.
Približno 5% se ga s sečem izloči v nespremenjeni obliki.
The plasma elimination half-life is approximately 19 hours.
Plazemska razpolovna doba izločanja traja približno 19 ur.
The geometric mean plasma clearance is approximately 50 litres/ hour (coefficient of variation 21.7%).
21, 7%).
As with other HMG-CoA reductase inhibitors, the hepatic uptake of rosuvastatin involves the membrane transporter OATP-C.
Tako kot pri drugih zaviralcih reduktaze HMG- CoA sodeluje tudi pri privzemu rosuvastatina v jetra membranski prenosnik OATP- C.
Systemic exposure of rosuvastatin increases in proportion to dose.
Sistemska izpostavljenost rosuvastatinu se zvečuje proporcionalno z njegovim odmerkom.
Age and sex:
Starost in spol:
There was no clinically relevant effect of age or sex on the pharmacokinetics of rosuvastatin.
Starost in spol nimata klinično pomembnega vpliva na farmakokinetiko rosuvastatina.
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.
V farmakokinetičnih raziskavah so ugotovili, da je srednja vrednost AUC in Cmax pri Japoncih, ki živijo na Japonskem in Kitajcih, živečih v Singapurju, približno dvakrat večja kot pri belcih, ki živijo na zahodu.
A population pharmacokinetic analysis revealed no clinically relevant differences in pharmacokinetics between Caucasian and Black groups.
V populacijski farmakokinetični analizi niso odkrili klinično pomembnih razlik pri farmakokinetičnih lastnostih belcev in rncev. č
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.
V raziskavi, v kateri so sodelovali preiskovanci z različnimi stopnjami ledvične okvare, blaga do zmerna huda ledvična bolezen ni vplivala na plazemske koncentracije rosuvastatina ali njegovega N- demetilnega presnovka.
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.
Pri bolnikih s hudo okvaro (kreatininski očistek < 30 ml/ min) je bila plazemska koncentracija rosuvastatina trikrat večja kot pri zdravih prostovoljcih, N- demetilnega presnovka pa devetkrat večja.
Steady-state plasma concentrations of rosuvastatin in subjects undergoing haemodialysis were approximately 50% greater compared to healthy volunteers.
Koncentracija rosuvastatina v stanju dinamičnega ravnovesja je bila pri ljudeh na hemodializi približno za 50% večja kot pri zdravih prostovoljcih.
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.
V raziskavi, v kateri so sodelovali preiskovanci z različnimi stopnjami jetrne okvare, niso dokazali zvečanja izpostavljenosti rosuvastatinu pri bolnikih, ocenjenih s 7 ali manj točkami po Child- Pughovi lestvici.
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.
Pri dveh preiskovancih, ocenjenih z 8 in 9 točkami po Child- Pughovi lestvici, je bila sistemska izpostavljenost najmanj dvakrat večja kot pri tistih z nižjo oceno po tej lestvici.
There is no experience in subjects with Child-Pugh scores above 9.
Ni izkušenj s preiskovanci, ocenjenimi z več kot 9 točkami po Child- Pughovi lestvici.
15 survival.
15 Predklinični podatki na osnovi običajnih študij farmakološke varnosti, toksičnosti pri ponavljajočih se odmerkih, genotoksičnosti in kancerogenega potenciala ne kažejo posebnega tveganja za loveka.
Tablet core Lactose monohydrate Microcrystalline cellulose Calcium phosphate Crospovidone Magnesium stearate
jedro tablete laktoza monohidrat mikrokristalna celuloza kalcijev fosfat krospovidon magnezijev stearat
Tablet coat Lactose monohydrate Hypromellose Glycerol triacetate Titanium dioxide (E171) Ferric oxide, yellow (E172)
obloga tablete laktoza monohidrat hipromeloza gliceriltriacetat titanov dioksid (E171) železov oksid, rumeni (E172)
Blisters:
Blistri:
Store in the original package.
Zdravilo shranjujte pri temperaturi do 30 ºC v originalni ovojnini.
HDPE bottles:
Plastenke DHPE:
Do not store above 30°C.
Zdravilo shranjujte pri temperaturi do 30 ºC.
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.
Blistri iz aluminijevega laminata/ aluminijeve folije po 7, 14, 15, 20, 28, 30, 42, 50, 60, 84, 98 in 100 tablet in plastenke DHPE po 30 in 100 tablet.
