natgillin/translations-raw huggingface dataset:
Ifølge dets metabolisme forekommer metaboliske interaktioner med andre lægemidler højst sandsynligt ikke, selvom rivastigmin kan hæmme den butyrylkolinesterase- medierede metabolisme af andre stoffer.
According to its metabolism, metabolic interactions with other medicinal products appear unlikely, although rivastigmine may inhibit the butyrylcholinesterase mediated metabolism of other substances.
Der blev ikke observeret effekt på fertiliteten eller fosterudviklingen hos rotter og kaniner undtaget doser, der medførte maternel toksicitet.
No effects on fertility or embryofoetal development were observed in rats and rabbits, except at doses related to maternal toxicity.
I peri - / postnatale undersøgelser på rotter blev der observeret forlænget drægtighedsperiode.
In peri/ postnatal studies in rats, an increased gestation time was observed.
59 Rivastigmin udskilles i mælken hos dyr.
In animals, rivastigmine is excreted into milk.
4. 7 Virkning på evnen til at føre motorkøretøj eller betjene maskiner
59 4.7 Effects on ability to drive and use machines
Alzheimers sygdom kan medføre en gradvis forringelse af køreegenskaberne eller nedsætte evnen til at betjene maskiner.
Alzheimer’ s disease may cause gradual impairment of driving performance or compromise the ability to use machinery.
Som følge heraf har rivastigmin en mild eller moderat indvirkning på evnen til at føre motorkøretøj eller betjene maskiner.
As a consequence, rivastigmine has minor or moderate influence on the ability to drive and use machines.
46, 0% af patienterne på placebo rapporterede bivirkninger).
The overall incidence of adverse events (AEs) in patients treated with Exelon 9.5 mg/ 24 h transdermal patches was lower than the rate in patients who received 3 to 12 mg/ day Exelon capsule treatment (50.5% with Exelon 9.5 mg/ 24 h transdermal patches vs 63.3% with Exelon capsules; 46.0% of patients on placebo reported AEs).
5, 0% og 3, 3% af patienterne på placebo rapporterede henholdsvis kvalme og opkastning).
Gastrointestinal adverse reactions, including nausea and vomiting, were the most common adverse reactions in patients who received active treatment, and occurred at a substantially lower rate in the Exelon 9.5 mg/ 24 h transdermal patch group compared to the Exelon capsule group (7.2% vs 23.1% for nausea and 6.2% vs 17.0% for vomiting; 5.0% and 3.3% of patients on placebo reported nausea and vomiting, respectively).
Tabel 1 viser de bivirkninger (bivirkninger, som med rimelighed må antages at være forårsaget af præparatet), som blev rapporteret hos 291 patienter med Alzheimers demens behandlet med Exelon depotplastre ved måldosen 9, 5 mg/ 24 timer (4, 6 mg/ 24 timer titreret til 9, 5 mg/ 24 timer) i et specifikt 24- ugers, dobbeltblindet, placebo - og aktivkontrolleret klinisk studie.
Table 1 displays the adverse reactions (events reasonably believed to be causally related to the medicinal product) reported in 291 patients with Alzheimer’ s dementia treated in a specific 24-week double-blind, placebo and active-controlled clinical study with Exelon transdermal patches at target dose of 9.5 mg/ 24 h (4.6 mg/ 24 h titrated to 9.5 mg/ 24 h).
Bivirkningerne er ordnet under frekvenskategorier, den mest almindelige først ved at anvende følgende frekvensberegninger:
Adverse reactions are ranked under headings of frequency, the most frequent first, using the following convention:
Meget almindelig (≥1/ 10), almindelig (≥1/ 100 til, < 1/ 10), ikke almindelig (≥1/ 1. 000 til, < 1/ 100), sjælden (≥1/ 10. 000 til, < 1/ 1. 000), meget sjælden (< 1/ 10. 000).
Very common (≥ 1/ 10); common (≥ 1/ 100, < 1/ 10); uncommon (≥ 1/ 1,000, < 1/ 100); rare (≥ 1/ 10,000, < 1/ 1,000); very rare (< 1/ 10,000).
