natgillin/translations-raw huggingface dataset:
Inhibition af ACE resulterer i nedsat plasma angiotensin II koncentration, hvilket medfører en nedsat vasokonstriktorisk aktivitet og en reduceret aldosteronsekretion.
Inhibition of ACE results in decreased concentrations of angiotensin II which results in decreased vasopressor activity and reduced aldosterone secretion.
Det sidst nævnte kan endvidere medføre en forhøjelse af serum - kaliumkoncentrationen.
The latter decrease may result in an increase in serum potassium concentration.
Selv om lisinopril primært menes at sænke blodtrykket via en suppression af renin- angiotension - aldosteron systemet, er det vist, at lisinopril også har en antihypertensiv effekt hos patienter med lav - renin hypertension.
Whilst the mechanism through which lisinopril lowers blood pressure is believed to be primarily suppression of the renin-angiotensin-aldosterone system, lisinopril is antihypertensive even in patients with low renin hypertension.
ACE er identisk med kininase II, et enzym, der nedbryder bradykinin.
ACE is identical to kininase II, an enzyme that degrades bradykinin.
Bradykinin er et potentielt vasodepressivt peptid, og hvorvidt det forhøjede bradykinin- niveau spiller en rolle for lisinoprils terapeutiske effekt er endnu ikke kla rlagt.
Whether increased levels of bradykinin, a potent vasodilatory peptide, play a role in the therapeutic effects of lisinopril remains to be elucidated.
Zestrils effekt på mortalitet og morbiditet ved hjerteinsufficiens er undersøgt ved at sammenligne en høj dosis (32, 5 mg eller 35 mg en gang dagligt) med en lav dosis (2, 5 mg eller 5 mg en gang dagligt).
The effect of Zestril on mortality and morbidity in heart failure has been studied by comparing a high dose (32.5 mg or 35 mg once daily) with a low dose (2.5 mg or 5 mg once daily).
Høj dosis i forhold til lav dosis reducerede risikoen med 8% i ’ alle typer af mortalitet ’ og ’ kardiovaskulær hospitalsindlæggelse ’ (p=0, 036).
In a study of 3164 patients, with a median follow up period of 46 months for surviving patients, high dose Zestril produced a 12% risk reduction in the combined endpoint of all-cause mortality and all-cause hospitalisation (p = 0.002) and an 8% risk reduction in all-cause mortality and cardiovascular hospitalisation (p = 0.036) compared with low dose.
Der sås en reduktion af risikoen for ’ alle typer af mortalitet ’ (8%; p=0, 128) og ’ kardiovaskulær mortalitet ’ (10%; p=0, 073).
Risk reductions for all-cause mortality (8%; p = 0.128) and cardiovascular mortality (10%; p = 0.073) were observed.
Post- hoc analyser viste, at antallet af hospitalsindlæggelser for hjerteinsufficiens blev reduceret med 24% (p=0, 002) hos patienter i behandling med høj- dosis Zestril sammenlignet med lav dosis.
In a post-hoc analysis, the number of hospitalisations for heart failure was reduced by 24% (p=0.002) in patients treated with high-dose Zestril compared with low dose.
De symptomatiske fordele ved behandlin g med høj og lav dosis af Zestril var sammenlignelige.
Symptomatic benefits were similar in patients treated with high and low doses of Zestril.
Studiets resultater viste, at de overordnede bivirkningsprofiler hos patienter i behandling med høj eller lav dosis af Zestril var sammenlignelige i både art og antal.
The results of the study showed that the overall adverse event profiles for patients treated with high or low dose Zestril were similar in both nature and number.
Forudsigelige hændelser som følge af ACE- hæmning såsom hypotension eller ændret nyrefunktion var håndterbare og medførte sjældent tilbagetrækning fra behandlingen.
Predictable events resulting from ACE inhibition, such as hypotension or altered renal function, were manageable and rarely led to treatment withdrawal.
Hoste sås mindre hyppigt hos patienter i behandling med høj dosis Zestril i forhold til lav dosis.
