natgillin/translations-raw huggingface dataset:
Bivirkningerne er ordnet under frekvenskategorier med den mest almindelige først og med 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) og ikke kendt (kan ikke estimeres ud fra forhåndenværende data)
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) and not known (cannot be estimated from the available data).
Psykiske lidelser
Urinary infection
Sygdomme i nervesystemet
Psychiatric disorders Nervous
Meget almindelig Almindelig Almindelig Almindelig Ikke almindelig Sjælden Meget sjælden
Common Common Uncommon Uncommon Very rare system disorders Very common Common Common Common Uncommon Rare Very rare
Svimmelhed Hovedpine Somnolens Tremor Besvimelsesanfald Krampeanfald Ekstrapyramidale symptomer (inklusive forværring af Parkinsons sygdom)
Agitation Confusion Insomnia Depression Hallucinations Dizziness Headache Somnolence Tremor Syncope Seizures Extrapyramidal symptoms (including worsening of Parkinson’ s disease)
Hjertesygdomme
Cardiac
Sjælden Meget sjælden
disorders Rare Very rare
Angina pectoris Kardielle arrhythmier (f. eks. bradykardi, atrio- ventrikulært blok, ateriel flimren og takykardi)
Angina pectoris Cardiac arrhythmia (e. g. bradycardia, atrio-ventricular block, atrial fibrillation and tachycardia)
Meget almindelig Meget almindelig Meget almindelig Almindelig Sjælden Meget sjælden
Very common Very common Very common Common Rare Very rare Very rare Not known
Pankreatitis Nogle tilfælde af alvorlig opkastning blev associeret med esophagusruptur (se pkt 4. 4).
Nausea Vomiting Diarrhoea Abdominal pain and dyspepsia Gastric and duodenal ulcers Gastrointestinal haemorrhage Pancreatitis Some cases of severe vomiting were associated with oesophageal rupture (see section 4.4).
Metabolisme - og ernæringsforstyrrelser
Metabolism and nutritional disorders
Sygdomme i lever og galdeveje
Hepatobiliary disorders
Sygdomme i hud og subkutane væv
5 Skin and subcutaneous tissue disorders General
Almindelig Sjælden
Common Rare disorders and administration
Øget svedtendens Udslæt
Sweating increased Rashes
Almene lidelser og reaktioner på indgivelsesstedet
site conditions
Træthed og asteni Generel utilpashed Fald ved uheld
Fatigue and asthenia Malaise Accidental fall
Følgende bivirkninger er blevet observeret med Exelon depotplaster: angst, delirium, feber (almindelig).
The following additional adverse reactions have been observed with Exelon transdermal patches: anxiety, delirium, pyrexia (common).
Tabel 2 viser de bivirkninger, der er rapporteret hos patienter, som modtog behandling med Exelon, og som havde med demens, der var associeret med Parkinsons sygdom.
Table 2 shows the adverse reactions reported in patients with dementia associated with Parkinson’ s disease treated with Exelon.
Psykiske forstyrrelser
Psychiatric disorders Nervous Cardiac
Almindelig Almindelig Almindelig
Common Common Common system disorders Very common Common Common Common Common Common Common Uncommon disorders Common Uncommon Uncommon
Søvnløshed Angst Rastløshed
Insomnia Anxiety Restlessness Tremor Dizziness Somnolence Headache Worsening of Parkinson’ s disease Bradykinesia Dyskinesia Dystonia Bradycardia Atrial Fibrillation Atrioventricular block
Nervesystemet Hjerte
Gastrointestinal disorders
Meget almindelig Almindelig Almindelig Almindelig Almindelig Almindelig Almindelig Ikke almindelig
Very common Very common Common Common Common
Tremor Svimmelhed Somnolens Hovedpine Forværring af Parkinsons sygdom Bradykinesi Dyskinesi Dystoni
Nausea Vomiting Diarrhoea Abdominal pain and dyspepsia Salivary hypersecretion
Almindelig Almindelig Ikke almindelig
Skin and subcutaneous tissue disorders
Bradykardi Atrieflimren Atrioventrikulært blok
Common
Mave- tarmkanalen Hud og
Sweating increased
6 Knogler, led, muskler og bindevæv
Musculoskeletal and connective tissue disorders
Metabolisme - og ernæringsforstyrrelser
Metabolism and nutritional disorders General
Almindelig Almindelig
Common Common disorders and administration
Anoreksi Dehydrering
Anorexia Dehydration
Almene symptomer og reaktioner på administrationsstedet
site conditions
Træthed og asteni Gangforstyrrelse
Fatigue and asthenia Gait abnormality
Tabel 3 angiver antallet og procentdelen af patienterne fra det specifikke 24- ugers studie, der blev udført med Exelon hos patienter med demens, der er associeret med Parkinsons sygdom med præ- definerede bivirkninger, der muligvis kan reflektere en forværring af Parkinsons symptomer.