Metabolisme og ernæringsforstyrrelser
Metabolism and nutrition disorders
Angst, depression, delirium
Anxiety, depression, delirium
Hovedpine, synkope Ekstrapyramidale symptomer
Headache, syncope Extrapyramidal symptoms
Kvalme, opkastning, diarré, dyspepsi, mavesmerter Mavesår
Nausea, vomiting, diarrhoea, dyspepsia, abdominal pain Gastric ulcer
60 Almene symptomer og reaktioner på administrationsstedet
General disorders and administration site conditions
Hudreaktioner på administrationsstedet (f. eks. erytem på administrationsstedet, kløe ved administrationsstedet, ødem ved administrationsstedet, dermatitis på administrationsstedet, irritation ved administrationsstedet), asteniske lidelser (f. eks. træthed, asteni), pyreksi, vægttab
Application site skin reactions (e. g. application site erythema, application site pruritus, application site oedema, application site dermatitis, application site irritation), asthenic conditions (e. g. fatigue, asthenia), pyrexia, weight decreased
Når der blev anvendt højere doser end 9, 5 mg/ 24 timer i ovennævnte studie, blev der observeret svimmelhed, søvnløshed, agitation, nedsat appetit, atrieflimren og hjertesvigt oftere end med 9, 5 mg/ 24 timer eller placebo.
When doses higher than 9.5 mg/ 24 h were used in the above-mentioned study, dizziness, insomnia, agitation, decreased appetite, atrial fibrillation and cardiac failure were observed more frequently than
Det tyder på en dosis- effekt- sammenhæng.
60 with 9.5 mg/ 24 h or placebo, suggesting a dose effect relationship.
Disse bivirkninger forekom dog ikke med en højere frekvens for Exelon 9, 5 mg/ 24 timer end for placebo.
However, these events did not occur at a higher frequency with Exelon 9.5 mg/ 24 h transdermal patches than with placebo.
Følgende bivirkninger er kun observeret med Exelon- kapsler og oral opløsning og ikke i kliniske studier med Exelon 9, 5 mg/ 24 timer:
The following adverse reactions have only been observed with Exelon capsules and oral solution and not in clinical studies with Exelon 9.5 mg/ 24 h transdermal patches:
Svimmelhed (meget almindelig), agitation, somnolens, utilpashed, tremor, konfusion, øget perspiration (almindelig), søvnløshed, fald ved uheld, forhøjet leverfunktionstest (ikke almindelig), krampeanfald, sår på tolvfingertarmen, angina pectoris (sjælden), hjertearytmier (f. eks. atrio- ventrikulært blok, atriefimren og tachykardi), hypertension, pankreatitis, gastrointestinal blødning, hallucinationer (meget sjælden), og nogle tilfælde af svære opkastninger blev associeret med øsofagusruptur (ukendt).
Dizziness (very common); agitation, somnolence, malaise, tremor, confusion, sweating increased (common); insomnia, accidental fall, elevated liver function tests (uncommon); seizures, duodenal ulcers, angina pectoris (rare); cardiac arrhythmia (e. g. atrio-ventricular block, atrial fibrillation and tachycardia), hypertension, pancreatitis, gastrointestinal haemorrhage, hallucination (very rare); and some cases of severe vomiting were associated with oesophageal rupture (unknown).
Hudirritation I kliniske forsøg blev hudreaktionerne ved hvert besøg målt i forhold til en hudirritationsskala, som målte graden af erytem, ødem, afskalning, fissurer, kløe og smerte/ svie/ brænden på administrationsstedet.
Skin irritation In clinical trials, skin reactions were measured at each visit using a skin irritation rating scale that rated the degree of erythema, oedema, scaling, fissures, pruritus and pain/ stinging/ burning at the application site.
I et 24- ugers dobbeltblindet studie var de mest almindeligt observerede symptomer (hudirritationsskalaen) med Exelon 9, 5 mg/ 24 timer depotplastre meget let (21, 8%), mildt (12, 5%) eller moderat (6, 5%) erytem eller meget let (11, 9%), mild (7, 3%) eller moderat (5, 0%) kløe.
In a 24-week double-blind study, the most commonly observed symptoms (skin irritation rating scale) with Exelon 9.5 mg/ 24 h transdermal patches were very slight (21.8%), mild (12.5%) or moderate (6.5%) erythema or very slight (11.9%), mild (7.3%) or moderate (5.0%) pruritus.
De mest almindeligt observerede svære symptomer med Exelon 9, 5 mg/ 24 timer depotplastre var kløe (1, 7%) og erytem (1, 1%).