Cough was less frequent in patients treated with high dose Zestril compared with low dose.
Forsøget omfattede 19, 394 patienter, som fik behandlingen i 6 uger indenfor 24 timer efter et akut myokardieinfarkt.
In the GISSI-3 trial, which used a 2x2 factorial design to compare the effects of Zestril and glyceryl trinitrate given alone or in combination for 6 weeks versus control in 19,394, patients who were administered the treatment within 24 hours of an acute myocardial infarction, Zestril produced a statistically significant risk reduction in mortality of 11% versus control (2p=0.03).
I gruppen der fik Zestril alene,
The risk reduction
CPMP/ 423/ 04 sås en signifikant risikonedsættelse af mortalitet
CPMP/423/04
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©EMEA 2004 0, 03).
©EMEA 2004
Men ved Zestril og Glyceryl trinitrat kombineret sås derimod en signifikant risikonedsættelse af mortalitet med 17% i forhold til kontrolgruppen (2p=0, 02).
with glyceryl trinitrate was not significant but the combination of Zestril and glyceryl trinitrate produced a significant risk reduction in mortality of 17% versus control (2p=0.02).
Hos en subgruppe af ældre (alder > 70 år) og kvinder, prædefineret som patienter med en høj mortalitetsrisiko, sås en signifikant fordel ved det kombinerede endepunkt mortalitet og hjertefunktion.
In the sub-groups of elderly (age > 70 years) and females, pre-defined as patients at high risk of mortality, significant benefit was observed for a combined endpoint of mortality and cardiac function.
Det kombinerede endepunkt for alle patienter, inklusiv højrisiko patienter, efter 6 måneder viste også en signifikant fordel for de der var blevet behandlet i 6 uger med Zestril eller Zestril + glyceryl trinitrat kombineret, hvilket er et tegn på at Zestril har en forebyggende effekt.
The combined endpoint for all patients, as well as the high-risk sub-groups, at 6 months also showed significant benefit for those treated with Zestril or Zestril plus glyceryl trinitrate for 6 weeks, indicating a prevention effect for Zestril.
Som det kan forventes med enhver vasodilator behandling, sås en øget hyppighed af hypotension og nedsat nyrefunktion i forbindelse med Zestril behandling, men medførte ikke en proportione l stigning i mortalitet.
As would be expected from any vasodilator treatment, increased incidences of hypotension and renal dysfunction were associated with Zestril treatment but these were not associated with a proportional increase in mortality.
I et dobbelt blindt, randomiseret, multicenter forsøg hvor Zestril blev sammenlignet med en calcium kanal hæmmer i 335 hypertensive type 2 diabetikere med begyndende nefropati k
In a double-blind, randomised, multicentre trial which compared Zestril with a calcium channel blocker in 335 hypertensive Type 2 diabetes mellitus subjects with incipient nephropathy characterised by microalbuminuria, Zestril 10 mg to 20 mg administered once daily for 12 months, reduced systolic/diastolic blood pressure by 13/10 mmHg and urinary albumin excretion rate by 40%.
Sammenlignet med calcium kanal hæmmeren, som gav en blodtrykssænkning i samme størrelsesorden, sås et signifikant større fald i urinalbuminudskillelseshastighed for Zestril, hvilket giver evidens for at Zestrils ACE - hæmmende effekt reducerede mikroalbuminuri ved en direkte effekt på nyrevævet ud over dets blodsænkende effekt.
When compared with the calcium channel blocker, which produced a similar reduction in blood pressure, those treated with Zestril showed a significantly greater reduction in urinary albumin excretion rate, providing evidence that the ACE inhibitory action of Zestril reduced microalbuminuria by a direct mechanism on renal tissues in addition to its blood pressure lowering effect.
Lisinopril behandling indvirker ikke på den glycæmiske kontrol hvilket kan ses på den manglende effekt på niveauet af glukosyleret hæmoglobin (HbAlc).