Table 3 lists the number and percentage of patients from the specific 24-week clinical study conducted 6 with Exelon in patients with dementia associated with Parkinson’ s disease with pre-defined adverse events that may reflect worsening of parkinsonian symptoms.
Prædefinerede bivirkninger, der muligvis kan reflektere en forværring af Parkinsons symptomer hos patienter med demens, der er associeret med Parkinsons sygdom
Pre-defined adverse events that may reflect worsening of parkinsonian symptoms in patients with dementia associated with Parkinson’ s disease
Totalt antal patienter i studiet Totalt antal patienter med prædefinerede bivirkninger Tremor Fald Parkinsons sygdom (forværring) Øget spytsekretion Dyskinesi Parkinsonisme Hypokinesi Bevægelsesforstyrrelser Bradykinesi Dystoni Abnorm måde at gå på Muskelstivhed Balanceforstyrrelser Muskuloskeletal stivhed Rigor Motorisk dysfunktion
Total patients studied Total patients with pre-defined AE(s) Tremor Fall Parkinson’ s disease (worsening) Salivary hypersecretion Dyskinesia Parkinsonism Hypokinesia Movement disorder Bradykinesia Dystonia Gait abnormality Muscle rigidity Balance disorder Musculoskeletal stiffness Rigors Motor dysfunction
Symptomer De fleste tilfælde af tilfældig overdosering 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 have not been associated with any clinical signs or symptoms and almost all of the patients concerned continued rivastigmine treatment.
På grund af kolinesterasehæmmeres vagotoniske effekt på hjerterytmen kan der også forekomme bradykardi og/ eller synkope.
Due to the known vagotonic effect of cholinesterase inhibitors on heart rate, bradycardia and/ or syncope may also occur.
9 timer, anbefales det i tilfælde af asymptomatisk overdosering ikke at indgive yderligere dosis af rivastigmin i de efterfølgende 24 timer.
Treatment As rivastigmine has a plasma half-life of about 1 hour and a duration of acetylcholinesterase inhibition of about 9 hours, it is recommended that in cases of asymptomatic overdose no further dose of rivastigmine should be administered for the next 24 hours.
7 bivirkninger bør gives, hvis det skønnes nødvendigt.
Symptomatic treatment for other adverse reactions should be given as necessary.
En initial dosis på 0, 03 mg/ kg intravenøs atropinsulfat anbefales med efterfølgende doser afhængig af klinisk respons.
An initial dose of 0.03 mg/ kg intravenous atropine sulphate is recommended, with subsequent doses based on clinical response.
Kolinesterasehæmmer, 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.
Rivastigmine is an acetyl- and butyrylcholinesterase inhibitor of the carbamate type, thought to facilitate cholinergic neurotransmission by slowing the degradation of acetylcholine released by
Følgelig har rivastigmin muligvis en forbedrende effekt på kolinergmedierede kognitive udfald af demens, som er forbundet med Alzheimers sygdom og Parkinsons sygdom.
Thus, rivastigmine may have an ameliorative effect on cholinergic-mediated cognitive deficits in dementia associated with Alzheimer’ s disease and Parkinson’ s disease.
40% inden for den første 1, 5 time efter indgift.
In healthy young men, an oral 3 mg dose decreases acetylcholinesterase (AChE) activity in CSF by approximately 40% within the first 1.5 hours after administration.
9 timer efter, at den maksimale hæmmende effekt er opnået.