The most commonly observed severe symptoms with Exelon 9.5 mg/ 24 h transdermal patches were pruritus (1.7%) and erythema (1.1%).
De fleste hudreaktioner var begrænset til administrationsstedet og resulterede kun i afbrydelse hos 2, 4% af patienterne i Exelon 9, 5 mg/ 24 timer depotplastre- behandlingsgruppen.
Most skin reactions were limited to the application site and resulted in discontinuation in only 2.4% of the patients in the Exelon 9.5 mg/ 24 h transdermal patch group.
Symptomer De fleste tilfælde af tilfældig overdosering med oral rivastigmin har ikke været forbundet med kliniske tegn eller symptomer, og næsten alle de pågældende patienter fortsatte behandlingen med rivastigmin.
Symptoms Most cases of accidental overdose of oral rivastigmine have not been associated with any clinical signs or symptoms and almost all of the patients concerned continued rivastigmine treatment.
Efter traditionel behandling kom patienten sig fuldstændigt inden for 24 timer.
Ingestion of 46 mg of oral rivastigmine occurred in one case; following conservative management the patient fully recovered within 24 hours.
Der er på nuværende tidspunkt ingen data om overdosering med Exelon depotplastre.
There are currently no data on overdose with Exelon transdermal patches.
9 timer, anbefales det i tilfælde af asymptomatisk overdosering, at alle Exelon depotplastre straks fjernes, og at der ikke påføres nye depotplastre inden for de næste 24 timer.
Treatment As rivastigmine has a plasma half-life of about 3.4 hours and a duration of acetylcholinesterase inhibition of about 9 hours, it is recommended that in cases of asymptomatic overdose all Exelon transdermal patches should be removed immediately and no further transdermal patch should be applied for the next 24 hours.
En initialdosis på 0, 03 mg/ kg intravenøs atropinsulfat anbefales med efterfølgende doser afhængigt af klinisk respons.
An initial dose of 0.03 mg/ kg intravenous atropine sulphate is recommended, with subsequent doses based on clinical response.
Farmakoterapeutisk klassifikation: antikolinesteraser, ATC- kode:
Pharmacotherapeutic group: anticholinesterases, ATC code:
Rivastigmin er en acetyl - og butyrylkolinesterasehæmmer af carbamattypen, som menes at lette kolinerg neurotransmission ved at nedsætte nedbrydningen af acetylkolin, som er frigjort af funktionelt intakte kolinerge neuroner.
Thus, rivastigmine may have an ameliorative effect on
Følgelig har rivastigmin muligvis en forbedrende effekt på kolinergmedierede kognitive udfald ved demens, som er forbundet med Alzheimers sygdom.
61 cholinergic-mediated cognitive deficits in dementia associated with Alzheimer’ s disease.
Hos patienter med Alzheimers sygdom var rivastigmins hæmning af AChE i CSF dosisafhængig op til 6 mg, der blev indgivet to gange dagligt, som var den højeste dosis, der blev testet.
In patients with Alzheimer’ s disease, inhibition of AChE in CSF by oral rivastigmine was dose-dependent up to 6 mg given twice daily, the highest dose tested.
Rivastigmins hæmning af butyrylkolinesterase- aktivitet i CSF hos 14 patienter med Alzheimers var sammenlignelig med hæmningen af AChE.
Inhibition of butyrylcholinesterase activity in CSF of 14 Alzheimer patients treated by oral rivastigmine was similar to that of AChE.
Kliniske undersøgelser af Alzheimers demens Effekten af Exelon depotplastre hos patienter med Alzheimers demens er blevet påvist i et 24- ugers dobbeltblindet kernestudie og dets open label- forlængelsesfase.
Clinical studies in Alzheimer’ s dementia The efficacy of Exelon transdermal patches in patients with Alzheimer’ s dementia has been demonstrated in a 24-week double-blind core study and its open-label extension phase.
Patienterne i studiet havde en MMSE - score (Mini- Mental State Examination) på 10- 20.
Patients involved in this study had an MMSE (Mini-Mental State Examination) score of 10– 20.
