qanastek/EMEA-V3 huggingface dataset:
In these trials, patients were initially required to be stable on the lowest effective dose of anti- Parkinsonian medicinal products (dopamine agonist) and to remain on the same anti-Parkinsonian medicinal products and dosages throughout the study.
Šajos p t jumos pacientu st voklis vispirms tika stabiliz ts ar maz ko efekt vo pretparkinsonisma l dzek a (dopam na agonista) devu, un p t juma laik pretparkinsonisma l dzekli un t devu nedr kst ja main t.
Olanzapine was started at 2.5 mg/ day and titrated to a maximum of 15 mg/ day based on investigator judgement.
Olanzap na lietošanu s ka ar 2, 5 mg dien un titr ja maksim li l dz 15 mg dien p c p tnieka ieskatiem.
Neuroleptic Malignant Syndrome (NMS) NMS is a potentially life-threatening condition associated with antipsychotic medicinal product.
aundab gais neiroleptiskais simptoms (NS) NS ir iesp jami dz v bai b stams st voklis, ko izraisa antipsihotiski l dzek i.
Rare cases reported as NMS have also been received in association with olanzapine.
Lietojot olanzap nu, retos gad jumos ar zi ots par NS rašanos.
Clinical manifestations of NMS are hyperpyrexia, muscle rigidity, altered mental status, and evidence of autonomic instability (irregular pulse or blood pressure, tachycardia, diaphoresis, and cardiac dysrhythmia).
NS kl nisk s izpausmes ir hiperpireksija, musku u rigidit te, psihiski trauc jumi un ve etat v s nervu sist mas labilit tes izpausmes (main gs pulss vai asinsspiediens, tahikardija, pastiprin ta sv šana un sirds ritma trauc jumi).
Additional signs may include elevated creatinine phosphokinase, myoglobinuria (rhabdomyolysis), and acute renal failure.
Citas izpausmes var b t paaugstin ts kreatin nfosfokin zes l menis, mioglob n rija (rabdomiol ze) un ak ta nieru mazsp ja.
If a patient develops signs and symptoms indicative of NMS, or presents with unexplained high fever without additional clinical manifestations of NMS, all antipsychotic medicines, including olanzapine must be discontinued.
Ja pacientam tiek konstat tas NS paz mes vai simptomi vai neskaidras cilmes izteikts drudzis bez cit m NS kl nisk m izpausm m, j p rtrauc visu antipsihotisko l dzek u, ar olanzap na, lietošana.
Hyperglycaemia and diabetes Hyperglycaemia and/ or development or exacerbation of diabetes occasionally associated with ketoacidosis or coma has been reported rarely, including some fatal cases (see section 4.8).
Hiperglik mija un diab ts Retos gad jumos zi ots par hiperglik miju un/ vai jau esoša cukura diab ta paasin jumu, kas reiz m saist ts ar ketoacidozi vai komu, to vid ar par dažiem let liem gad jumiem (skat t apakšpunktu 4. 8).
In some cases, a prior increase in body weight has been reported which may be a predisposing factor.
Dažos gad jumos zi ots par iepriekš bijušu palielin tu erme a masu, kas var b t predispon jošs faktors.
Appropriate clinical monitoring is advisable particularly in diabetic patients and in patients with risk factors for the development of diabetes mellitus for which regular glucose control is recommended.
Cukura diab ta slimniekiem un pacientiem ar cukura diab ta riska faktoriem paši ieteicama atbilstoša kl niska nov rošana ar regul ru glikozes l me a kontroli asin s.
Lipid alterations Undesirable alterations in lipids have been observed in olanzapine-treated patients in placebo- controlled clinical trials (see section 4.8).
Lip du izmai as Ar placebo kontrol tos kl niskos p t jumos pacientiem, kuri tika rst ti ar olanzap nu, nov roja nev lamas lip du izmai as (skat t apakšpunktu 4. 8 Nev lam s blakuspar d bas).
Lipid alterations should be managed as clinically appropriate, particularly in dyslipidemic patients and in patients with risk factors for the development of lipids disorders.
Lip du izmai u gad jum j r kojas atbilstoši kl niskajai ainai, paši pacientiem ar dislipid miju un cilv kiem ar dislipid mijas riska faktoriem.
4 Anticholinergic activity While olanzapine demonstrated anticholinergic activity in vitro, experience during the clinical trials revealed a low incidence of related events.
Ta u, t k kl nisk pieredze par olanzap na lietošanu
However, as clinical experience with olanzapine in patients with concomitant illness is limited, caution is advised when prescribing for patients with prostatic hypertrophy, or paralytic ileus and related conditions.
4 pacientiem ar blakusslim b m ir ierobežota, j iev ro piesardz ba, ordin jot medikamentu pacientiem ar prostatas hipertrofiju, paral tisku ileusu vai l dz g m slim b m.
Hepatic function Transient, asymptomatic elevations of hepatic transaminases, alanine transferase (ALT), aspartate transferase (AST) have been seen commonly, especially in early treatment.
Aknu darb ba Bieži, paši rst šanas s kum konstat ta p rejoša asimptom tiska aknu transamin žu, AlAT un AsAT l me a paaugstin šan s.
Caution should be exercised in patients with elevated ALT and/ or AST, in patients with signs and symptoms of hepatic impairment, in patients with pre-existing conditions associated with limited hepatic functional reserve, and in patients who are being treated with potentially hepatotoxic medicines.
Piesardz ba j iev ro pacientiem ar paaugstin tu AlAT un/ vai AsAT l meni, aknu boj juma paz m m un simptomiem, iepriekš bijuš m slim b m, kas saist tas ar funkcion liem aknu trauc jumiem, un pacientiem, kas tiek rst ti ar iesp jami hepatotoksiskiem prepar tiem.
In the event of elevated ALT and/ or AST during treatment, follow-up should be organised and dose reduction should be considered.
Ja rst šanas laik paaugstin s AlAT un/ vai AsAT l menis, pacients j nov ro un j apsver devas samazin šana.
In cases where hepatitis (including hepatocellular, cholestatic or mixed liver injury) has been diagnosed, olanzapine treatment should be discontinued.
Gad jumos, kad diagnostic ts hepat ts (ieskaitot hepatocelul rus, holest tiskus vai jauktus aknu boj jumus), olanzap na terapija j p rtrauc.
Neutropenia Caution should be exercised in patients with low leukocyte and/ or neutrophil counts for any reason, in patients receiving medicines known to cause neutropenia, in patients with a history of drug-induced bone marrow depression/ toxicity, in patients with bone marrow depression caused by concomitant illness, radiation therapy or chemotherapy and in patients with hypereosinophilic conditions or with myeloproliferative disease.