Activity of the enzyme returns to baseline levels about 9 hours after the maximum inhibitory effect has been achieved.
Hos patienter med Alzheimers sygdom var rivastigmins hæmning af AChE i CSF afhængig af dosis op til 6 mg, der blev indgivet to gange daglig, som var den højeste dosis, som blev testet.
In patients with Alzheimer’ s disease, inhibition of AChE in CSF by rivastigmine was dose-dependent up to 6 mg given twice daily, the highest dose tested.
Rivastigmins hæmning af butyrylcholinesterase- aktivitet i CSF hos 14 patienter med Alzheimer var sammenlignelig med hæmningen af AChE.
Inhibition of butyrylcholinesterase activity in CSF of 14 Alzheimer patients treated by rivastigmine was similar to that of AChE.
Kliniske undersøgelser af Alzheimers demens Effekten af rivastigmin er blevet påvist ved brug af tre uafhængige og domænespecifikke vurderingsredskaber, som blev vurderet med periodiske intervaller gennem 6 måneders behandlingsperioder.
Clinical studies in Alzheimer’ s dementia The efficacy of rivastigmine has been established through the use of three independent, domain specific, assessment tools which were assessed at periodic intervals during 6 month treatment periods.
Disse omfatter ADAS- Cog (en præstationsbaseret måling af kognition), CIBIC - Plus (en omfattende global vurdering af patienten, der dannes af den behandlende læge med input fra den omsorgsgivende person) og PDS (den omsorgsgivende persons vurdering af dagligdagsaktiviteter, som indbefatter personlig hygiejne, fødeindtagelse, påklædning, husføring som indkøb, opretholdelse af evner så som at orientere sig i forhold til omgivelserne og involvere sig i økonomiske anliggender, og så videre).
These include the ADAS-Cog (a performance based measure of cognition), the CIBIC-Plus (a comprehensive global assessment of the patient by the physician incorporating caregiver input), and the PDS (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 relating to finances, etc.).
Patienterne i studiet havde en MMSE (Mini- Mental State Examination) score på 10– 24.
The patients studied had an MMSE (Mini-Mental State Examination) score of 10– 24.
Resultaterne for patienter med klinisk relevant respons, der var poolet fra to fleksible dosisundersøgelser ud af tre pivotale 26- ugers multicenterundersøgelser hos patienter med mild til moderat svær Alzheimers demens, er vist i Tabel 4 nedenfor.
The results for clinically relevant responders pooled from two flexible dose studies out of the three pivotal 26-week multicentre studies in patients with mild-to-moderately severe Alzheimer’ s Dementia, are provided in Table 4 below.
Klinisk relevant forbedring var i disse undersøgelser på forhånd defineret som en mindst 4- pointsforbedring af ADAS- Cog, forbedring af CIBIC- Plus eller en forbedring på mindst 10% af PDS.
Clinically relevant improvement in these studies was defined a priori as at least 4-point improvement on the ADAS-Cog, improvement on the CIBIC-Plus, or at least a 10% improvement on the PDS.
Ydermere er en post- hoc definition af respons vist i samme tabel.
In addition, a post-hoc definition of response is provided in the same table.
Den sekundære definition af respons krævede en mindst 4- pointsforbedring af ADAS- Cog, ingen forværring af CIBIC- Plus og ingen forværring af PDS.
The secondary definition of response required a 4-point or greater improvement on the ADAS-Cog, no worsening on the CIBIC-Plus, and no worsening on the PDS.
Den gennemsnitlige aktuelle dagsdosis for responderende i 6– 12 mg gruppen, der svarede til denne definition, var 9, 3 mg.
The mean actual daily dose for responders in the 6– 12 mg group, corresponding to this definition, was 9.3 mg.
8 Tabel 4
Table 4
Last Observation Carried Forward
Last Observation Carried Forward
ADAS- Cog: mindst 4 - pointsforbedring
ADAS-Cog: improvement of at least 4 points
CIBIC- Plus: forbedring PDS: mindst 10% forbedring Mindst 4- pointsforbedring af ADAS- Cog med ingen forværring af CIBIC- Plus og PDS
CIBIC-Plus: improvement PDS: improvement of at least 10%
29 *** 26 *** 10 *
29*** 26***
18 17 6
18 32*** 17 30***
19 18 6
19 18
Kliniske undersøgelser af demens, der er associeret med Parkinsons sygdom Effekten af rivastigmin ved demens, der er associeret med Parkinsons sygdom, er demonstreret i et 24 - ugers multicenter, dobbelt- blindt, placebo- kontrolleret hovedstudie og dets 24- ugers open- label forlængelsesfase.
