natgillin/translations-raw huggingface dataset:
Patienter behandlet med olanzapin havde en lavere forekomst af parkinsonisme, akatisi og dystoni sammenlignet med titrerede doser haloperidol.
Olanzapine-treated patients had a lower incidence of parkinsonism, akathisia and dystonia compared with titrated doses of haloperidol.
På grund af manglende detaljeret information om tidligere individuelle akutte og tardive ekstrapyramidale bevægelsesforstyrrelser, kan det for nuværende ikke konkluderes, at olanzapin forårsager mindre tardiv dyskinesi og/ eller andre tardive ekstrapyramidale syndromer.
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.
8 Associerede kliniske manifestationer (f. eks. gynækomasti, galaktoré og brystforstørrelse) var sjældne.
8 Associated clinical manifestations (e. g., gynaecomastia, galactorrhoea, and breast enlargement) were rare.
Hos de fleste patienter vendte niveauerne tilbage til normalområdet uden ophør af behandling.
In most patients, levels returned to normal ranges without cessation of treatment.
Langvarig eksposition (mindst 48 uger) Andelen af patienter, som fik kritisk, klinisk signifikante ændringer i vægtøgning, glucose, total/ LDL/ HDL- cholesterol eller triglycerider, blev forøget over tid.
Long-term exposure (at least 48 weeks) The proportion of patients who had adverse, clinically significant changes in weight gain, glucose, total/ LDL/ HCL cholesterol or triglycerides increased over time.
4- 6 måneder.
In adult patients who completed 9-12 months of therapy, the rate of increase in mean blood glucose slowed after approximately 4-6 months.
4. 4).
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 also section 4.4).
Meget almindelige bivirkninger i forbindelse med brugen af olanzapin til denne patientgruppe var
Very common adverse reactions associated with the use of olanzapine in this patient group were abnormal gait and falls.
I kliniske forsøg med patienter med lægemiddelinduceret psykose (dopaminagonist) i forbindelse med Parkinsons sygdom, blev der rapporteret forværring af Parkinson symptomatologi og hallucinationer meget almindeligt og hyppigere end med placebo.
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.
En potentielt medvirkende faktor kunne være høje niveauer af valproat i plasma.
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.
Olanzapin administreret sammen med lithium eller valproat resulterede i øgede værdier (≥ 10%) af rysten, mundtørhed, øget appetit og øget vægt.
Olanzapine administered with lithium or valproate resulted in increased levels (≥ 10%) of tremor, dry mouth, increased appetite, and weight gain.
Under behandling med olanzapin sammen med lithium eller valproat forekom en stigning på ≥ 7% af baseline legemsvægt hos 17, 4% af patienterne ved akut behandling (op til 6 uger).
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).
Langvarig olanzapinbehandling (op til 12 måneder) forebyggende mod tilbagefald hos patienter med bipolær sygdom blev forbundet med en stigning på ≥7% af baseline legemsvægt hos 39, 9% af patienterne.
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.
Børn og unge Olanzapin er ikke godkendt til behandling af børn og unge under 18 år.
9 Children and adolescents Olanzapine is not indicated for the treatment of children and adolescent patients below 18 years.
Klinisk signifikant vægtøgning (≥ 7%) synes at forekomme hyppigst i den unge population sammenlignet med ældre med sammelignelig eksposition.
Clinically significant weight gain (≥ 7%) appears to occur more frequently in the adolescent population compared to adults with comparable exposures.
Størrelsen af vægtøgning og andelen af unge patienter, som havde klinisk signifikant vægtøgning, var større ved langvarig eksposition (mindst 24 uger) end ved kortvarig eksposition.
The magnitude of weight gain and the propotion of adolescent patients who had clinically significant weight gain were greater with long-term exposure (at least 24 weeks) than with short-term exposure.
Meget almindelig (≥ 10%), almindelig (≥ 1% og < 10%).
Very common (≥ 10%), common (≥ 1% and < 10%).
Øget vægt9, forhøjede triglyceridniveauer10, øget appetit..
Weight gain9, elevated triglyceride levels10, increased appetite.
Forhøjede kolesterolniveauer11 Nervesystemet Meget almindelig:
Elevated cholesterol levels11 Nervous system disorders Very common:
Sedation (inklusive: hypersomni, letargi, somnolens).
Sedation (including: hypersomnia, lethargy, somnolence).
Mundtørhed Lever og galdeveje Meget almindelig:
Dry mouth Hepato-biliary disorders Very common:
4. 4).