6.6 Instructions for use and handling< and disposal >
6. 6 Navodila za pripravo in ravnanje z zdravilom < in odlaganje >
< [See Annex I- to be completed nationally] >
< Glejte Dodatek I - Izpolni država lanic] > č
[To be completed nationally]
< Izpolni država lanica > č
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
SEZNAM IMEN, FARMACEVTSKIH OBLIK, JAKOSTI ZDRAVILA, POTI UPORABE ZDRAVILA, PREDLAGATELJEV, IMETNIKOV DOVOLJENJA ZA PROMET Z ZDRAVILOM V DRŽAVAH ČLANICAH
Marketing Authorisation Holder
Imetnik dovoljenja za promet z
oral
peroralna
4 Member State EU/ EEA
2 Država članica
Box 23490 Nicosia Cyprus
Box 23490 Nicosia Ciper
5 Member State EU/ EEA
3 Država članica
6 Member State EU/ EEA
4 Država članica
2 and 4, rue Lionel Terray 92500 RUEIL-MALMAISON France
2 and 4, rue Lionel Terray 92500 RUEIL- MALMAISON Francija
7 Member State EU/ EEA
5 Država članica
8 Member State EU/ EEA
6 Država članica
9 Member State EU/ EEA
7 Država članica
Marketing Authorisation Holder GR-144 51 Athens
Imetnik dovoljenja za promet z
Hard gelatine capsules
Hard gelatine capsules
10 Member State EU/ EEA
8 Država članica
11 Member State EU/ EEA
9 Država članica
Ireland
zdravila
12 Member State EU/ EEA
10 Država članica
Hard capsules
Hard capsules
13 Member State EU/ EEA
11 Država članica
Lithuania
zdravilom
14 Member State EU/ EEA
12 Država članica
15 Member State EU/ EEA
13 Država članica
Norway
zdravila
16 Member State EU/ EEA
14 Država članica
Portugal
zdravila
Prague Czech Republic
Prague Češka republika
17 Member State EU/ EEA
15 Država članica
Slovenia
zdravila
18 Member State EU/ EEA
16 Država članica
19 Member State EU/ EEA
17 Država članica
20 Member State EU/ EEA
18 Država članica
21 Member State EU/ EEA
19 Država članica
22 ANNEX II
20 DODATEK II
SCIENTIFIC CONCLUSIONS AND GROUNDS FOR AMENDMENT OF THE SUMMARIES OF PRODUCT CHARACTERISTICS, LABELLING AND PACKAGE LEAFLET PRESENTED BY THE EMEA
ZNANSTVENI ZAKLJUČKI IN PODLAGA ZA DOPOLNILO POVZETKA GLAVNIH ZNAČILNOSTI ZDRAVILA, OZNAČEVANJA IN NAVODIL ZA UPORABO, KI JIH JE PREDSTAVILA EVROPSKA AGENCIJA ZA ZDRAVILA
23 SCIENTIFIC CONCLUSIONS
21 ZNANSTVENI ZAKLJUČKI
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.
Ker zdravilo Diovan nima enakega povzetka glavnih značilnosti zdravila v vseh državah članicah EU, na Islandiji in Norveškem, je bilo vključeno na seznam zdravil, za katera je treba uskladiti povzetke glavnih značilnosti zdravila, ki ga je sestavil CMD( h) v skladu s členom 30( 2) Direktive 2001/ 83/ ES, kakor je bila spremenjena.
Critical Evaluation A number of areas of disharmony in the product information for Diovan have been evaluated by the CHMP and a revised PI was adopted.
Kritično vrednotenje CHMP je ovrednotil številna neusklajena področja v informacijah o zdravilu Diovan in sprejel revidirano različico informacij o zdravilu.
4.1 - Therapeutic Indications
4. 1 - Terapevtske indikacije
“ Treatment of essential hypertension”
„ Zdravljenje esencialne hipertenzije. “
“ Treatment of clinically stable patients with symptomatic heart failure or asymptomatic left ventricular systolic dysfunction after a recent (12 hours – 10 days) myocardial infarction”
„ Zdravljenje klinično stabilnih bolnikov s simptomatskim srčnim popuščanjem ali asimptomatsko sistolično disfunkcijo levega prekata po nedavnem (12 ur– 10 dni) miokardnem infarktu. “
The therapeutic indication for heart failure is supported primarily by a large long-term morbidity trial Valsartan Heart Failure Trial (Val-HeFT) Valsartan reduced the risk related to first morbid event, mortality, the total number of Heart Failure (HF) hospitalizations.
Valsartan je zmanjšal tveganje za prvo obolevnost, umrljivost ter skupno število hospitalizacij zaradi srčnega popuščanja.
“ Treatment of symptomatic heart failure when Angiotensin Converting Enzyme (ACE) inhibitors could not be used, or as add-on therapy to ACE inhibitors when beta blockers could not be used”
„ Zdravljenje simptomatskega srčnega popuščanja, kadar ni mogoče uporabiti zaviralcev angiotenzinske konvertaze (ACE), ali kot dodatna terapija k zdravljenju z zaviralci ACE, kadar ni mogoče uporabiti zaviralcev beta receptorjev (BB). “
4.2 - Posology
4. 2 - Odmerjanje
The dosing schedule for the therapeutic use of valsartan in heart failure was based on the Val-HeFT study.