Neitrop nija Piesardz ba j iev ro pacientiem ar jebkuras cilmes mazu leikoc tu un/ vai neitrof lo skaitu, pacientiem, kas sa em zin mas neitrop niju izraisošas z les, pacientiem ar z u izrais tu kaulu smadze u funkcijas nom kumu/ toksicit ti anamn z, pacientiem ar blakusslim bu, staru vai mijterapijas izrais tu kaulu smadze u nom kumu un pacientiem ar hipereozinofiliju vai mieloproliferat vu slim bu.
Neutropenia has been reported commonly when olanzapine and valproate are used concomitantly (see section 4.8).
Vienlaikus lietojot olanzap nu un valpro tu, bieži zi ots par neitrop niju (skat t apakšpunktu 4. 8).
Discontinuation of treatment Acute symptoms such as sweating, insomnia, tremor, anxiety, nausea, or vomiting have been reported very rarely (< 0.01%) when olanzapine is stopped abruptly.
rst šanas p rtraukšana oti reti (< 0, 01%) p c p kš as olanzap na lietošanas p rtraukšanas zi ots par t diem ak tiem simptomiem k sv šana, bezmiegs, tr ce, trauksme, slikta d ša vai vemšana.
QT interval In clinical trials, clinically meaningful QTc prolongations (Fridericia QT correction [QTcF] 500 milliseconds [msec] at any time post baseline in patients with baseline QTcF < 500 msec) were uncommon (0.1% to 1%) in patients treated with olanzapine, with no significant differences in associated cardiac events compared to placebo.
QT interv ls Kl niskos p t jumos pacientiem, kuri tika rst ti ar olanzap nu (sal dzinot ar placebo grupu), reti (0, 1% l dz 1%) tika nov rota kl niski noz m ga QTc interv la pagarin šan s (Fridericia QT korekcija [QTcF] 500 msec jebkur laik no p t juma s kuma pacientiem ar s kotn jo QTcF < 500 msec).
However, as with other antipsychotics, caution should be exercised when olanzapine is prescribed with medicines known to increase QTc interval, especially in the elderly, in patients with congenital long QT syndrome, congestive heart failure, heart hypertrophy, hypokalaemia or hypomagnesaemia.
Tom r, t pat k citu antipsihotisku l dzek u lietošanas gad jum, j iev ro piesardz ba, lietojot olanzap nu kop ar medikamentiem, kas pagarina QTc interv lu, paši vec ka gadag juma pacientiem, pacientiem ar iedzimtu gara QT sindromu, sastr guma sirds mazsp ju, sirds hipertrofiju, hipokali miju vai hipomagni miju.
Thromboembolism Temporal association of olanzapine treatment and venous thromboembolism has very rarely (< 0.01%) been reported.
Trombembolija oti reti (< 0, 01%) ir zi ots par slaic gu saist bu starp olanzap na terapiju un venozo trombemboliju.
A causal relationship between the occurrence of venous thromboembolism and treatment with olanzapine has not been established.
Nav konstat ta c loniska saist ba starp venozo trombemboliju un olanzap na terapiju.
However, since patients with schizophrenia often present with acquired risk factors for venous thromboembolism all possible risk factors of VTE e. g. immobilisation of patients, should be identified and preventive measures undertaken.
Tom r, emot v r to, ka šizofr nijas pacientiem bieži ir nov rojami ieg ti venoz s trombembolijas riska faktori, ir j apzina visi iesp jamie riska faktori, kas var tu izrais t venozo trombemboliju (piem., pacienta imobiliz cija), un j nodrošina atbilstoša profilakse.
General CNS activity Given the primary CNS effects of olanzapine, caution should be used when it is taken in combination with other centrally acting medicines and alcohol.
Visp r g ietekme uz CNS T k olanzap nam ir prim ra ietekme uz CNS, j iev ro piesardz ba, ja to lieto kombin cij ar citiem centr las darb bas l dzek iem un alkoholu.
As it exhibits in vitro dopamine antagonism, olanzapine may antagonize the effects of direct and indirect dopamine agonists.
T k olanzap nam in vitro rakstur gs dopam na antagonisms, tas var darboties pret ji tiešu un netiešu dopam na agonistu iedarb bai.
Seizures Olanzapine should be used cautiously in patients who have a history of seizures or are subject to factors which may lower the seizure threshold.
Krampji Olanzap ns piesardz gi j lieto pacientiem, kam anamn z ir krampji vai kas pak auti krampju slieksni pazeminošu faktoru ietekmei.
Seizures have been reported to occur rarely in patients when treated with olanzapine.
Pacientiem, kas lieto olanzap nu, par krampju rašanos zi ots reti.
In most of these cases, a history of seizures or risk factors for seizures were reported.
Liel kai da ai šo pacientu tika zi ots par krampjiem anamn z vai krampju riska faktoriem.
5 Tardive Dyskinesia In comparator studies of one year or less duration, olanzapine was associated with a statistically significant lower incidence of treatment emergent dyskinesia.
Tard v diskin zija Sal dzinošos p t jumos, kas ilga vienu gadu vai maz k, olanzap ns statistiski noz m gi maz k izrais ja diskin zijas, kam nepieciešama rst šana.
However the risk of tardive dyskinesia increases with long term exposure, and therefore if signs or symptoms of tardive dyskinesia appear in a patient on olanzapine, a dose reduction or discontinuation should be considered.
Tom r tard v s diskin zijas risks palielin s ilgstošas terapijas laik, t d j apsver devas mazin šana vai lietošanas p rtraukšana, ja pacientam olanzap na terapijas laik rodas tard v s diskin zijas simptomi.
These symptoms can temporally deteriorate or even arise after discontinuation of treatment.
P c terapijas p rtraukšanas šie simptomi var slaic gi pastiprin ties vai pat rasties.
Postural hypotension Postural hypotension was infrequently observed in the elderly in olanzapine clinical trials.
5 Postur la hipotensija Kl niskos p t jumos ar vec ka gadag juma pacientiem, kas lietoja olanzap nu, dažk rt tika nov rota postur la hipotensija.
As with other antipsychotics, it is recommended that blood pressure is measured periodically in patients over 65 years.
T pat k citu antipsihotisko l dzek u lietošanas gad jum, pacientiem p c 65 gadu vecuma ieteicams regul ri m r t asinsspiedienu.
Use in children and adolescents under 18 years of age Olanzapine is not indicated for use in the treatment of children and adolescents.
Lietošana b rniem un pusaudžiem l dz 18 gadu vecumam Olanzap ns nav indic ts b rnu un pusaudžu rst šanai.
Studies in patients aged 13-17 years showed various adverse reactions, including weight gain, changes in metabolic parameters and increases in prolactin levels.
P t jumos ar pacientiem vecum no 13 l dz 17 gadiem tika konstat tas daž das blakuspar d bas, tostarp svara pieaugums, metabolisko r d t ju izmai as un prolakt na l me a izmai as.