Lisinopril treatment does not affect glycaemic control as shown by a lack of significant effect on levels of glycated haemoglobin (HbA 1c).
Lisinopril er en peroralt aktiv ACE- hæmmer som ikke indeholder sulphydryl.
5.2 Pharmacokinetic properties Lisinopril is an orally active non-sulphydryl-containing ACE inhibitor.
AMI patienter har dog udvist en tendens til lidt længere tid til peak plasmakoncentration.
Absorption Following oral administration of lisinopril, peak serum concentrations occur within about 7 hours, although there was a trend to a small delay in time taken to reach peak serum concentrations in acute myocardial infarction patients.
Urinudskillelsesmålinger viser at middel absorptionsfraktionen af lisinopril er cirka 25%, med en variation imellem patienter på 6- 60% i dosis intervallet 5- 80 mg..
Based on urinary recovery, the mean extent of absorption of lisinopril is approximately 25% with inter-patient variability of 6-60% over the dose range studied (5-80 mg).
Den absolute biotilgængelighed hos patienter med hjerteinsufficiens er omkring 16% lavere.
The absolute bioavailability is reduced approximately 16% in patients with heart failure.
Lisinoprilabsorptionen påvirkes ikke af føde.
Lisinopril absorption is not affected by the presence of food.
Fordeling Lisinopril synes ikke at bindes til andre serumproteiner end circulerende angiotensin konverterende enzym (ACE).
Distribution Lisinopril does not appear to be bound to serum proteins other than to circulating angiotensin converting enzyme (ACE).
Forsøg med rotter har vist, at lisinopril passerer blod- hjerne- barrieren i ringe omfang.
Studies in rats indicate that lisinopril crosses the blood-brain barrier poorly.
Eliminering Lisinopril metaboliseres ikke og udskilles fuldstændigt og uforandret i urinen.
Elimination Lisinopril does not undergo metabolism and is excreted entirely unchanged into the urine.
Ved gentagen dosering har lisinopril en effektiv halveringstid på 12, 6 timer.
On multiple dosing lisinopril has an effective half-life of accumulation of 12.6 hours.
Lisinopril clearance hos raske individer er på omkring 50 ml/ min.
The clearance of lisinopril in healthy subjects is approximately 50 ml/min.
Faldende serumkoncentrationer udviser en forlænget terminal fase, der ikke bidrager til lægemiddel akkumulering.
Declining serum concentrations exhibit a prolonged terminal phase, which does not contribute to drug accumulation.
Denne terminale fase repræsenterer sandsynligvis en mættet binding til ACE og er ikke proportional med dosis.
This terminal phase probably represents saturable binding to ACE and is not proportional to dose.
Nedsat leverfunktion Ved nedsat leverfunktion i forbindelse med levercirrose sås nedsat lisinopril absorption (omkring 30% bestemt ud fra urin udskillelsen) men en øget eksponering (omkring 50%) sammenlignet med raske individer på grund af nedsat clearance.
Hepatic impairment Impairment of hepatic function in cirrhotic patients resulted in a decrease in lisinopril absorption (about 30% as determined by urinary recovery) but an increase in exposure (approximately 50%) compared to healthy subjects due to decreased clearance.
Dette bliver dog kun klinisk vigtigt, når den glomerulære filtrationshastighed er lavere end 30 ml/ min.
Renal impairment Impaired renal function decreases elimination of lisinopril, which is excreted via the kidneys, but this decrease becomes clinically important only when the glomerular filtration rate is below 30 ml/min.
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Lisinopril kan fjernes ved dialyse.
Lisinopril can be removed by dialysis.
Under 4 timers hæmodialyse, faldt plasma lisinopril koncentration med 60% i gennemsnit, med en dialyse clearance på mellem 40 til 55 ml/ min.
During 4 hours of haemodialysis, plasma lisinopril concentrations decreased on average by 60%, with a dialysis clearance between 40 and 55 ml/min.
