natgillin/translations-raw huggingface dataset:
Atosiban should only be used when pre-term labour has been diagnosed between 24 and 33 completed weeks of gestation.
Atosiban se sme uporabiti le, če je postavljena diagnoza prezgodnjega porajanja med 24 in 33 dopolnjenimi tedni gestacije.
In atosiban clinical trials no effects were observed on lactation.
V kliničnih raziskavah atosibana niso opazili učinkov na dojenje.
Small amounts of atosiban have been shown to pass from plasma into the breast milk of lactating women.
Ugotovljeno je, da majhna količina atosibana preide iz plazme v mleko doječih žensk.
Embryo-fetal toxicity studies have not shown toxic effects of atosiban.
Raziskave embriofetalne toksičnosti niso odkrile toksičnih učinkov atosibana.
No studies were performed that covered fertility and early embryonic development (see section 5.3).
Raziskave, ki bi obsegale vpliv na plodnost in zgodnji embrionalni razvoj niso bile izvedene (glejte poglavje 5. 3).
Possible undesirable effects of atosiban were described for the mother during the use of atosiban in clinical trials.
V kliničnih raziskavah so bili med uporabo atosibana opisani možni neželeni učinki atosibana pri materi.
The observed undesirable effects were generally of a mild severity.
Opaženi neželeni učinki so bili praviloma blagi.
In total 48% of the patients treated with atosiban experienced undesirable effects.
V celoti je doživelo neželene učinke 48% bolnic, ki so dobivale atosiban.
For the newborn, the clinical trials did not reveal any specific undesirable effects of atosiban.
Pri novorojenčkih klinične raziskave niso pokazale nobenih specifičnih neželenih učinkov atosibana.
The infant adverse events were in the range of normal variation and were comparable with both placebo and beta-mimetic group incidences.
Neželeni dogodki pri dojenčkih so bili v območju normalnih variacij in po pogostnosti primerljivi s tistimi v placebni skupini in v skupini z beta- simpatikomimetiki.
4 The undesirable effects in the women were the following:
4 Neželeni učinki pri ženskah so bili:
Very common (> 1/ 10)
Zelo pogosti (> 1/ 10)
Gastrointestinal disorders: nausea.
Bolezni prebavil: navzeja.
Metabolism and nutrition disorders: hyperglycaemia Nervous system disorders: headache, dizziness Cardiac disorders: tachycardia, Vascular disorders: hot flush, hypotension Gastrointestinal disorders: vomiting General disorders and administration site conditions: injection site reaction
Splošne težave in spremembe na mestu aplikacije: reakcija na injekcijskem mestu.
Uncommon (> 1/ 1000, < 1/ 100)
Občasni (> 1/ 1. 000, < 1/ 100) Psihiatrične motnje: nespečnost.
Psychiatric disorders: insomnia Skin and subcutaneous tissue disorders: pruritis, rash General disorders and administration site conditions: pyrexia
Splošne težave in spremembe na mestu aplikacij: zvišana telesna temperatura.
Rare (> 1/ 10,000, < 1/ 1,000)
Redki Opisani so bili posamezni primeri maternične krvavitve oz. atonije (> 1/ 10. 000, < 1/ 1000)
Incidental cases of uterine haemorrhage/ uterine atony were reported.
maternice.
The frequency did not exceed that of the control groups in clinical trials.
Njihova pogostnost ni presegala pogostnosti v kontrolnih skupinah kliničnih raziskav.
One case of allergic reaction was reported, which was considered to be probably related to atosiban.
Opisan je en primer alergijske reakcije, za katero so ocenili, da je verjetno povezana z atosibanom.
Few cases of atosiban overdosing were reported, they occurred without any specific signs or symptoms.
Opisanih je bilo nekaj primerov prevelikega odmerjanja atosibana; pojavili so se brez specifičnih znakov ali simptomov.
There is no known specific treatment in case of an overdose.
Specifično zdravljenje prevelikega odmerjanja ni znano.
Pharmacotherapeutic group:
Farmakoterapevtska skupina: drugi ginekološki pripravki.
Other gynecologicals, ATC code:
Oznaka ATC:
TRACTOCILE contains atosiban (INN), a synthetic peptide ([Mpa1, D-Tyr(Et)2, Thr4, Orn8]-oxytocin) which is a competitive antagonist of human oxytocin at receptor level.