Long-term outcomes associated with these events have not been studied and remain unknown (see sections 4.8 and 5.1).
Šo blakuspar d bu ietekme ilgtermi nav p t ta un nav zin ma (skat t apakšpunktus 4. 8 un 5. 1).
Phenylalanine ZYPREXA VELOTAB orodispersible tablet contains aspartame, which is a source of phenylalanine.
Fenilalan ns ZYPREXA VELOTAB mut disper jam s tablet s ir aspart ms, kas ir fenilalan na avots.
May be harmful for people with phenylketonuria.
Tas var b t b stams cilv kiem ar fenilketon riju.
Mannitol ZYPREXA VELOTAB orodispersible tablet contains mannitol.
ZYPREXA VELOTAB mut disper jam s tablet s ir mann ts.
Sodium methyl parahydroxybenzoate and sodium propyl parahydroxybenzoate Olanzapine orodispersible tablet contains sodium methyl parahydroxybenzoate and sodium propyl parahydroxybenzoate.
Olanzap na mut disper jam s tablet s ir n trija metilparahidroksibenzo ts un n trija propilparahidroksibenzo ts.
These preservatives are known to cause urticaria.
Šie konservanti var izrais t n treni.
Generally, delayed type reactions such as contact dermatitis may occur, but rarely immediate reactions with bronchospasm may occur.
Parasti iesp jamas v l na tipa reakcijas, piem ram, kontaktdermat ts, bet retos gad jumos var b t t l t jas reakcijas ar bronhu spazm m.
Interaction studies have only been performed in adults.
P t jumi par mijiedarb bu ir veikti tikai ar pieaugušajiem.
Potential interactions affecting olanzapine Since olanzapine is metabolised by CYP1A2, substances that can specifically induce or inhibit this isoenzyme may affect the pharmacokinetics of olanzapine.
Iesp jam olanzap nu ietekm još mijiedarb ba T k olanzap nu metaboliz CYP1A2, vielas, kas var specifiski induc t vai inhib t šo izoenz mu, var ietekm t olanzap na farmakokin tiku.
Induction of CYP1A2 The metabolism of olanzapine may be induced by smoking and carbamazepine, which may lead to reduced olanzapine concentrations.
CYP1A2 indukcija Olanzap na metabolismu var induc t sm šana un karbamazep ns, kas var izrais t olanzap na koncentr cijas pazemin šanos.
Only slight to moderate increase in olanzapine clearance has been observed.
Nov rota tikai neliela vai m reni izteikta olanzap na kl rensa palielin šan s.
The clinical consequences are likely to be limited, but clinical monitoring is recommended and an increase of olanzapine dose may be considered if necessary (see section 4.2).
Kl nisk s sekas var tu b t nelielas, ta u nepieciešam bas gad jum ieteicama kl niska nov rošana un olanzap na devas palielin šana (skat t apakšpunktu 4. 2).
Inhibition of CYP1A2 Fluvoxamine, a specific CYP1A2 inhibitor, has been shown to significantly inhibit the metabolism of olanzapine.
CYP1A2 inhib cija Nov rots, ka fluvoksam ns – specifisks CYP1A2 inhibitors – stipri kav olanzap na metabolismu.
The mean increase in olanzapine Cmax following fluvoxamine was 54% in female non- smokers and 77% male smokers.
P c fluvoksam na lietošanas olanzap na Cmax palielin j s vid ji par 54% nesm još m sieviet m un par 77% sm jošiem v riešiem.
The mean increase in olanzapine AUC was 52% and 108% respectively.
Olanzap na LZL palielin j s attiec gi par 52% un 108%.
A lower starting dose of olanzapine should be considered in patients who are using fluvoxamine or any other CYP1A2 inhibitors, such as ciprofloxacin.
Pacientiem, kas lieto fluvoksam nu vai k du citu CYP1A2 inhibitoru, piem ram, ciprofloksac nu, j apsver maz kas olanzap na s kuma devas lietošana.
A decrease in the dose of olanzapine should be considered if treatment with an inhibitor of CYP1A2 is initiated.
Ja tiek s kta rst šana ar CYP1A2 inhibitoru, j apsver olanzap na devas samazin šanas nepieciešam ba.
Decreased bioavailability Activated charcoal reduces the bioavailability of oral olanzapine by 50 to 60% and should be taken at least 2 hours before or after olanzapine.
Samazin ta biolo isk pieejam ba Aktiv t ogle samazina iekš gi lietota olanzap na biolo isko pieejam bu par 50 – 60%, un t j lieto vismaz 2 stundas pirms vai p c olanzap na lietošanas.
6 Fluoxetine (a CYP2D6 inhibitor), single doses of antacid (aluminium, magnesium) or cimetidine have not been found to significantly affect the pharmacokinetics of olanzapine.
Nav nov rots, ka fluokset ns (CYP2D6 inhibitors), atseviš as antac du (alum nija, magnija) vai cimetid na devas noz m gi ietekm tu olanzap na farmakokin tiku.
Potential for olanzapine to affect other medicinal products Olanzapine may antagonise the effects of direct and indirect dopamine agonists.
Olanzap na sp ja ietekm t citas z les Olanzap ns var darboties pret ji tiešas un netiešas darb bas dopam na agonistiem.
1A2, 2D6, 2C9, 2C19, 3A4).
Olanzap ns in vitro neinhib galvenos CYP450 izoenz mus (piem ram, 1A2, 2D6, 2C9, 2C19, 3A4).
Thus no particular interaction is expected as verified through in vivo studies where no inhibition of metabolism of the following active substances was found: tricyclic antidepressant (representing mostly CYP2D6 pathway), warfarin (CYP2C9), theophylline (CYP1A2) or diazepam (CYP3A4 and 2C19).
T p c nav gaid ma paša mijiedarb ba, k apstiprin ts in vivo p t jumos, kur netika nov rota š du akt vo vielu metabolisma kav šana: tricikliskie antidepresanti (p rst v galvenok rt CYP2D6 ce u), varfar ns (CYP2C9), teofil ns (CYP1A2) un diazep ms (CYP3A4 un 2C19).
Olanzapine showed no interaction when co-administered with lithium or biperiden.
6 Olanzap nam nav nov rota mijiedarb ba, lietojot kop ar litiju vai biperid nu.
Therapeutic monitoring of valproate plasma levels did not indicate that valproate dosage adjustment is required after the introduction of concomitant olanzapine.
Valpro ta plazmas l me a terapeitiska kontrole neliecin ja, ka p c vienlaic gas olanzap na lietošanas s kšanas valpro ta deva b tu j piel go.
General CNS activity Caution should be exercised in patients who consume alcohol or receive medicinal products that can cause central nervous system depression.