Hjerteinsufficiens Patienter med hjerteinsufficiens har en større lisinopril eksponering sammenlignet med raske individer (en stigning i AUC på 125% i gennemsnit), men baseret på urin udskillelsen af lis inopril, nedsættes absorptionen med 16% i sammenligning med raske individer.
Heart failure Patients with heart failure have a greater exposure of lisinopril when compared to healthy subjects (an increase in AUC on average of 125%), but based on the urinary recovery of lisinopril, there is reduced absorption of approximately 16% compared to healthy subjects.
Ældre Ældre patienter har højere blod- værdier og højere AUC- værdier end unge patienter (stigning på omkring 60%).
Elderly Older patients have higher blood levels and higher values for the area under the plasma concentration time curve (increased approximately 60%) compared with younger subjects.
Prækliniske data viser ingen specielle risici for mennesker baseret på konventionelle generelle farmakologi forsøg, gentaget dosis toksicitet, gentoksicitet og det karcinogene potentiale.
5.3 Preclinical safety data Preclinical data reveal no special hazard for humans based on conventional studies of general pharmacolo gy, repeated dose toxicity, genotoxicity, and carcinogenic potential.
Som klasse er det vist at ACE- hæmmere kan inducere bivirkninger under den sene fosterudvikling, førende til fosterdød og medfødte misdannelser, med speciel indvirkning på kraniet.
Angiotensin converting enzyme inhibitors, as a class, have been shown to induce adverse effects on the late foetal development, resulting in foetal death and congenital effects, in particular affecting the skull.
Fostertoksicitet, interuterin vækstretardering samt patent ductus arteriosus er set.
Foetotoxicity, intrauterine growth retardation and patent ductus arteriosus have also been reported.
Det anses at udviklingsanomalier skyldes ACE - hæmmernes direkte påvirkning af fosterets renin- angiotensin system samt delvis på grund af iskæmi som følge af moderens hypotension og nedsat blodgennemstrømning mellem foster og placenta og levering af ilt og næring til fosteret.
These developmental anomalies are thought to be partly due to a direct action of ACE inhibitors on the foetal renin-angiotensin system and partly due to ischaemia resulting from maternal hypotension and decreases in foetal-placental blood flow and oxygen/nutrients delivery to the foetus.
6. 1 Fortegnelse over hjælpestoffer
[To be implemented nationally]
Mannitol.
6.2 Incompatibilities
Calciumhydrogenphosphat.
[To be implemented nationally]
Magnesiumstearat.
6.3 Shelf life
6. 2 Uforligeligheder
[To be implemented nationally]
Ingen kendte
6.4 Special precautions for storage
6. 3 Opbevaringstid
[To be implemented nationally]
4 år.
6.5 Nature and contents of container
6. 4 Særlige opbevaringsforhold
[To be implemented nationally]
Opbevares under 30°C.
6.6 Instructions for use and handling
6. 5 Emballage (art og indhold)
[To be implemented nationally]
HDPE pakninger (60 og 100).
MARKETING AUTHORISATION NUMBER
CPMP/ 423/ 04 AL/ PVC blisterpakning Aluminium PVC/ PVDC blisterpakning Polypropylen rør
CPMP/423/04
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41/42
INDEHAVER AF MARKEDSFØRINGSTILLADELSEN
DATE OF FIRST AUTHORISATION/RENEWAL OF AUTHORISATION
REVISION AF PRODUKTRESUMÉ
DATE OF (PARTIAL) REVISION OF THE TEXT
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FORTEGNELSE OVER LÆGEMIDLERNES NAVNE, LÆGEMIDDELFORMER, STYRKER, INDGIVELSESVEJ, INDEHAVERE AF MARKEDSFØRINGSTILLADELSE, EMBALLAGE OG PAKNINGSSTØRRELSER I MEDLEMSSTATERNE
LIST OF THE NAMES, PHARMACEUTICAL FORM, STRENGTHS OF THE MEDICINAL PRODUCTS, ROUTE OF ADMINISTRATION, MARKETING AUTHORISATION HOLDERS IN THE MEMBER STATES
CPMP/ 459/ 04
CPMP/ 459/ 04
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Medlemsstat
Marketing Authorisation Holder
Addresse
Invented name
Donau- City Strasse 6 1220 - Wien, Austria
Donau-City Strasse 6 1220 - Wien, Austria
ZOCORD
ZOCORD
Filmovertrukket tabletter
film coated tablets
Tabletter
film coated tablets
Succursale belge Chaussée de Waterloo 1135 1180 Bruxelles Belgique
Succursale belge Chaussée de Waterloo 1135 1180 Bruxelles Belgique
ZOCOR
ZOCOR
2/ 39 Styrke
2/ 46
Indgivelsesvej
Merck Sharp & Dohme B. V.