Elevations of hepatic transaminases (ALT/ AST; see section 4.4).
Nedsat total bilirubin, øget GGT, forhøjede niveauer af plasmaprolaktin12.
Decreased total bilirubin, increased GGT, elevated plasma prolactin levels12.
9 Øget vægt ≥ 7% af baseline legemsvægt (kg) var meget almindelig og ≥ 15% af baseline legemsvægt var almindelig.
9 Weight gain ≥ 7% of baseline body weight (kg) was very common and ≥ 15% of baseline body weight was common.
Ved langvarig eksposition (mindst 24 uger) tog ca. halvdelen af de unge patienter ≥ 15% og næsten en tredjedel ≥ 25% af deres baseline kropsvægt på.
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.
Blandt de unge patienter var den gennemsnitlige vægtøgning størst hos de patienter, som var overvægtige eller fede ved baseline.
Among adolescent patients, mean weight gain was greatest in patients who were overweight or obese at baseline.
10 Observerede normalniveauer ved faste ved baseline (< 1. 016 mmol/ l, som steg til (≥ 1. 467 mmol/ l) og ændringer i triglycerider ved faste fra grænser ved baseline (≥ 1. 016 mmol/ l - < 1. 467 mmol/ l) op til (≥ 1. 467 mmol/ l).
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 11 Ændringer i de totale kolesterolniveauer ved faste fra normale ved baseline (< 4. 39 mmol/ l) op til (≥ 5. 17 mmol/ l) blev observeret almindeligt.
11 Changes in total fasting cholesterol levels from normal at baseline (< 4.39 mmol/ l) to high (≥ 5.17 mmol/ l) were observed commonly.
Ændringer i de totale kolesterolniveauer ved faste fra grænser ved baseline (≥ 4. 39 - < 5. 17 mmol/ l) op til (≥ 5. 17 mmol/ l) var meget almindeligt.
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.
12 Forhøjede plasmaprolaktinniveauer blev rapporteret hos 47% af de unge patienter.
12 Elevated plasma prolactin levels were reported in 47.4% of adolescent patients.
Tegn og symptomer Meget almindelige symptomer på overdosering (forekomst > 10%) inkluderer takykardi, agitation/ aggressivitet, dysartri, forskellige ekstrapyramidale symptomer og nedsat bevidsthedsniveau, varierende fra sedation til koma.
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.
Andre medicinsk signifikante sequelae efter overdosering inkluderer delirium, kramper, koma, muligt malignt neuroleptikasyndrom, respirationsbesvær, aspiration, hypertension eller hypotension, hjertearytmi (< 2% af overdoseringstilfældene) og kardiopulmonært ophør.
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.
Dødelig udgang er rapporteret efter akut overdosering med ned til 450 mg, men overlevelse er også rapporteret efter akut overdosering med 1500 mg.
Fatal outcomes have been reported for acute overdoses as low as 450mg but survival has also been reported following acute overdose of 1,500 mg.
Behandling af overdosering Der er ingen specifik antidot til olanzapin.
Management of overdose 10 There is no specific antidote for olanzapine.
Standard procedurer til behandling af overdosering kan være indiceret (fx ventrikelskylning, administration af aktivt kul).
Standard procedures for management of overdose may be indicated (i. e. gastric lavage, administration of activated charcoal).
Samtidig administration af aktivt kul har vist at nedsætte den perorale biotilgængelighed af olanzapin med 50- 60%.
The concomitant administration of activated charcoal was shown to reduce the oral bioavailability of olanzapine by 50 to 60%.
Brug ikke adrenalin, dopamin eller andre sympatomimetiske midler med beta - agonist aktivitet, da beta- stimulation kan forværre hypotension.
Do not use epinephrine, dopamine, or other sympathomimetic agents with beta agonist activity since beta stimulation may worsen hypotension.
Antipsykotikum, ATC- kode:
Diazepines, oxazepines and thiazepines, ATC code:
I prækliniske undersøgelser udviste olanzapin affinitet (Ki; < 100 nM) til serotonin 5 HT2A/ 2C, 5 HT3, 5 HT6, dopamin D1, D2, D3, D4, D5, kolinerge muskarine receptorer m1- m5, α1- adrenerge og histamin H1 receptorer.
In preclinical studies, olanzapine exhibited a range of receptor affinities (Ki; < 100 nM) for serotonin 5 HT2A/ 2C, 5 HT3, 5 HT6; dopamine D1, D2, D3, D4, D5; cholinergic muscarinic receptors m1-m5; α 1 adrenergic; and histamine H1 receptors.