Visp r ga ietekme uz CNS Piesardz ba j iev ro pacientiem, kas lieto alkoholu vai medikamentus, kuri izraisa centr l s nervu sist mas nom kumu.
The concomitant use of olanzapine with anti-Parkinsonian medicinal products in patients with Parkinson's disease and dementia is not recommended (see section 4.4).
Olanzap nu nav ieteicams lietot vienlaic gi ar z l m Parkinsona slim bas rst šanai pacientiem ar Parkinsona slim bu un demenci (skat t apakšpunktu 4. 4).
QTc interval Caution should be used if olanzapine is being administered concomitantly with medicinal products known to increase QTc interval (see section 4.4).
QTc interv ls J uzman s, lietojot olanzap nu vienlaic gi ar z l m, kuras palielina QTc interv lu (skat t apakšpunktu 4. 4).
There are no adequate and well-controlled studies in pregnant women.
Nav atbilstošu un labi kontrol tu p t jumu gr tniec m.
Patients should be advised to notify their physician if they become pregnant or intend to become pregnant during treatment with olanzapine.
Pacientes j br dina, ka, olanzap na terapijas laik iest joties gr tniec bai vai pl nojot to, tas j pazi o rstam.
Nevertheless, because human experience is limited, olanzapine should be used in pregnancy only if the potential benefit justifies the potential risk to the foetus.
T k lietošanas pieredze cilv kiem ir ierobežota, š s z les gr tniec bas laik dr kst lietot tikai tad, ja iesp jamais terapijas guvums attaisno iesp jamo risku auglim.
Spontaneous reports have been very rarely received on tremor, hypertonia, lethargy and sleepiness, in infants born to mothers who had used olanzapine during the 3rd trimester.
oti reti sa emti br vpr t gie zi ojumi par tr ci, hipertoniju, letar iju un miegain bu jaundzimušajiem, kuru m tes 3. trimestra laik lietojušas olanzap nu.
In a study in breast-feeding, healthy women, olanzapine was excreted in breast milk.
P t jum vesel m sieviet m z d šanas period olanzap ns izdal j s m tes pien.
Mean infant exposure (mg/ kg) at steady state was estimated to be 1.8% of the maternal olanzapine dose (mg/ kg).
Apr in ts, ka vid j l dzsvara koncentr cija (mg/ kg) z dainim bija 1, 8% no m tei ievad t s olanzap na devas (mg/ kg).
Patients should be advised not to breast-feed an infant if they are taking olanzapine.
Pacient m olanzap na lietošanas laik j iesaka p rtraukt z d šanu.
No studies on the effects on the ability to drive and use machines have been performed.
Nav veikti p t jumi par ietekmi uz sp ju vad t transportl dzek us un apkalpot meh nismus.
Because olanzapine may cause somnolence and dizziness, patients should be cautioned about operating machinery, including motor vehicles.
T k olanzap ns var izrais t miegain bu un reiboni, pacientiem j iesaka uzman ties, str d jot ar meh nismiem, ar vadot transportl dzek us.
Adults The most frequently (seen in 1% of patients) reported adverse reactions associated with the use of olanzapine in clinical trials were somnolence, weight gain, eosinophilia, elevated prolactin, cholesterol, glucose and triglyceride levels (see section 4.4), glucosuria, increased appetite, dizziness, akathisia, parkinsonism (see section 4.4), dyskinesia, orthostatic hypotension, anticholinergic effects,
Pieaugušie Visbiež k (≥ 1% pacientu) nov rot s blakuspar d bas, kas rad s olanzap na lietošanas laik kl niskos p t jumos, bija miegain ba, erme a masas palielin šan s, eozinofilija, paaugstin ts prolakt na, holester na, glikozes un triglicer du l menis (skat t apakšpunktu 4. 4), glikoz rija, palielin ta apet te, reibonis, akat zija, parkinsonisms (skat t apakšpunktu 4. 4), diskin zija, ortostatiska hipotensija, antihol ner iskas ietekmes, p rejoša asimptom tiska aknu transamin žu l me a paaugstin šan s (skat t apakšpunktu 4. 4), izsitumi, ast nija, nogurums un t ska.
7 transient asymptomatic elevations of hepatic transaminases (see section 4.4), rash, asthenia, fatigue and oedema.
7 Tabul uzskait tas blakuspar d bas un laboratoriskie izmekl jumi, kas ieg ti no spont najiem zi ojumiem un kl niskajiem p t jumiem.
Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
Katr biežuma grup blakuspar d bas uzskait tas to nopietn bas samazin juma sec b.
Very common (10%), common (1% and < 10%), uncommon (0.1% and < 1%), rare (0.01% and < 0.1%), very rare (< 0.01%), not known (cannot be estimated from the data available).
Biežuma kategorijas ir š das: oti bieži (≥ 10%), Bieži (no ≥ 1% l dz < 10%), Ret k (no ≥ 0, 1% l dz < 1%), Reti (no ≥ 0, 01% l dz < 0, 1%), oti reti (< 0, 01%) un Nav zin ms (nav iesp jams noteikt p c pieejam s inform cijas).