5 mg
80 mg
Filmovertrukket tabletter
tablets
Box 581 2003PC Haarlem, The Netherlands
Box 581 2003PC Haarlem, The Netherlands
3/ 39 Styrke
4/ 46
Lægemiddel- form
Marketing Authorisation Holder
Danmark
Strength
Merck Sharp & Dohme B. V.
Pharmaceutical Form
Filmovertrukket tabletter
Route of administration
Box 581 2003 PC Haarlem, The Netherlands
Box 581 2003 PC Haarlem, The Netherlands
Oy Leiras Finland Ab Yliopistonkatu 34 A 20100 Turku, Finland
Oy Leiras Finland Ab Yliopistonkatu 34 A 20100 Turku, Finland
COROLIN
COROLIN
4/ 39 Styrke
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Addresse
Pharmaceutical Form
Laboratoires Merck Sharp & Dohme Chibret 3, Avenue Hoche 75008 Paris, France
Laboratoires Merck Sharp & Dohme Chibret 3, Avenue Hoche 75008 Paris, France
Laboratoires SANOFI- SYNTHELABO FRANCE 174, Avenue de France 75013 Paris, France
Laboratoires SANOFI-SYNTHELABO FRANCE 174, Avenue de France 75013 Paris, France
LODALES
LODALES
Styrke
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2004
 EMEA 2004
Dieckmann Arzneimittel GmBH Lindenplatz 1 85540 Haar, Germany
Dieckmann Arzneimittel GmBH Lindenplatz 1 85540 Haar, Germany
ZOCOR FORTE
ZOCOR FORTE
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8/ 46
Særnavn
Germany
Lægemiddel- form
ZOCOR FORTE XL 80
Indgivelsesvej
film coated tablets
MSD Sharp & Dohme GmbH Lindenplatz 1 85540 Haar, Germany
MSD Sharp & Dohme GmbH Lindenplatz 1 85540 Haar, Germany
LIPOCARD
LIPOCARD
ZEMOX
ZEMOX
Boehringer Ingelheim Pharma KG Binger Strasse 173 55216 Ingelheim am Rhein, Germany
Boehringer Ingelheim Pharma KG Binger Strasse 173 55216 Ingelheim am Rhein, Germany
DENAN
DENAN
Marketing Authorization Holder Merck & Co., INC Whitehouse Station, N. J.
Marketing Authorization Holder Merck & Co., INC Whitehouse Station, N. J.
Tatoioy Street P. O.
Tatoioy Street P. O.
Box 52894 146 10N.
Box 52894 146 10N.
Erithrea, Greece
Erithrea, Greece
Addresse
Greece
9/ 39 Styrke
11/ 46
Lægemiddel- form
oral use
Indgivelsesvej
Ireland
Medlemsstat
tablets
Addresse
oral use
Merck Sharp & Dohme Limited Hertford Road, Hoddesdon Herts EN11 9BU United Kingdom
Merck Sharp & Dohme Limited Hertford Road, Hoddesdon Herts EN11 9BU United Kingdom
Merck Sharp & Dohme (Italia) SpA.
Merck Sharp & Dohme (Italia) SpA.
Fabbroni 6 00191 Rome, Italy
Fabbroni 6 00191 Rome, Italy
SINVACOR
SINVACOR
Istituto Gentili SpA.