Dyreadfærdsundersøgelser af olanzapin indikerede 5 HT, dopamin og kolinerg antagonisme i overensstemmelse med receptorbindingsprofilen.
Animal behavioral studies with olanzapine indicated 5HT, dopamine, and cholinergic antagonism, consistent with the receptor-binding profile.
Olanzapin udviste større affinitet til serotonin 5HT2 end til dopamin D2 receptorerne i in vitro undersøgelser og større 5 HT2 - end D2 - aktivitet i in vivo modeller.
Olanzapine demonstrated a greater in vitro affinity for serotonin 5HT2 than dopamine D2 receptors and greater 5 HT2 than D2 activity in vivo, models.
Olanzapin hæmmede et klassisk betinget respons (conditioned avoidance response), en test der indikerer antipsykotisk aktivitet, ved lavere doser end de, der frembringer katalepsi, en effekt der indikerer motoriske bivirkninger.
Olanzapine reduced a conditioned avoidance response, a test indicative of antipsychotic activity, at doses below those producing catalepsy, an effect indicative of motor undesirable-effects.
I modsætning til visse andre antipsykotika øger olanzapin responset ved en "anxiolytisk" test.
Unlike some other antipsychotic agents, olanzapine increases responding in an “ anxiolytic” test.
I en enkeltdosis (10 mg) Positron Emission Tomography (PET) undersøgelse hos raske forsøgspersoner bandt olanzapin til flere 5HT2A end til dopamin D2 receptorer.
In a single oral dose (10 mg) Positron Emission tomography (PET) study in healthy volunteers, olanzapine produced a higher 5 HT2A than dopamine D2 receptor occupancy.
Desuden afslørede en 11 SPECT undersøgelse af skizofrene patienter, at olanzapin- responderende patienter havde en lavere striatal D2- binding end visse andre antipsykotika - og risperidon- responderende patienter, hvorimod det var sammenligneligt med clozapin- responderende patienter.
In addition, a 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.
I 2 ud af 2 placebo - og 2 ud af 3 komparatorkontrollerede undersøgelser af mere end 2. 900 skizofrene patienter med både positive og negative symptomer blev olanzapin forbundet med statistisk signifikante større forbedringer af negative såvel som af positive symptomer.
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.
Undersøgelsen viste en prospektiv sekundær analyse af ændring i stemningslejeniveauet fra før behandling til endt behandling en statistisk signifikant forbedring (p=0, 001) til fordel for patienter behandlet med olanzapin (- 6, 0) i forhold til patienter behandlet med haloperidol (- 3, 1).
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).
I en undersøgelse af patienter i behandling med lithium eller valproat i minimum 2 uger medførte samtidig behandling med olanzapin 10 mg (kombinationsterapi med lithium eller valproat) en større reduktion af symptomerne på mani efter 6 uger end ved lithium - eller valproat- monoterapi.
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.
Olanzapin viste sig statistisk signifikant overlegen overfor placebo på det primære slutpunkt for bipolære tilbagefald.
11 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.
Olanzapin viste sig ikke ringere end lithium på det primære slutpunkt for bipolære tilbagefald (olanzapin 30, 0%, lithium 38, 3%; p = 0, 055)
In a second 12 month recurrence prevention study in manic episode patients who achieved remission with a combination of olanzapine and lithium and were then randomised to olanzapine or lithium alone, olanzapine was statistically non-inferior to lithium on the primary endpoint of bipolar recurrence (olanzapine 30.0%, lithium 38.3%; p = 0.055).
I et 18 måneders co- terapi studie af maniske eller blandede episoder hos patienter stabiliseret med olanzapin samt en stemningsstabilisator (lithium eller valproat), viste langtids olanzapin co- terapi med lithium eller valproat sig ikke statistisk signifikant overlegen overfor lithium eller valproat alene i forsinkelse bipolære tilbagefald, defineret i overensstemmelse med det syndromiske (diagnostiske) kriterium.
In an 18-month co-therapy study in manic or mixed episode patients stabilised with olanzapine plus a mood stabiliser (lithium or valproate), long-term olanzapine co-therapy with lithium or valproate was not statistically significantly superior to lithium or valproate alone in delaying bipolar recurrence, defined according to syndromic (diagnostic) criteria.