Very common
oti bieži Asins un limfatisk s sist
Common
Bieži mas trauc jumi
Not known
Nav zin ms
Leukopenia Neutropenia
Leikop nija Neitrop nija
Thrombocytopenia
Trombocitop nija
Immune system disorders Allergic reaction Metabolism and nutrition disorders Weight gain1
Im n s sist mas trauc jumi Aler iska reakcija Metabolisma un barošan s trauc jumi Svara pieaugums1
Elevated cholesterol levels2,3 Elevated glucose levels4 Elevated triglyceride levels2,5 Glucosuria Increased appetite
Paaugstin ts holester na l menis2, 3 Paaugstin ts glikozes l menis4 Paaugstin ts triglicer du l menis2, 5 Glikoz rija Pastiprin ta stgriba
Development or exacerbation of diabetes occasionally associated with ketoacidosis or coma, including some fatal cases (see section 4.4) Hypothermia
Diab ta att st šan s vai saasin šan s (reiz m izraisot ketoacidozi vai komu), t. sk. daži let li gad jumi (skat t apakšpunktu 4. 4) Hipotermija
Nervous system disorders Somnolence Cardiac disorders
Nervu sist mas trauc jumi Miegain ba
Dizziness Akathisia6 Parkinsonism6 Dyskinesia6
Reibonis Akat zija6 Parkinsonisms6 Diskin zija6
Seizures where in most cases a history of seizures or risk factors for seizures were reported Neuroleptic malignant syndrome (see section 4.4) Dystonia (including oculogyration) Tardive dyskinesia Discontinuation symptoms7
Krampji, kur liel kaj da gad jumu tika zi ots par krampjiem vai krampju riska faktoriem anamn z aundab gais neiroleptiskais simptoms (skat t apakšpunktu 4. 4) Distonija (tostarp acs bola neapzin tas kust bas) Tard v diskin zija P rtraukšanas simptomi7
Vascular disorders
Sirds funkcijas trauc jumi Asinsvadu sist mas trauc jumi
Bradycardia QTc prolongation (see section 4.4)
Bradikardija QTc interv la pagarin šan s (skat t apakšpunktu 4. 4)
Ventricular tachycardia/ fibrillation, sudden death (see section 4.4)
Ventrikul ra tahikardija/ fibril cija, p kš a n ve (skat t apakšpunktu 4. 4)
Thromboembolism (including pulmonary embolism and deep vein thrombosis)
Trombembolija (t. sk. plaušu embolija un dzi o v nu tromboze)
8 Hepato-biliary disorders
8 Ku a- zarnu trakta trauc jumi
Transient, asymptomatic elevations of hepatic transaminases (ALT, AST), especially in early treatment (see section 4.4)
P rejoša, asimptom tiska aknu transamin žu (AlAT, AsAT) l me a paaugstin šan s, paši rst šanas s kum (skat t apakšpunktu 4. 4)
Hepatitis (including hepatocellular, cholestatic or mixed liver injury)
Hepat ts (t. sk. hepatocelul ri, holest tiski vai jaukti aknu boj jumi)
Skin and subcutaneous tissue disorders
das un zem das audu boj jumi
Photosensitivity reaction Alopecia
Fotosensitivit tes reakcijas Matu izkrišana
Musculoskeletal and connective tissue disorders Rhabdomyolysis Renal and urinary disorders Urinary hesitation Reproductive system and breast disorders Priapism General disorders and administration site conditions Asthenia Fatigue Oedema Investigations Elevated plasma prolactin levels8 1
Skeleta- musku u un saistaudu sist mas boj jumi Rabdomiol ze Nieru un ur nce u trauc jumi Ur na aizture Reprodukt v s sist mas un kr ts slim bas Priapisms Visp r ji trauc jumi un reakcijas ievad šanas viet Ast nija Nogurums T ska Izmekl jumi Paaugstin ts proakt na l menis plazm 8 1
High creatine phosphokinase Increased total bilirubin
Augsts kreat nfosfokin zes l menis Paaugstin ts kop j bilirub na l menis
Increased alkaine phosphatase
Paaugstin ts s rmain s fosfat zes l menis
Patients gaining 25% of their baseline body weight with long-term exposure were very common.
Tika nov rota kl niski noz m ga erme a masas palielin šan s vis s s kotn j erme a masas indeksa (MI) kategorij s. erme a masas palielin šan s 7% no s kotn j s erme a masas bija oti bieži un 15% no s kotn j s erme a masas – bieži. oti bieži pacientiem, kuri prepar tu lietoja ilgstoši, erme a masas palielin šan s bija par 25% no s kotn j s erme a masas.
2 Mean increases in fasting lipid values (total cholesterol, LDL cholesterol, and triglycerides) were greater in patients without evidence of lipid dysregulation at baseline.
2 Lip du (kop j holester na, ZBL holester na un triglicer du) l me a tukš d š vid j palielin šan s bija liel ka pacientiem bez lip du l me a p rmai m p t juma s kum.
3 Observed for fasting normal levels at baseline (< 5.17 mmol/ l) which increased to high (6.2 mmol/ l).
3 Nov rots norm ls l menis tukš d š p t juma s kum (< 5, 17 mmol/ l), kas palielin j s l dz augstam (6, 2 mmol/ l).
Changes in total fasting cholesterol levels from borderline at baseline (5.17- < 6.2 mmol/ l) to high (6.2 mmol/ l) were very common.
Kop j holester na l me a tukš d š p rmai as no robežv rt bas p t juma s kum (5, 17 - < 6, 2 mmol/ l) l dz augstam (6, 2 mmol/ l) bija oti bieži.
4 Observed for fasting normal levels at baseline (< 5.56 mmol/ l) which increased to high (7 mmol/ l).
4 Nov rots norm ls l menis tukš d š p t juma s kum (< 5, 56 mmol/ l), kas palielin j s l dz augstam (7 mmol/ l).
Changes in fasting glucose from borderline at baseline (5.56 - < 7 mmol/ l) to high (7 mmol/ l) were very common.
Glikozes l me a tukš d š p rmai as no s kotn j lieluma (5, 56 - < 7 mmol/ l) l dz augstam (7 mmol/ l) bija oti bieži.
5 Observed for fasting normal levels at baseline (< 1.69 mmol/ l) which increased to high (2.26 mmol/ l).
5 Nov rots norm ls l menis tukš d š p t juma s kum (< 1, 69 mmol/ l), kas palielin j s l dz augstam (2, 26 mmol/ l).
Changes in fasting triglycerides from borderline at baseline (1.69 mmol/ l - < 2.26 mmol/ l) to high (2.26 mmol/ l) were very common.
Triglicer du l me a tukš d š p rmai as no robežv rt bas p t juma s kum (1, 69 mmol/ l - < 2, 26 mmol/ l) l dz augstam (2, 26 mmol/ l) bija oti bieži.
6 In clinical trials, the incidence of parkinsonism and dystonia in olanzapine-treated patients was numerically higher, but not statistically significantly different from placebo.
9 6 Kl niskajos p t jumos ar olanzap nu rst tiem pacientiem parkinsonismu un distoniju nov roja skaitliski vair k gad jumos, ta u tas statistiski noz m gi neatš r s no placebo grupas.
Olanzapine-treated patients had a lower incidence of parkinsonism, akathisia and dystonia compared with titrated doses of haloperidol.
Ar olanzap nu rst tiem pacientiem ret k nek ar titr tu haloperidola devu rst tiem pacientiem nov roja parkinsonismu, akat ziju un distoniju.
In the absence of detailed information on the pre-existing history of individual acute and tardive extrapyramidal movement disorders, it can not be concluded at present that olanzapine produces less tardive dyskinesia and/ or other tardive extrapyramidal syndromes.
T k nav detaliz tas inform cijas par ak tiem un tard viem ekstrapiramid liem kust bu trauc jumiem individu l s pacientu anamn z s, pašlaik nav iesp jams secin t, ka olanzap ns maz k izraisa tard vo diskin ziju un/ vai citus tard vus ekstrapiramid lus sindromus.
9 7 Acute symptoms such as sweating, insomnia, tremor, anxiety, nausea and vomiting have been reported when olanzapine is stopped abruptly.
7 P c p kš as olanzap na lietošanas p rtraukšanas zi ots par t diem ak tiem simptomiem k sv šana, bezmiegs, tr ce, trauksme, slikta d ša vai vemšana.