Istituto Gentili SpA.
Via Mazzini 112 56125 Pisa, Italy
Via Mazzini 112 56125 Pisa, Italy
LIPONORM
LIPONORM
Sigma Tau SpA Via Pontina Km 30, 400 Pomezia (Rome) Italy
Sigma Tau SpA Via Pontina Km 30, 400 Pomezia (Rome) Italy
SIVASTIN
SIVASTIN
Mediolanum SpA Via S. G.
Mediolanum SpA Via S. G.
Cottolengo 15 20143 Milano, Italy
Cottolengo 15 20143 Milano, Italy
MEDIPO
MEDIPO
Succursale belge Chaussée de Waterloo 1135 1180 Bruxelles/ Brussel, Belgique
Succursale belge Chaussée de Waterloo 1135 1180 Bruxelles/ Brussel, Belgique
80 mg
40 mg
P. O.
40 mg
Box 581 2003 PC Haarlem, The Netherlands
Merck Sharp & Dohme B. V.
12/ 39 Styrke
15/ 46
BOZARA
BOZARA
Norge
ZOCOR
13/ 39 Styrke
17/ 46
20 mg
40 mg
Merck Sharp & Dohme, Lda, Quinta da Fonte Edifício Vasco da Gama, 19 P. O.
Merck Sharp & Dohme, Lda, Quinta da Fonte Edifício Vasco da Gama, 19 P. O.
Box 214 Porto Salvo 2780- 730 Paço de Arcos, Portugal
Box 214 Porto Salvo 2780-730 Paço de Arcos, Portugal
Filmovertrukket tabletter
film-coated tablets
14/ 39 Styrke
18/ 46
Medlemsstat
Invented name
Lægemiddel- form
administration
Indgivelsesvej
Member State
Laboratórios Químico- Farmacêuticos Chibret, Lda.
Laboratórios Químico-Farmacêuticos Chibret, Lda.
Quinta da Fonte Edifício Vasco da Gama, 19 P. O.
Quinta da Fonte Edifício Vasco da Gama, 19 P. O.
Box 216 Porto Salvo P- 2780- 730 Paço de Arcos, Portugal
Box 216 Porto Salvo P-2780-730 Paço de Arcos, Portugal
VACOLEST
VACOLEST
Merck Sharp & Dohme de España SA C/ Josefa Valcárcel, 38 28027 Madrid, Spain
Merck Sharp & Dohme de España SA C/ Josefa Valcárcel, 38 28027 Madrid, Spain
ZOCO
ZOCO
LACER, SA Sardenya, 350 080254 Barcelona, Spain
LACER, SA Sardenya, 350 080254 Barcelona, Spain
PANTOK
PANTOK
15/ 39 Styrke
19/ 46
Indgivelsesvej
film-coated tablets
Uriach & Cia SA Avda Camí Reial, 51- 57 08184 Palau- solitá I Plegamans - Barcelona, Spain
Uriach & Cia SA Avda Camí Reial, 51-57 08184 Palau-solitá I Plegamans- Barcelona, Spain
COLEMIN
COLEMIN
Sverige
oral use
16/ 39 Styrke
21/ 46
Merck Sharp & Dohme Limited Hertford Road Hoddesdon Herts EN11 9BU United Kingdom
Merck Sharp & Dohme Limited Hertford Road Hoddesdon Herts EN11 9BU United Kingdom
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23/ 46
FAGLIGE KONKLUSIONER OG BEGRUNDELSER FOR ÆNDRINGEN AF PRODUKTRESUMEET FREMLAGT AF EMEA
SCIENTIFIC CONCLUSIONS AND GROUNDS FOR AMENDMENT OF THE SUMMARIES OF PRODUCT CHARACTERISTICS PRESENTED BY THE EMEA
CPMP/ 459/ 04 FAGLIGE KONKLUSIONER
CPMP/ 459/ 04 SCIENTIFIC CONCLUSIONS
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EMEA 2004
@EMEA 2004
SAMLET RESUME AF DEN FAGLIGE VURDERING AF ZOCORD OG TILKNYTTEDE NAVNE (se bilag I)
OVERALL SUMMARY OF THE SCIENTIFIC EVALUATION OF ZOCORD AND ASSOCIATED NAMES (see Annex I)
Terapeutiske indikationer
Section 4.1 Therapeutic Indications
Indehaveren af markedsføringstilladelsen blev anmodet om at foreslå og videnskabeligt dokumentere en fælles fremgangsmåde for hele EU, da der var forskelle mellem de enkelte landes godkendelser af brugen af Zocord i forbindelse med:
The MAH was requested to propose and scientifically justify a common EU wide approach as there were divergences between national approvals regarding the use of Zocord in:
Sekundær forebyggelse af kardiovaskulære hændelser er blevet godkendt i alle medlemsstater, Island og Norge.