Pædiatrisk population Erfaringen med unge (alder 13 – 17 år) omfatter mindre end 200 unge og er begrænset til kortvarige effektdata ved skizofreni (6 uger) og mani i forbindelse med bipolar I- sygdom (3 uger).
Paediatric population The experience in adolescents (ages 13 to 17 years) is limited to short term efficacy data in schizophrenia (6 weeks) and mania associated with bipolar I disorder (3 weeks), involving less than 200 adolescents.
Olanzapin blev brugt i en fleksibel dosis, som begyndte med 2, 5 mg, og som gik op til 20 mg daglig.
Olanzapine was used as a flexible dose starting with 2.5 and ranging up to 20 mg/ day.
4. 4 og 4. 8) var større hos unge end hos voksne.
The magnitude of changes in fasting total cholesterol, LDL cholesterol, triglycerides, and prolactin (see sections 4.4 and 4.8) were greater in adolescents than in adults.
4. 4 og 4. 8).
There are no data on maintenance of effect and limited data on long term safety (see sections 4.4 and 4.8).
12 Olanzapin metaboliseres i leveren via konjugering og oxidation.
Olanzapine is metabolized in the liver by conjugative and oxidative pathways.
Den overvejende cirkulerende metabolit er 10- N- glucuronid, som ikke passerer blod- hjerne barrieren.
The major circulating metabolite is the 10-N-glucuronide, which does not pass the blood brain barrier.
Cytochrom P450- CYP1A2 og P450- CYP2D6 bidrager til dannelsen af N- desmethyl og 2- hydroxymethyl metabolitterne, der udviser signifikant mindre in vivo farmakologisk aktivitet end olanzapin i dyreundersøgelser.
Cytochromes P450- CYP1A2 and P450-CYP2D6 contribute to the formation of the N-desmethyl and 2-hydroxymethyl metabolites, both exhibited significantly less in vivo pharmacological activity than olanzapine in animal studies.
Hos raske ældre forsøgspersoner (> 65 år) var den gennemsnitlige eliminationshalveringstid forlænget (51, 8 versus 33, 8 timer) og clearance var reduceret (17, 5 versus 18, 2 l/ time).
In healthy elderly (65 and over) versus non-elderly subjects, the mean elimination half-life was prolonged (51.8 versus 33.8 hr) and the clearance was reduced (17.5 versus 18.2 l/ hr).
Den farmakokinetiske variation hos ældre forsøgspersoner er indenfor variationen hos ikke- ældre.
The pharmacokinetic variability observed in the elderly is within the range for the non-elderly.
Hos 44 patienter > 65 år med skizofreni gav dosering med 5- 20 mg/ dag ingen udsving i bivirkningsprofilen.
In 44 patients with schizophrenia > 65 years of age, dosing from 5 to 20 mg/ day was not associated with any distinguishing profile of adverse events.
Hos kvinder versus mænd var den gennemsnitlige halveringstid en del forlænget (36, 7 versus 32, 3 timer) og clearance reduceret (18, 9 versus 27, 3 l/ time).
In female versus male subjects the mean elimination half life was somewhat prolonged (36.7 versus 32.3 hr) and the clearance was reduced (18.9 versus 27.3 l/ hr).
Olanzapin (5- 20 mg) udviste imidlertid en sammenlignelig sikkerhedsprofil hos kvindelige (n=467) som hos mandlige patienter (n=869).
However, olanzapine (5-20 mg) demonstrated a comparable safety profile in female (n=467) as in male patients (n=869).
Hos patienter med nedsat nyrefunktion (kreatinin clearance < 10 ml/ min) versus raske forsøgspersoner fandtes ingen signifikant forskel i den gennemsnitlige eliminationshalveringstid (37, 7 versus 32, 4 timer) eller clearance (21, 2 versus 25, 0 l/ time).
In renally impaired patients (creatinine clearance < 10 ml/ min) versus healthy subjects, there was no significant difference in mean elimination half-life (37.7 versus 32.4 hr) or clearance (21.2 versus 25.0 l/ hr).
En undersøgelse af den totale omsætning af olanzapin viste imidlertid, at omkring 57% radioaktivt mærket olanzapin genfandtes i urinen, hovedsageligt som metabolitter.
A mass balance study showed that approximately 57% of radiolabelled olanzapine appeared in urine, principally as metabolites.
Hos rygere med let leverfunktionsnedsættelse var den gennemsnitlige eliminationshalveringstid (39, 3 timer) forlænget, og clearance (18, 0 l/ time) reduceret i overensstemmelse med raske ikke- rygende forsøgspersoner (henholdsvis 48, 8 timer og 14, 1 l/ time).