8 Associated clinical manifestations (e. g., gynaecomastia, galactorrhoea, and breast enlargement) were rare.
8 Saist t s kl nisk s izpausmes (piem., ginekomastija, galaktoreja un kr šu palielin šan s) bija retas.
In most patients, levels returned to normal ranges without cessation of treatment.
Vairumam pacientu l menis normaliz j s, nep rtraucot rst šanu.
Long-term exposure (at least 48 weeks) The proportion of patients who had adverse, clinically significant changes in weight gain, glucose, total/ LDL/ HDL cholesterol or triglycerides increased over time.
Ilgstoša lietošana Laika gait palielin j s to pacientu patsvars, kuriem tika konstat tas nelabv l gas, kl niski noz m gas svara, k ar glikozes, kop j / ZBL/ ABL holester na vai triglicer du l me a palielin šan s izmai as.
In adult patients who completed 9-12 months of therapy, the rate of increase in mean blood glucose slowed after approximately 4-6 months.
Pieaugušajiem p c 9- 12 m nešu rstniec bas kursa vid j glikozes l me a asin s palielin šan s k uva l n ka p c aptuveni 4- 6 m nešiem.
Additional information on special populations In clinical trials in elderly patients with dementia, olanzapine treatment was associated with a higher incidence of death and cerebrovascular adverse reactions compared to placebo (see section 4.4).
Papildu inform cija par paš m pacientu grup m Kl niskos p t jumos gados veciem pacientiem ar demenci olanzap na lietošana tika saist ta ar liel ku miršanas gad jumu skaitu un cerebrovaskul r m probl m m sal dzin jum ar placebo (skat t ar apakšpunktu 4. 4). oti bieži (> 10%) šiem pacientiem saist b ar olanzap na lietošanu nov rot s blakuspar d bas bija patolo iska gaita un krišana.
Very common adverse reactions associated with the use of olanzapine in this patient group were abnormal gait and falls.
Bieži (1 – 10%) tika nov rota pneimonija, paaugstin ta erme a temperat ra, letar ija, erit ma, redzes halucin cijas un ur na nesatur šana.
In clinical trials in patients with drug-induced (dopamine agonist) psychosis associated with Parkinson’ s disease, worsening of Parkinsonian symptomatology and hallucinations were reported very commonly and more frequently than with placebo.
Kl niskos p t jumos pacientiem ar z u (dopam na agonista) izrais tu psihozi Parkinsona slim bas gad jum oti bieži, un biež k nek lietojot placebo, zi ots par parkinsonisma simptomu pastiprin šanos un halucin cij m.
In one clinical trial in patients with bipolar mania, valproate combination therapy with olanzapine resulted in an incidence of neutropenia of 4.1%; a potential contributing factor could be high plasma valproate levels.
Iesp jamais veicinošais faktors var tu b t augsts valpro ta l menis plazm.
Olanzapine administered with lithium or valproate resulted in increased levels (≥ 10%) of tremor, dry mouth, increased appetite, and weight gain.
Olanzap ns, lietots kop ar litiju vai valpro tu, biež k (> 10%) izrais ja tr ci, mutes sausumu, pastiprin tu stgribu un erme a masas palielin šanos.
During treatment with olanzapine in combination with lithium or divalproex, an increase of ≥ 7% from baseline body weight occurred in 17.4% of patients during acute treatment (up to 6 weeks).
Bieži tika zi ots ar par runas trauc jumiem (1 – 10%). rst šanas laik ar olanzap nu kombin cij ar litiju vai divalproeksu, 17, 4% pacientu ak t s rst šanas f z (l dz 6 ned m) erme a masa sal dzin jum ar s kotn jo palielin j s par > 7%.
Long-term olanzapine treatment (up to 12 months) for recurrence prevention in patients with bipolar disorder was associated with an increase of ≥ 7% from baseline body weight in 39.9% of patients.
Ilgstoša olanzap na terapija (l dz 12 m nešiem) recid vu profilaksei 39, 9% pacientiem ar bipol riem trauc jumiem bija saist ta ar erme a masas palielin šanos par > 7% sal dzin jum ar s kotn jo.
Children and adolescents Olanzapine is not indicated for the treatment of children and adolescent patients below 18 years.
B rni un pusaudži Olanzap ns nav indic ts b rnu un pusaudžu l dz 18 gadu vecumam rst šanai.
Although no clinical studies designed to compare adolescents to adults have been conducted, data from the adolescent trials were compared to those of the adult trials.
Lai ar nav veikti kl niskie p t jumi, lai sal dzin tu pusaudžus un pieaugušos, p t jumos ar pusaudžiem ieg t inform cija tika sal dzin ta ar inform ciju, kura tika ieg ta p t jumos ar pieaugušajiem.
The following table summarises the adverse reactions reported with a greater frequency in adolescent patients (aged 13-17 years) than in adult patients or adverse reactions only identified during short- term clinical trials in adolescent patients.
Zem k esošaj tabul ir apkopotas blakuspar d bas par kur m biež k zi ots saist b ar pusaudžiem (vecum no 13 l dz 17 gadiem), sal dzinot ar pieaugušajiem, k ar blakuspar d bas, kuras tika konstat tas tikai slaic gos kl niskajos p t jumos ar pusaudžiem.
The magnitude of weight gain and the proportion of adolescent patients who had clinically significant weight gain were greater with long-term exposure (at least 24 weeks) than with short-term exposure.
Kl niski noz m ga erme a masas palielin šan s (7%) ir biež k nov rojama pusaudžiem, sal dzinot ar pieaugušajiem, kuri prepar tu lietoja l dz gi ilgi. erme a masas palielin šan s apjoms un to pusaudžu patsvars, kuriem bija kl niski noz m ga erme a masas palielin šan s, bija liel ks, ja prepar ts tika lietots ilgstoši (vismaz 24 ned as) (sal dzin jum ar slaic gu lietošanu).
Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness.
Katr biežuma grup blakuspar d bas ir uzskait tas to nopietn bas pak pes samazin juma sec b.
Very common (10%), common (1% and < 10%).
Biežuma kategorijas ir š das: oti bieži (10%), bieži (no 1% l dz < 10%).
Common:
10 Metabolisma un barošan s trauc jumi oti bieži: svara pieaugums9, paaugstin ts triglicer du l menis10, pastiprin ta stgriba.
Sedation (including: hypersomnia, lethargy, somnolence).
Bieži: paaugstin ts holester na l menis11 Nervu sist mas trauc jumi oti bieži: sed cija (t. sk. hypersomnia, letar ija, miegain ba).
Elevations of hepatic transaminases (ALT/ AST; see section 4.4).
Ku a- zarnu trakta trauc jumi Bieži: sausa mute Aknu un/ vai žultsce u trauc jumi oti bieži: paaugstin ts aknu transamin žu (AlAT/ AsAT) l menis (skat t apakšpunktu 4. 4).