8 Clinical studies in dementia associated with Parkinson’ s disease The efficacy of rivastigmine in dementia associated with Parkinson’ s disease has been demonstrated in a 24-week multicentre, double-blind, placebo-controlled core study and its 24-week open-label extension phase.
Patienter, der var involveret i dette studie, havde en MMSE- score (Mini- Mental State Examination) på 10– 24.
Patients involved in this study had an MMSE (Mini-Mental State Examination) score of 10– 24.
ADAS- Cog, en måling af kognition og den globale måling ADCS- CGIC (Alheimer’ s Disease Cooperative Study- Clinician’ s Global Impression of Change).
Efficacy has been established by the use of two independent scales which were assessed at regular intervals during a 6-month treatment period as shown in Table 5 below: the ADAS-Cog, a measure of cognition, and the global measure ADCS-CGIC (Alzheimer’ s Disease Cooperative Study- Clinician ’ s Global Impression of Change).
Demens associeret med Parkinsons sygdom
Dementia associated with Parkinson’ s Disease
ADCS- CGIC Placebo
ADCS-CGIC Placebo
Gennemsnitlig baseline ± SD Gennemsnitsændring ved 24 uger ± SD
Mean baseline ± SD Mean change at 24 weeks ± SD Adjusted treatment
ikke relevant 3, 8 ± 1, 4
n/ a 3.8 ± 1.4
ikke relevant 4, 3 ± 1, 5
n/ a 4.3 ± 1.5
Justeret behandlingsforskel
difference
ikke relevant
n/ a
p- værdi versus placebo
p-value versus placebo
ITT - LOCF population
ITT - LOCF population
ikke relevant 3, 7 ± 1, 4
n/ a 3.7 ± 1.4
p- værdi versus placebo 1
p-value versus placebo 1
ANCOVA med behandling og land som faktorer og baseline ADAS- Cog som en co- variat.
Based on ANCOVA with treatment and country as factors and baseline ADAS-Cog as a covariate.
2 Middeldata vist for belejlighed, kategorisk analyse, der blev udført ved brug af van Elteren- test ITT:
2 Mean data shown for convenience, categorical analysis performed using van Elteren test ITT:
Retrieved Drop Outs; LOCF:
Retrieved Drop Outs; LOCF:
Last Observation Carried Forward.
Last Observation Carried Forward
Selvom behandlingseffekten blev demonstreret i den samlede studiepopulation, indikerede data, at en større behandlingseffekt i forhold til placebo blev set i subgruppen af patienter med moderat demens, der var associeret med Parkinsons sygdom.
Although a treatment effect was demonstrated in the overall study population, the data suggested that a larger treatment effect relative to placebo was seen in the subgroup of patients with moderate dementia associated with Parkinson’ s disease.
9 hos patienter med visuelle hallucinationer (se tabel 6).
Similarly a larger treatment effect was observed in those patients with visual hallucinations (see Table 6).
Demens, der er associeret med Parkinsons sygdom
Dementia associated with Parkinson’ s Disease
ADAS- C og Exelon
ADAS-Cog Exelon
ADAS- C og ADAS- C og Placebo Exelon
ADAS-Cog ADAS-Cog Placebo Exelon
ADAS- C og Placebo
ADAS-Cog Placebo
Patienter med moderat demens (MMSE 10- 17)
Patients with moderate dementia (MMSE 10-17)
Patienter med mild (MMSE 18- 24)
Patients with mild (MMSE 18-24)
demens
dementia
Baseret på ANCOVA med behandling og land som faktorer og baseline ADAS- Cog som covariat.
Based on ANCOVA with treatment and country as factors and baseline ADAS-Cog as a covariate.
Retrieved Drop Outs
Retrieved Drop Outs
Absorption Rivastigmin absorberes hurtigt og fuldstændigt.