TRACTOSILE vsebuje atosiban (INN), sintetičen peptid ([Mpa1, D- Tyr( Et) 2, Thr4, Orn8] - oksitocin), ki je kompetitiven antagonist človeškega oksitocina na receptorski ravni.
In human pre-term labour, atosiban at the recommended dosage antagonises uterine contractions and induces uterine quiescence.
Pri prezgodnjem porajanju pri človeku atosiban v priporočenem odmerjanju zavira kontrakcije maternice in maternico umiri.
The onset of uterus relaxation following atosiban is rapid, uterine contractions being significantly reduced within 10 minutes to achieve stable uterine quiescence (≤ 4 contractions/ hour) for 12 hours.
Sprostitev maternice se po atosibanu pojavi hitro in kontrakcije se v 10 minutah pomembno zmanjšajo, tako da je dosežena stabilna umiritev maternice (≤ 4 kontrakcije/ uro) za 12 ur.
Phase III clinical trials (CAP-001 studies) include data from 742 women who were diagnosed with pre-term labour at 23– 33 weeks of gestation and were randomised to receive either atosiban (according to this labelling) or β -agonist (dose-titrated).
Klinične raziskave III. faze (raziskave CAP- 001) zajemajo podatke 742 žensk, pri katerih je bilo diagnosticirano prezgodnje porajanje v obdobju od 22. do 33. tedna gestacije in so bile randomizirane na atosiban (v skladu s tem dokumentom) ali β- agonist (odmerno titriran).
5 treatment failures in CAP-001 were caused by poor tolerability.
Glavno merilo učinkovitosti je bil delež žensk, ki niso rodile in v 7 dneh od začetka zdravljenja niso potrebovale alternativne tokolize.
Treatment failures caused by insufficient efficacy were significantly (p=0.0003) more frequent in atosiban (n=48, 14.2%) than in the β -agonist-treated women (n=20, 5.8%).
Podatki kažejo, da ni rodilo in v 7 dneh po začetku zdravljenja ni potrebovalo drugačne tokolize 59, 6% (n = 201) žensk, ki so dobivale atosiban, in 47, 7% (n = 163) žensk, ki so dobivale β- agonist (p = 0, 0004).
In the CAP-001 studies the probability of remaining undelivered and not requiring alternative tocolytics within 7 days of treatment initiation was similar for atosiban and beta-mimetics treated women at gestational age of 24-28 weeks.
Verjetnost, da ne pride do poroda in da v 7 dneh od začetka zdravljenja niso potrebni alternativni tokolitiki, je bila v raziskavah CAP- 001 pri ženskah, zdravljenih v obdobju od 24. do 28. tedna gestacije, podobna kot pri prejemnicah atosibana in beta- mimetikov.
Secondary endpoints: secondary efficacy parameters included the proportion of women remaining undelivered within 48 h of treatment initiation.
Sekundarna merila učinkovitosti so vključevala delež žensk, ki niso rodile v 48 urah po začetku zdravljenja.
There was no difference between the atosiban and beta-mimetic groups with regard to this parameter.
Skupini na atosibanu in beta- mimetiku se v tem pogledu nista razlikovali.
Mean (SD) gestational age at delivery was the same in the two groups:
Povprečna (SD) gestacijska starost ob porodu je bila v obeh skupinah enaka:
35.6 (3.9) and 35.3 (4.2) weeks for the atosiban and β -agonist groups, respectively (p=0.37).
35, 6 (3, 9) tedna v skupini z atosibanom in 35, 3 (4, 2) tedna v skupini z β- agonistom (p = 0, 37).
Admission to a neonatal intensive care unit (NICU) was similar for both treatment groups (approximately 30%), as was length of stay and ventilation therapy.
Delež sprejemov v neonatalno enoto za intenzivno nego je bil v obeh zdravljenih skupinah podoben (približno 30%), prav tako trajanje bivanja in ventilacijska terapija.
Mean (SD) birth weight was 2491 (813) grams in the atosiban group and 2461 (831) grams in the β -agonist group (p=0.58).
Povprečna (SD) porodna masa je bila v skupini z atosibanom 2. 491 (813) gramov in v skupini z β- agonistom 2. 461 (831) gramov (p = 0, 58).
Fetal and maternal outcome did apparently not differ between the atosiban and the β -agonist group, but the clinical studies were not powered enough to rule out a possible difference.