Secondary prevention of cardiovascular events has been approved in all Member States, Iceland and Norway.
Imidlertid er ordvalget (og dermed den præcise betydning) af teksten til indikationen meget forskellig fra land til land.
However, the wording (and therefore the precise meaning) of the indication is very different from country to country.
Primær hyperkolesterolæmi (Fredrickson, type IIa og IIb) er blevet godkendt i alle medlemsstater, Island og Norge.
Primary hypercholesterolemia (Fredrickson´s type’ s IIa and IIb) has been approved in all Member States, Iceland and Norway.
Imidlertid er ordvalget (og dermed den præcise betydning) af teksten til indikationen meget forskellig i de nationalt godkendte produktresumeer.
However, the wording (and therefore the precise meaning) of the indication is very different in the nationally approved SPCs.
Dysbetalipoproteinæmi (Fredrickson, type III) er kun blevet godkendt i nogle medlemsstater.
Dysbetalipoproteinemia (Fredrickson’ s type III) has only been granted in some Member States.
Hypertriglyceridæmi (Fredrickson, type IV) er kun blevet godkendt i nogle medlemsstater.
Hypertriglyceridemia (Fredrickson’ s type’ s IV) has only been granted in some Member States.
Homozygot familiær hyperkolesterolæmi er blevet godkendt som “ supplement til diæt og andre ikke - diætmæssige foranstaltninger, når disse foranstaltninger har været utilstrækkelige ” i nogle medlemsstater, og i andre er det blevet godkendt som “ supplement til diæt og andre ikke- diætmæssige foranstaltninger, når diætmæssige og andre ikke- farmakologiske foranstaltninger har været utilstrækkelige ”.
Homozygous familial hypercholesterolemia has been granted as “ an adjunct to diet and other non- dietary measures when those measures have been inadequate” in some Member States and in others it has been granted as “ an adjunct to diet and other non-dietary measures when diet and other non- pharmacological measures have been inadequate”.
• Behandling af primær hyperkolesterolæmi eller kombineret dyslipidæmi, behandling af homozygot familiær hyperkolesterolæmi.
• Treatment of primary hypercholesterolaemia or mixed dyslipidaemia, treatment of homozygous familial hypercholesterolaemia.
Simvastatin har vist sig at reducere både normale og forhøjede low- density lipoprotein - (LDL) kolesterolkoncentrationer.
Simvastatin has been shown to reduce both normal and elevated low-density lipoproteins (LDL) cholesterol concentrations.
LDL dannes fra very- low- density lipoprotein (VLDL) og kataboliseres primært ved hjælp af LDL- receptorer med høj affinitet.
LDL are formed from very-low-density protein (VLDL) and are catabolised predominantly by the high affinity LDL receptor.
Den LDL- reducerende effekt af simvastatin kan involvere både reduktion af VLDL- kolesterolkoncentration og induktion af LDL- receptoren, medførende reduceret produktion og øget katabolisme af LDL- kolesterol.
The mechanism of the LDL-lowering effect of simvastatin may involve both reduction of VLDL cholesterol concentration and induction of the LDL receptor, leading to reduced production and increased catabolism of LDL cholesterol.