Disse omfatter ADAS- Cog (en præstationsbaseret måling af kognition), ADCS- CGIC (en omfattende global vurdering af patienten, der dannes af den behandlende læge med input fra den omsorgsgivende person) og ADCS- ADL (den omsorgsgivende persons vurdering af dagligdagsaktiviteter herunder personlig hygiejne, fødeindtagelse, påklædning, husføring såsom indkøb, opretholdelse af evnen til at orientere sig i forhold til omgivelserne og involvere sig i økonomiske anliggender).
These include the ADAS-Cog (a performance-based measure of cognition) and the ADCS-CGIC (a comprehensive global assessment of the patient by the physician incorporating caregiver input), and the ADCS-ADL (a caregiver-rated assessment of the activities of daily living including personal hygiene, feeding, dressing, household chores such as shopping, retention of ability to orient oneself to surroundings as well as involvement in activities related to finances).
62 Tabel 2
Table 2
depotplastre 9, 5 mg/ 24 t
transdermal patches
kapsler 12 mg dagligt
capsules
ITT- LOCF- population ADAS- Cog
ITT-LOCF population ADAS-Cog
Gennemsnitsbaseline ± SD Gennemsnitsændring ved uge 24 ± SD
Mean baseline ± SD Mean change at week 24 ± SD p-value versus placebo ADCS-CGIC
27, 0 ± 10, 3 - 0, 6 ± 6, 4
27.0 ± 10.3 -0.6 ± 6.4 0.005*1
Gennemsnitsscore ± SD p- værdi versus placebo ADCS- ADL
Mean score ± SD p-value versus placebo ADCS-ADL
Gennemsnitsbaseline ± SD Gennemsnitsændring ved uge 24 ± SD
Mean baseline ± SD Mean change at week 24 ± SD p-value versus placebo * p≤ 0.05 versus placebo
49, 3 ± 15, 8 - 0, 5 ± 9, 5
50.1 ± 16.3 -0.1 ± 9.1 0.013*1
Last Observation Carried Forward 1 Baseret på ANCOVA med behandling og land som faktorer og baselineværdi som co- variant.
Last Observation Carried Forward 1 Based on ANCOVA with treatment and country as factors and baseline value as a covariate.
Negative ADAS- Cog- ændringer tyder på forbedring.
Negative ADAS-Cog changes indicate improvement.
Positive ADCS- ADL- ændringer tyder på forbedring.
Positive ADCS-ADL changes indicate improvement.
2 Baseret på CMH- testblokning (van Elteren- test) for land.
2 Based on CMH test (van Elteren test) blocking for country.
ADCS- CGIC- scorer < 4 tyder på forbedring.
ADCS-CGIC scores < 4 indicate improvement.
Resultaterne for patienter med klinisk relevant respons fra de 24 ugers studie er angivet i tabel 3.
The results for clinically relevant responders from the 24-week study are provided in Table 3.
Klinisk relevant forbedring var på forhånd defineret som mindst en 4- pointsforbedring på ADAS- Cog, ingen forværring på ADCS- CGIC og ingen forværring på ADCS- ADL.
Clinically relevant improvement was defined a priori as at least 4-point improvement on the ADAS- Cog, no worsening on the ADCS-CGIC, and no worsening on the ADCS-ADL.
Tabel 3
62 Table 3
Exelon kapsler
Exelon Exelon
12
9.5
mg dagligt N = 256
12 mg/ day
ITT- LOCF- population
ITT-LOCF population At least 4 points improvement on ADAS-Cog with no worsening on ADCS- CGIC and ADCS-ADL
N = 251
= 251 17.4
N = 282
= 282 10.5
Som antydet ved compartment- modellen viste 9, 5 mg/ 24 timer depotplastre eksponering tilsvarende den, der fås ved en oral dosis på 12 mg dagligt.
As suggested by compartmental modelling, 9.5 mg/ 24 h transdermal patches exhibited exposure similar to that provided by an oral dose of 12 mg/ day.
63 5. 2 Farmakokinetiske egenskaber
5.2 Pharmacokinetic properties
Absorption Rivastigmin fra Exelon depotplastre absorberes langsomt.
Absorption Absorption of rivastigmine from Exelon transdermal patches is slow.
Efter den første dosis observeres der påviselige plasmakoncentrationer efter et interval på 0, 5- 1 time.
After the first dose, detectable plasma concentrations are observed after a lag time of 0.5-1 hour.
Cmax nås efter 10- 16 timer.
Cmax is reached after 10-16 hours.