Decreased total bilirubin, increased GGT, elevated plasma prolactin levels12.
Izmekl jumi oti bieži: pazemin ts kop j bilirub na l menis, paaugstin ts GGT, paaugstin ts prolakt na l menis plazm 12.
9 Weight gain 7% of baseline body weight (kg) was very common and 15% of baseline body weight was common.
9 Svara pieaugums par 7% no erme a masas (kg) p t juma s kum bija oti bieži, un par 15% no erme a masas p t juma s kum bija bieži.
With long-term exposure (at least 24 weeks), approximately half of adolescent patients gained 15% and almost a third gained 25% of their baseline body weight.
Lietojot prepar tu ilgstoši (vismaz 24 ned as), aptuveni pusei pusaudžu vecuma pacientu erme a masas palielin šan s bija par 15%, bet gandr z trešda ai – par 25% no erme a masas p t juma s kum.
Among adolescent patients, mean weight gain was greatest in patients who were overweight or obese at baseline.
Pacientiem pusaudžu vecum vid j erme a masas palielin šan s bija visizteikt k tiem pacientiem, kuri bija ar lieko svaru vai aptaukošanos p t juma s kum.
10 Observed for fasting normal levels at baseline (< 1.016 mmol/ l) which increased to high (1.467 mmol/ l) and changes in fasting triglycerides from borderline at baseline (1.016 mmol/ l - < 1.467 mmol/ l) to high (1.467 mmol/ l).
10 Nov rots norm ls l menis tukš d š p t juma s kum (< 1, 016 mmol/ l), kas palielin j s l dz augstam (1, 467 mmol/ l) un triglicer du l me a tukš d š p rmai as no robežv rt bas p t juma s kum (1, 016 - < 1, 467 mmol/ l) l dz augstam (1, 467 mmol/ l).
Changes in total fasting cholesterol levels from borderline at baseline (4.39 - < 5.17 mmol/ l) to high (5.17 mmol/ l) were very common.
11 Bieži tika konstat tas kop j holester na l me a tukš d š izmai as no norm la p t juma s kum (< 4, 39 mmol/ l) l dz augstam (5, 17 mmol/ l). oti bieži tika konstat tas kop j holester na l me a tukš d š izmai as no robežv rt bas p t juma s kum (4, 39 - < 5, 17 mmol/ l) l dz augstam (5, 17 mmol/ l).
12 Elevated plasma prolactin levels were reported in 47.4% of adolescent patients.
12 Par paaugstin tu prolakt na l meni plazm tika zi ots 47, 4% pusaudžu.
Signs and symptoms Very common symptoms in overdose (> 10% incidence) include tachycardia, agitation/ aggressiveness, dysarthria, various extrapyramidal symptoms, and reduced level of consciousness ranging from sedation to coma.
Paz mes un simptomi oti bieži v rojami simptomi (> 10% gad jumu) p rdoz šanas gad jum ir tahikardija, uzbudin jums/ agresivit te, dizartrija, daž di ekstrapiramid li simptomi un pazemin ts apzi as l menis, kas vari no sed cijas l dz komai.
Other medically significant sequelae of overdose include delirium, convulsion, coma, possible neuroleptic malignant syndrome, respiratory depression, aspiration, hypertension or hypotension, cardiac arrhythmias (< 2% of overdose cases) and cardiopulmonary arrest.
Citas medic niski noz m gas p rdoz šanas sekas ir del rijs, krampji, koma, iesp jams aundab gais neiroleptiskais sindroms, elpošanas nom kums, aspir cija, hipertensija vai hipotensija, sirds aritmijas (< 2% p rdoz šanas gad jumu) un sirds un plaušu funkcijas p rtraukšana.
Fatal outcomes have been reported for acute overdoses as low as 450 mg but survival has also been reported following acute overdose of 1,500 mg.
Ak tas p rdoz šanas gad jum par let lu izn kumu zi ots pat tikai p c 450 mg lietošanas, ta u zi ots ar par izdz vošanu p c ak tas 1500 mg p rdoz šanas.
Management of overdose There is no specific antidote for olanzapine.
P rdoz šanas rst šana Olanzap nam nav specifiska antidota.
Induction of emesis is not recommended.
Nav ieteicams ierosin t vemšanu.
Standard procedures for management of overdose may be indicated (i. e. gastric lavage, administration of activated charcoal).
Var b t indic tas standarta p rdoz šanas rst šanas proced ras (t. i., ku a skalošana, aktiv t s ogles lietošana).
The concomitant administration of activated charcoal was shown to reduce the oral bioavailability of olanzapine by 50 to 60%.
Vienlaikus aktiv t s ogles lietošana mazina olanzap na biolo isko pieejam bu p c peror las lietošanas par 50 – 60%.
Symptomatic treatment and monitoring of vital organ function should be instituted according to clinical presentation, including treatment of hypotension and circulatory collapse and support of respiratory function.
emot v r kl nisko ainu, j s k simptom tiska rst šana un dz v bai svar go org nu funkcijas kontrole, to vid hipotensijas un asinsrites kolapsa rst šana un elpošanas uztur šana.
Do not use epinephrine, dopamine, or other sympathomimetic agents with beta- agonist activity since beta stimulation may worsen hypotension.
Nelietojiet epinefr nu, dopam nu vai citus simpatomim tiskus l dzek us ar beta agonista darb bu, jo beta receptoru stimul cija var pastiprin t hipotensiju.
Close medical supervision and monitoring should continue until the patient recovers.
J veic sirds un asinsvadu sist mas nep rtraukta nov rošana, lai
11 5.
11 noteiktu iesp jamas aritmijas rašanos.
Pharmacotherapeutic group: antipsychotic, ATC code:
Farmakoterapeitisk grupa: antipsihotisks l dzeklis, AT kods:
Olanzapine is an antipsychotic, antimanic and mood stabilising agent that demonstrates a broad pharmacologic profile across a number of receptor systems.
Olanzap ns ir antipsihotisks, pretm nijas un garast vokli stabiliz jošs l dzeklis, kam piem t plaša farmakolo iska iedarb ba uz daudz m receptoru sist m m.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki; < 100 nM) for serotonin 5HT2A/ 2C, 5HT3, 5HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors m1-m5; α 1 adrenergic; and histamine H1 receptors.
Pirmskl niskos p t jumos olanzap ns izr d ja afinit ti (Ki < 100 nM) pret seroton na 5- HT2A/ 2C, 5HT3, 5HT6 receptoriem, dopam na D1, D2, D3, D4, D5 receptoriem, muskar njut giem hol ner iskiem M1- 5 receptoriem, α1 adrenoreceptoriem un histam na H1 receptoriem.