12 In smoking subjects with mild hepatic dysfunction, mean elimination half-life (39.3 hr) was prolonged and clearance (18.0 l/ hr) was reduced analogous to non-smoking healthy subjects (48.8 hr and 14.1 l/ hr, respectively).
Hos ikke- rygere versus rygere (mænd og kvinder) var den gennemsnitlige eliminations halveringstid forlænget (38, 6 versus 30, 4 timer) og clearance reduceret (18, 6 versus 27, 7 l/ time).
In non-smoking versus smoking subjects (males and females) the mean elimination half-life was prolonged (38.6 versus 30.4 hr) and the clearance was reduced (18.6 versus 27.7 l/ hr).
Olanzapins plasmaclearance er lavere hos: ældre end hos yngre personer, kvinder end hos mænd og ikke- rygere end hos rygere.
The plasma clearance of olanzapine is lower in elderly versus young subjects, in females versus males, and in non-smokers versus smokers.
1000 ng/ ml.
The plasma protein binding of olanzapine was about 93% over the concentration range of about 7 to about 1000 ng/ ml.
Olanzapin er overvejende bundet til albumin og orosomukoid (et surt α- glycoprotein).
Olanzapine is bound predominantly to albumin and α 1-acid-glycoprotein.
Pædiatrisk population Unge (alder 13 – 17 år):
Paediatric population Adolescents (ages 13 to 17 years):
Den gennemsnitlige eksponering med olanzapin var i kliniske forsøg ca.
The pharmacokinetics of olanzapine are similar between adolescents and adults.
27% højere hos unge.
In clinical studies, the average olanzapine exposure was approximately 27% higher in adolescents.
Akut (enkelt- dosis) toksicitet Den observerede perorale toksicitet hos gnavere er karakteristisk for potente antipsykotiske lægemiddelstoffer: hypoaktivitet, coma, tremor, kloniske kramper, spytsekretion og hæmmet vægtøgning.
Acute (single-dose) toxicity Signs of oral toxicity in rodents were characteristic of potent neuroleptic compounds: hypoactivity, coma, tremors, clonic convulsions, salivation, and depressed weight gain.
210 mg/ kg (mus) og 175 mg/ kg (rotter).
The median lethal doses were approximately 210 mg/ kg (mice) and 175 mg/ kg (rats).
Hunde tolererede perorale enkeltdoser på op til 100 mg/ kg uden mortalitet.
Dogs tolerated single oral doses up to 100 mg/ kg without mortality.
13 tremor, øget hjertefrekvens, anstrengt respiration, miosis og anoreksi.
Clinical signs included sedation, ataxia, tremors, increased heart rate, labored respiration, miosis, and anorexia.
Hos aber medførte perorale enkelt- doser på op til 100 mg/ kg afkræftelse og højere doser medførte halvt bevidstløs tilstand.
In monkeys, single oral doses up to 100 mg/ kg resulted in prostration and, at higher doses, semi-consciousness.
Toksicitet ved gentagen dosis I undersøgelser af op til 3 måneders varighed af mus og op til 1 års varighed af rotter og hunde var CNS depression, antikolinerge effekter og perifere hæmatologiske forstyrrelser de dominerende effekter.
Repeated-dose toxicity In studies up to 3 months duration in mice and up to 1 year in rats and dogs, the predominant effects were CNS depression, anticholinergic effects, and peripheral haematological disorders.
Hæmatologisk toksicitet:
Haematologic toxicity:
Der sås imidlertid ingen tegn på knoglemarvscytotoksicitet.
Effects on haematology parameters were found in each species, including dose-related reductions in circulating leukocytes in mice and non-specific reductions of circulating leukocytes in rats; however, no evidence of bone marrow cytotoxicity was found.
Reversibel neutropeni, trombocytopeni eller anæmi udvikledes hos enkelte hunde, som blev behandlet med 8 eller 10 mg/ kg/ dag (total olanzapin dosis (AUC) var 12- 15 gange højere end human dosis på 12 mg).
Reversible neutropenia, thrombocytopenia, or anemia developed in a few dogs treated with 8 or 10 mg/ kg/ day (total olanzapine exposure [AUC] is 12- to 15-fold greater than that of a man given a 12 mg dose).
Reproduktiv toksicitet Olanzapin udviste ingen teratogene virkninger.
Reproductive toxicity Olanzapine had no teratogenic effects.