Efter at have nået den maksimale koncentration mindskes plasmakoncentrationen langsomt over den resterende del af 24- timers- behandlingsperioden.
After the peak, plasma concentrations slowly decrease over the remainder of the 24-hour period of application.
8 timer.
With multiple dosing (such as at steady state), after the previous transdermal patch is replaced with a new one, plasma concentrations initially decrease slowly for about 40 minutes on average, until absorption from the newly applied transdermal patch becomes faster than elimination, and plasma levels begin to rise again to reach a new peak at approximately 8 hours.
50% af de maksimale niveauer i modsætning til oral administration, hvor koncentrationerne falder næsten til nul mellem doserne.
At steady state, trough levels are approximately 50% of peak levels, in contrast to oral administration, with which concentrations fall off to virtually zero between doses.
Eksponeringen for rivastigmin (Cmax og AUC) steg overproportionalt med en faktor på 2, 6 ved skift fra 4, 6 mg/ 24 timer til 9, 5 mg/ 24 timer, hvilket er mindre udtalt end ved den orale formulering.
Although less pronounced than with the oral formulation, exposure to rivastigmine (Cmax and AUC) increased over-proportionally by a factor of 2.6 when escalating from 4.6 mg/ 24 h to 9.5 mg/ 24 h.
Fluktuationsindekset (FI), som er et mål for den relative forskel mellem højeste og laveste koncentration ((Cmax- Cmin) / Cavg), var 0, 58 for Exelon 4, 6 mg/ 24 timer depotplastre og 0, 77 for Exelon 9, 5 mg/ 24 timer depotplastre og viste dermed et mindre udsving mellem laveste og højeste koncentration end den orale formulering (FI = 3, 96 (6 mg dagligt) og 4, 15 (12 mg dagligt)).
The fluctuation index (FI), a measure of the relative difference between peak and trough concentrations((Cmax-Cmin)/ Cavg), was 0.58 for Exelon 4.6 mg/ 24 h transdermal patches and 0.77 for Exelon 9.5 mg/ 24 h transdermal patches, thus demonstrating a much smaller fluctuation between trough and peak concentrations than for the oral formulation (FI = 3.96 (6 mg/ day) and 4.15 (12 mg/ day)).
I forhold til plasmakoncentrationen over 24 timer, kan der ikke direkte sættes lighedstegn mellem dosen af rivastigmin frigivet fra depotplastret over 24 timer (mg/ 24 timer) og mængden (mg) rivastigmin en kapsel indeholder.
The dose of rivastigmine released from the transdermal patch over 24 hours (mg/ 24 h) cannot be directly equated to the amount (mg) of rivastigmine contained in a capsule with respect to plasma concentration produced over 24 hours.
Enkelt- dosis inter- patientvariationerne i rivastigmins farmakokinetiske parametre (normaliseret til dosis/ kg legemsvægt) var 43% (Cmax) og 49% (AUC0- 24h) efter transdermal administration mod henholdsvis 74% og 103% efter den orale formulering.
The single-dose inter-subject variability in rivastigmine pharmacokinetic parameters (normalised to dose/ kg bodyweight) was 43% (Cmax) and 49% (AUC0-24h) after transdermal administration versus 74% and 103%, respectively, after the oral form.
Inter- patientvariationerne i et steady state - studie af Alzheimers demens var højst 45% (Cmax) og 43% (AUC0- 24h) efter brug af depotplasteret, og henholdsvis 71% og 73% efter administration af den orale formulering.
The inter-patient variability in a steady-state study in Alzheimer’ s dementia was at most 45% (Cmax) and 43% (AUC0-24h) after use of the transdermal patch, and 71% and 73%, respectively, after administration of the oral form.
Der blev observeret en sammenhæng mellem eksponering for aktive stoffer ved steady state (rivastigmin og metabolit NAP226- 90) og legemsvægt hos patienter med Alzheimers demens.
A relationship between active substance exposure at steady state (rivastigmine and metabolite NAP226-90) and bodyweight was observed in Alzheimer’ s dementia patients.
4. 4).
The effect of bodyweight on active substance exposure suggests special attention to patients with very low body weight during up-titration (see section 4.4).
20- 30% lavere, når det blev påført maven eller låret.