Shema odmerjanja za terapevtsko uporabo valsartana pri srčnem popuščanju je temeljila na študiji Val - HeFT.
Therefore in the situation of potential use of the triple combination
Zato je bilo za primere morebitne uporabe trojne kombinacije besedilo v povzetku
24 the text within the SPC has been adjusted to indicate that caution (rather than “ not recommended”) is appropriate
22 glavnih značilnosti zdravila prilagojeno, in sicer tako, da se navede, da je potrebna previdnost (namesto navedbe „ ni priporočljiva “).
In CHMP’ s opinion the wording “ not recommended” should be used until there is more solid supportive benefit/ risk-profile evidence to triple combination.
Po mnenju CHMP se mora uporabljati izraz „ ni priporočljiva “, dokler se ne zberejo trdnejši dokazi, ki bi podprli razmerje med koristmi in tveganji trojne kombinacije.
Therefore the MAH should address the lack of (additional) clinical benefit and increased adverse events In conclusion; the CHMP adopts the revised text: “ The recommended starting dose of Diovan is 40 mg twice daily.
„ Priporočljiv začetni odmerek zdravila Diovan je 40 mg dvakrat dnevno.
The maximum daily dose administered in clinical trials is 320 mg in divided doses.
Največji dnevni odmerek, uporabljen v kliničnih preskušanjih, je bil 320 mg v ločenih odmerkih.
However, the triple combination of an ACE inhibitor, a beta blocker and valsartan is not recommended (see sections 4.4 and 5.1).
Vendar pa trojna kombinacija zaviralca ACE, beta zaviralca in valsartana ni priporočljiva (glejte poglavji 4. 4 in 5. 1).
Evaluation of patients with heart failure should always include assessment of renal function .”
Ocena bolnikov s srčnim popuščanjem mora vedno vključevati oceno delovanja ledvic. “
Acknowledging the comments from the CHMP and the Rapporteurs and in the absence of any new data regarding triple therapy with valsartan, the MAH proposed to substitute the wording “ the triple combination of an ACE inhibitor, a beta blocker and valsartan is not recommended” in chronic heart failure as requested in the relevant sections of the SPC (sections 4.2 and 4.4).
Ob upoštevanju pripomb odbora CHMP in poročevalcev ter zaradi pomanjkanja novih podatkov v zvezi s trojno terapijo, ki vključuje valsartan, je imetnik dovoljenja za promet z zdravilom predlagal zamenjavo besedila „ trojna kombinacija zaviralca ACE, beta zaviralca in valsartana ni priporočljiva “ pri kroničnem srčnem popuščanju, kot se to zahteva v zadevnih poglavjih povzetka glavnih značilnosti zdravila (poglavji 4. 2 in 4. 4).
In section 4.2 there are also differences in SPC across Member States in relation to the dosage recommendation in patients with renal and hepatic impairment.
Povzetki glavnih značilnosti zdravila držav članic se razlikujejo tudi v poglavju 4. 2, in sicer v zvezi s priporočljivim odmerkom za bolnike z okvaro ledvic in jeter.
Regarding renal impairment, the use of valsartan 80 mg as the starting dose, with no dosage adjustment, in patients with reduced renal function (creatinine clearance rate > 10 ml/ min) is supported by both efficacy and safety data from Study 27 and by pharmacokinetic data from Study 12.
Pri okvari ledvic je 80- miligramski začetni odmerek valsartana brez prilagoditve odmerka pri bolnikih z zmanjšanim delovanjem ledvic (kreatininski očistek > 10 ml/ min) podprt s podatki o učinkovitosti in varnosti iz študije 27 in farmakokinetičnimi podatki iz študije 12.
In Study 27 the kinetic of valsartan was also investigated in hypertensive patients with impairment of renal function (creatine clearance rate:
V študiji 27 je bila raziskana tudi kinetika valsartana pri hipertenzivnih bolnikih z okvaro delovanja ledvic (kreatininski očistek:
16-116 mL/ min).
16– 116 ml/ min).
The CHMP considered that the elimination of valsartan at steady-state is similar in patients with renal impairment when compared with healthy volunteers and adopted the following wording: “ No dosage adjustment is required for patients with a creatinine clearance > 10 ml/ min .”
„ Prilagoditev odmerka ni potrebna pri bolnikih s kreatininskim očistkom > 10 ml/ min. “
Valsartan does not undergo extensive biotransformation and 70% of the available dose is excreted.
Pri valsartanu ne pride do obsežne biotransformacije, zato se 70% razpoložljivega odmerka izloči.