Animal behavioral studies with olanzapine indicated 5HT, dopamine, and cholinergic antagonism, consistent with the receptor-binding profile.
Dz vnieku uzved bas p t jumos ar olanzap nu tika atkl ts 5HT, dopam na un hol ner isks antagonisms atbilstoši z u saist bai ar receptoriem.
Olanzapine demonstrated a greater in vitro affinity for serotonin 5HT2 than dopamine D2 receptors and greater 5HT2 than D2 activity in vivo, models.
Olanzap nam in vitro bija rakstur ga liel ka afinit te pret seroton na 5HT2 receptoriem, sal dzinot ar afinit ti pret dopam na D2 receptoriem, k ar in vivo mode os liel ka 5HT2 aktivit te, sal dzinot ar D2 aktivit ti.
Electrophysiological studies demonstrated that olanzapine selectively reduced the firing of mesolimbic (A10) dopaminergic neurons, while having little effect on the striatal (A9) pathways involved in motor function.
Elektrofiziolo iskie p t jumi pier d ja, ka olanzap ns selekt vi mazina mezolimbisko (A10) dopam ner isko neironu uzbudin m bu, un tam ir neliela ietekme uz striat liem (A9) meh nismiem, kas saist ti ar kust bu funkcij m.
Olanzapine reduced a conditioned avoidance response, a test indicative of antipsychotic activity, at doses below those producing catalepsy, an effect indicative of motor side-effects.
Olanzap ns mazin ja nosac tu aizsargreakciju (tests, kas liecina par antipsihotisko aktivit ti), lietojot to t d s maz k s dev s, kas neizraisa katalepsiju – izpausmi, kas liecina par motor m blakuspar d b m.
Unlike some other antipsychotic agents, olanzapine increases responding in an “ anxiolytic” test.
Atš ir b no dažiem citiem antipsihotiskiem l dzek iem olanzap ns pastiprina atbildes reakciju “ anksiol tisk ” p rbaud.
In a single oral dose (10 mg) Positron Emission tomography (PET) study in healthy volunteers, olanzapine produced a higher 5HT2A than dopamine D2 receptor occupancy.
Pozitronu pl smas tomogr fijas (PPT) p t jum veseliem br vpr t giem cilv kiem p c vienreiz jas peror las devas (10 mg) lietošanas tika atkl ts, ka olanzap ns vair k saista 5HT2A receptorus, sal dzinot ar dopam na D2 receptoriem.
In addition, a Single Photon Emission Computed Tomography (SPECT) imaging study in schizophrenic patients revealed that olanzapine-responsive patients had lower striatal D2 occupancy than some other antipsychotic- and risperidone-responsive patients, while being comparable to clozapine-responsive patients.
Turkl t SPECT (Single Photon Emission Computed Tomography) p t jum šizofr nijas pacientiem tika atkl ts, ka pacientiem, kam olanzap ns rada uzlabošanos, bija maz k izteikta striat lo D2 receptoru saist šana, sal dzinot ar dažiem citiem pacientiem, kam uzlabošanos rad ja citi antipsihotiskie l dzek i vai risperidons, ta u pacientu grup, kam uzlabošanos rada klozap ns, rezult ti bija sal dzin mi.
In two of two placebo and two of three comparator controlled trials with over 2,900 schizophrenic patients presenting with both positive and negative symptoms, olanzapine was associated with statistically significantly greater improvements in negative as well as positive symptoms.
Divos no diviem ar placebo kontrol tiem p t jumiem un divos no trim ar sal dzin mu medikamentu kontrol tiem p t jumiem, kuros piedal j s vair k nek 2900 šizofr nijas pacientu, kam bija rakstur gi gan “ pozit vi ”, gan “ negat vi ” simptomi, olanzap ns izrais ja statistiski daudz izteikt ku gan “ negat vo ”, gan “ pozit vo ” simptomu mazin šanos.
In a multinational, double-blind, comparative study of schizophrenia, schizoaffective, and related disorders which included 1,481 patients with varying degrees of associated depressive symptoms (baseline mean of 16.6 on the Montgomery-Asberg Depression Rating Scale), a prospective secondary analysis of baseline to endpoint mood score change demonstrated a statistically significant improvement (p= 0.001) favouring olanzapine (-6.0) versus haloperidol (-3.1).
Daudznacion l, dubultakl, sal dzinoš p t jum par šizofr niju, šizoafekt viem un ar tiem saist tiem trauc jumiem, kur piedal j s 1481 pacients ar daž das pak pes asoci tas depresijas simptomiem (s kumst vokl vid ji 16, 6 p c Montgomery- Asberg Depresijas v rt juma skalas), garast vok a p rmai u s kotn jo un beigu rezult tu sekund ras anal zes pier d ja statistiski noz m gu uzlabošanos (p=0, 001) un olanzap na (- 6, 0) p r kumu, sal dzinot ar haloperidolu (- 3, 1).
In patients with a manic or mixed episode of bipolar disorder, olanzapine demonstrated superior efficacy to placebo and valproate semisodium (divalproex) in reduction of manic symptoms over 3 weeks.
Pacientiem ar m nijas vai jauktu bipol ru trauc jumu epizodi olanzap ns efekt v k par placebo un valpro ta semin trija s li (divalproeksu) mazin ja m nijas simptomus 3 ned u laik.
Olanzapine also demonstrated comparable efficacy results to haloperidol in terms of the proportion of patients in symptomatic remission from mania and depression at 6 and 12 weeks.
Olanzap nam nov roja ar haloperidola efektivit tei l dz gus rezult tus pacientu da as zi, kam p c 6 un 12 ned m bija simptom tiska m nijas un depresijas remisija.
In a co-therapy study of patients treated with lithium or valproate for a minimum of 2 weeks, the addition of olanzapine 10 mg (co-therapy with lithium or valproate) resulted in a greater reduction in symptoms of mania than lithium or valproate monotherapy after 6 weeks.
Papildterapijas p t jum ar litiju vai valpro tu vismaz 2 ned as rst tiem pacientiem 10 mg olanzap na pievienošana terapijai (kombin ta terapija ar litiju vai valpro tu) izrais ja lab ku m nijas simptomu mazin šanos p c 6 ned m nek litija vai valpro ta monoterapija.
In a 12-month recurrence prevention study in manic episode patients who achieved remission on olanzapine and were then randomised to olanzapine or placebo, olanzapine demonstrated statistically significant superiority over placebo on the primary endpoint of bipolar recurrence.
12 m nešu recid vu profilakses p t jum pacientiem m nijas epizod, kam ar olanzap nu tika sasniegta remisija un kas tad tika nejaušin ti iedal ti olanzap na vai placebo terapijai, olanzap ns statistiski lab k nek placebo ietekm ja prim ros bipol ru trauc jumu recid va raksturlielumus.