63 Exposure (AUC ∞) to rivastigmine (and metabolite NAP266-90) was highest when the transdermal patch was applied to the upper back, chest, or upper arm and approximately 20– 30% lower when applied to the abdomen or thigh.
Dog var plasmaniveauerne på andendagen højere end på førstedagen ved behandling med depotplaster.
There was no relevant accumulation of rivastigmine or the metabolite NAP226-90 in plasma in patients with Alzheimer’ s disease, except that plasma levels were higher on the second day of transdermal patch therapy than on the first.
40%).
Distribution Rivastigmine is weakly bound to plasma proteins (approximately 40%).
Det krydser let blod- hjerne- barrieren og har et tilsyneladende fordelingsvolumen på 1, 8- 2, 7 l/ kg.
It readily crosses the blood-brain barrier and has an apparent volume of distribution in the range of 1.8-2.7 l/ kg.
3, 4 timer efter fjernelse af depotplasteret.
Metabolism Rivastigmine is rapidly and extensively metabolised with an apparent elimination half-life in plasma of approximately 3.4 hours after removal of the transdermal patch.
Eliminationen var absorptionshastighedsbegrænset (flip- flop - kinetik), hvilket forklarer den længere t½ efter depotplaster (3, 4 timer) mod oral eller intravenøs indgift (1, 4 til 1, 7 time).
Elimination was absorption rate limited (flip-flop kinetics), which explains the longer t½ after transdermal patch (3.4 h) versus oral or intravenous administrations (1.4 to 1.7 h).
Metaboliseringen sker primært via kolinesterasemedieret hydrolyse til metabolitten
Metabolism is primarily via cholinesterase-mediated hydrolysis to the metabolite NAP226-90.
In vitro viser metabolitten minimal hæmning af acetylkolinesterase (< 10%).
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase (< 10%).
In vitro - og dyreforsøg har vist, at de større cytokrome P450- isoenzymer spiller en minimal rolle i metaboliseringen af rivastigmin.
Based on evidence from in vitro and animal studies, the major cytochrome P450 isoenzymes are minimally involved in rivastigmine metabolism.
130 liter/ time efter en intravenøs dosis på 0, 2 mg og faldt til 70 liter/ time efter en intravenøs dosis på 2, 7 mg, hvilket er konsistent med rivastigmins ikke- lineære, overproportionale farmakokinetik på grund af mætning af eliminationen.
Total plasma clearance of rivastigmine was approximately 130 litres/ h after a 0.2 mg intravenous dose and decreased to 70 litres/ h after a 2.7 mg intravenous dose, which is consistent with the non-linear, over-proportional pharmacokinetics of rivastigmine due to saturation of its elimination.
Det tyder på, at der forekom meget mindre metabolisering efter dermal behandling i forhold til oral behandling.
The metabolite-to-parent AUC∞ ratio was around 0.7 after transdermal patch versus 3.5 after oral administration, indicating that much less metabolism occurred after dermal compared to oral treatment.
Der dannes mindre NAP226- 90 efter påføring af depotplasteret, formodentlig på grund af manglende præsystemisk (hepatisk first pass) metabolisering i modsætning til oral indgift.
Less NAP226-90 is formed following application of the transdermal patch, presumably because of the lack of presystemic (hepatic first pass) metabolism, in contrast to oral administration.
Renal udskillelse af metabolitterne er den væsentligste udskillelsesvej efter administration af depotplaster.
Elimination Unchanged rivastigmine is found in trace amounts in the urine; renal excretion of the metabolites is the major route of elimination after transdermal patch administration.
Efter indgift af oral 14C- rivastigmin var den renale udskillelse hurtig og nærmest fuldstændig (> 90%) inden for 24 timer.
Following administration of oral 14C- rivastigmine, renal elimination was rapid and essentially complete (> 90%) within 24 hours.
Ældre patienter Alder havde ingen indvirkning på eksponering for rivastigmin hos patienter med Alzheimers demens, som blev behandlet med Exelon depotplastre.
Elderly subjects Age had no impact on the exposure to rivastigmine in Alzheimer’ s disease patients treated with Exelon transdermal patches.
Personer med nedsat leverfunktion Der er ikke udført nogen undersøgelser med Exelon depotplastre hos patienter med nedsat leverfunktion.
Subjects with hepatic impairment No study was conducted with Exelon transdermal patches in subjects with hepatic impairment.