Absorption Rivastigmine is rapidly and completely absorbed.
1 time.
Peak plasma concentrations are reached in approximately 1 hour.
1, 5 gange højere end forventet fra øgningen af dosis.
As a consequence of rivastigmine’ s interaction with its target enzyme, the increase in bioavailability is about 1.5-fold greater than that expected from the increase in dose.
36% ±13%.
Absolute bioavailability after a 3 mg dose is about 36%±13%.
30%.
Administration of rivastigmine with food delays absorption (tmax) by 90 min and lowers Cmax and increases AUC by approximately 30%.
40%.
Distribution Protein binding of rivastigmine is approximately 40%.
Det krydser let blodhjernebarrieren 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.
1 time), primært via kolinesterasemedieret hydrolyse til den decarbamylerede metabolit.
Metabolism Rivastigmine is rapidly and extensively metabolised (half-life in plasma approximately 1 hour), primarily via cholinesterase-mediated hydrolysis to the decarbamylated metabolite.
Resultater fra in vitro og dyreundersøgelser viser, at cytokrom- P450 iso- enzymer kun i ringe grad er involveret i rivastigmin- metabolisering.
In vitro, this metabolite shows minimal inhibition of acetylcholinesterase (< 10%).
Rivastigmins totale plasmaclearance var ca.
Based on evidence from in vitro and animal studies the major cytochrome P450 isoenzymes are minimally involved in rivastigmine metabolism.
130 l/ t efter en 0, 2 mg intravenøs dosis og faldt til 70 l/ t efter en 2, 7 mg intravenøs dosis.
Total plasma clearance of rivastigmine was approximately 130 l/ h after a 0.2 mg intravenous dose and decreased to 70 l/ h after a 2.7 mg intravenous dose.
Udskillelse Der findes ikke uændret rivastigmin i urinen; renal udskillelse af metabolitterne er den væsentligste
Excretion Unchanged rivastigmine is not found in the urine; renal excretion of the metabolites is the major route of elimination.
Efter indgift af 14C- rivastigmin var renal udskillelse hurtig og nærmest fuldstændig (> 90%) inden for 24 timer.
Following administration of 14C-rivastigmine, renal elimination was rapid and essentially complete (> 90%) within 24 hours.
Der er ikke nogen akkumulering af rivastigmin eller decarbamyleret metabolit hos patienter med Alzheimers sygdom.
There is no accumulation of rivastigmine or the decarbamylated metabolite in patients with Alzheimer’ s disease.
Ældre patienter Selv om biotilgængeligheden for rivastigmin er højere hos ældre end hos yngre raske frivillige forsøgspersoner, viste undersøgelser af Alzheimerpatienter i alderen mellem 50 og 92 år ingen ændring i biotilgængelighed med alderen.
Elderly subjects While bioavailability of rivastigmine is greater in elderly than in young healthy volunteers, studies in Alzheimer patients aged between 50 and 92 years showed no change in bioavailability with age.
Personer med nedsat leverfunktion Cmax for rivastigmin var cirka 60% højere, og AUC for rivastigmin var mere end dobbelt så høj hos personer med mild til moderat nedsat leverfunktion end hos raske personer.
Subjects with hepatic impairment The Cmax of rivastigmine was approximately 60% higher and the AUC of rivastigmine was more than twice as high in subjects with mild to moderate hepatic impairment than in healthy subjects.
Personer med nedsat nyrefunktion Cmax og AUC for rivastigmin var mere end dobbelt så høj hos personer med moderat nedsat nyrefunktion sammenlignet med raske personer; der var dog ingen ændringer af Cmax og AUC for rivastigmin hos personer med svært nedsat nyrefunktion.
Subjects with renal impairment Cmax and AUC of rivastigmine were more than twice as high in subjects with moderate renal impairment
Der blev ikke observeret nogen mål- organtoksicitet.
No target organ toxicity was observed.
Rivastigmin var ikke mutagen i et standardbatteri af in vitro - og in vivo- test, på nær i en kromosonal Abberation Test i humane perifere lymfocytter ved en dosis på 104 gange den maksimale kliniske relevante.
Rivastigmine was not mutagenic in a standard battery of in vitro and in vivo tests, except in a chromosomal aberration test in human peripheral lymphocytes at a dose 104 times the maximum clinical exposure.
In vivo Micronucleus- testen var negativ.
The in vivo micronucleus test was negative.
Når mængde og koncentration af rivastigmin og dets metabolitter blev sat i relation til arealet af legemsoverfladen var det omtrent ækvivalent til den maksimalt anbefalede humane daglige dosis på 12 mg; ved sammenligning med maksimal human dosis blev der dog opnået en seksdobling af dosis hos dyr.
When normalised to body surface area, the exposure to rivastigmine and its metabolites was approximately equivalent to the maximum recommended human dose of 12 mg/ day; however, when compared to the maximum human dose, a multiple of approximately 6-fold was achieved in animals.
Gelatine Magnesiumstearat Hypromellose Mikrokrystallinsk cellulose Silica, kolloid vandfri Gul jernoxid (E 172) Rød jernoxid (E 172) Titandioxid (E 171)
Gelatin Magnesium stearate Hypromellose Microcrystalline cellulose Silica, colloidal anhydrous Yellow iron oxide (E172) Red iron oxide (E172) Titanium dioxide (E171)
11 6. 3 Opbevaringstid
6.3 Shelf life
- Blister med klar PVC- bund og blåt folielåg med 14 kapsler.
- Blister of clear PVC tray with blue lidding foil with 14 capsules.
Hver æske indeholder 2, 4 eller
Each box contains 2, 4 or
8 blister.
8 blisters.
- HDPE- flaske med plastiklukke med indre tætningsanordning.
- HDPE bottles with plastic closure with induction innerseal.
250 kapsler.
Each bottle contains 250 capsules.
6. 6 Regler for destruktion
11 6.6 Special precautions for disposal
12. 05. 1998 Dato for seneste fornyelse:
12.05.1998 Date of latest renewal:
Exelon 3, 0 mg hårde kapsler
Exelon 3.0 mg hard capsules
Hver kapsel indeholder rivastigminhydrogentartrat svarende til 3, 0 mg rivastigmin.
Each capsule contains rivastigmine hydrogen tartrate corresponding to rivastigmine 3.0 mg.
Råhvidt til svagt gulligt pulver i en kapsel med orange hætte og orange skal, med ” EXELON 3 mg ” præget med rødt på kapselskallen.
Off-white to slightly yellow powder in a capsule with orange cap and orange body, with red imprint “ EXELON 3 mg ” on body.
13 Der kan foregå vedligeholdelsesbehandling så længe, der er terapeutisk effekt for patienten.
13 Maintenance treatment can be continued for as long as a therapeutic benefit for the patient exists.
14 overledningsdefekter (sino- atrialt blok, atrio- ventrikulært blok) (jævnfør afsnit 4. 8).
14 Care must be taken when using rivastigmine in patients with sick sinus syndrome or conduction defects (sino-atrial block, atrio-ventricular block) (see section 4.8).
Alzheimers sygdom kan medføre gradvis forringelse af køreegenskaber eller nedsætte evnen til at
Alzheimer’ s disease may cause gradual impairment of driving performance or compromise the ability to use machinery.
Derfor bør rivastigmin- behandlede demenspatienters evne til fortsat at køre bil eller betjene indviklede maskiner løbende vurderes af den behandlende læge.
15 continue driving or operating complex machines should be routinely evaluated by the treating physician.
Meget almindelig Meget almindelig Meget almindelig Almindelig Sjælden Meget sjælden Meget sjælden Ikke kendt
Very common Very common Very common Common Rare Very rare Very rare Not known
Kvalme Opkastning Diarré Abdominale smerter og dyspepsi Mavesår og sår på tolvfingertarmen Gastrointestinal blødning Pankreatitis Nogle tilfælde af alvorlig opkastning blev associeret med esophagusruptur (se pkt 4. 4).
Nausea Vomiting Diarrhoea Abdominal pain and dyspepsia Gastric and duodenal ulcers Gastrointestinal haemorrhage Pancreatitis Some cases of severe vomiting were associated with oesophageal rupture (see section 4.4).