Izid za plod in mater se v skupini z atosibanom po vsem sodeč ni razlikoval od izida v skupini z β- agonistom, toda moč kliničnih raziskav ni bila tolikšna, da bi izključila možno razliko.
Of the 361 women who received atosiban treatment in the phase III studies, 73 received at least one re- treatment, 8 received at least 2 re-treatments and 2 received 3 re-treatments (see section 4.4).
Od 361 žensk, zdravljenih z atosibanom v raziskavi III. faze, je bilo 73 deležnih vsaj enega ponovnega zdravljenja, 8 vsaj dveh, 2 pa sta bili ponovno zdravljeni trikrat (glejte poglavje 4. 4).
As the safety and efficacy of atosiban in women with a gestational age of less than 24 completed weeks has not been established in controlled randomised studies, the treatment of this patient group with atosiban is not recommended (see section 4.3).
Varnost in učinkovitost atosibana nista ugotovljeni s kontroliranimi randomiziranimi raziskavami pri ženskah z gestacijsko starostjo manj kot 24 dopolnjenih tednov, zato uporaba atosibana pri tej skupini bolnic ni priporočljiva (glejte poglavje 4. 3).
In a placebo-controlled study, fetal/ infant deaths were 5/ 295 (1.7%) in the placebo group and 15/ 288 (5.2%) in the atosiban group, of which two occurred at five and eight months of age.
V raziskavi, kontrolirani s placebom, je bilo smrti plodov/ dojenčkov v skupini s placebom 5/ 295 (1, 7%) in v skupini z atosibanom 15/ 288 (5, 2%), od tega dve v starosti pet in osem mesecev.
Eleven out of the 15 deaths in the atosiban group occurred in pregnancies with a gestational age of 20 to 24 weeks, although in this subgroup patient distribution was unequal (19 women on atosiban, 4 on placebo).
Enajst od 15 smrti v skupini z atosibanom je bilo pri nosečnostih z gestacijsko starostjo od 20 do 24 tednov, čeprav je bila porazdelitev bolnic v tej podskupini neenakomerna (19 prejemnic atosibana, 4 prejemnice placeba).
For women with a gestational age greater than 24 weeks there was no difference in mortality rate (1.7% in the placebo group and 1.5% in the atosiban group).
Pri ženskah z gestacijsko starostjo nad 24 tednov ni bilo razlik v umrljivosti (1, 7% v skupini s placebom in 1, 5% v skupini z atosibanom).
In healthy non-pregnant subjects receiving atosiban infusions (10 to 300 micrograms/ min over 12 hours), the steady state plasma concentrations increased proportionally to the dose.
Pri zdravih, nenosečih preiskovankah, ki so dobile infuzijo atosibana (od 10 do 300 mikrogamov/ min v 12 urah), je ravnotežna koncentracija v plazmi naraščala sorazmerno odmerku.
The clearance, volume of distribution and half-life were found to be independent of the dose.
Izkazalo se je, da očistek, volumen distribucije in razpolovni čas niso odvisni od odmerka.
In women in pre-term labour receiving atosiban by infusion (300 micrograms/ min for 6 to 12 hours), steady state plasma concentrations were reached within one hour following the start of the infusion (mean 442 ± 73 ng/ ml, range 298 to 533 ng/ ml).
Pri ženskah s prezgodnjim porajanjem, ki so dobile infuzijo atosibana (300 mikrogramov/ min od 6 do 12 ur), je bila ravnotežna koncentracija v plazmi dosežena v eni uri po začetku infuzije (povprečno 442 ± 73 ng/ ml, razpon od 298 do 533 ng/ ml).
Following completion of the infusion, plasma concentration rapidly declined with an initial (tα) and terminal (tβ) half-life of 0.21 ± 0.01 and 1.7 ± 0.3 hours, respectively.
Po koncu infundiranja je koncentracija v plazmi hitro upadla z začetnim razpolovnim časom (tα) 0, 21 ± 0, 01 ure in terminalnim razpolovnim časom (tβ) 1, 7 ± 0, 3 ure.
Mean value for clearance was 41.8 ± 8.2 litres/ h.
Srednja vrednost očistka je bila 41, 8 ± 8, 2 litrov/ uro.
Mean value of volume of distribution was 18.3 ± 6.8 litres.
Srednja vrednost volumna distribucije je bila 18, 3 ± 6, 8 litrov.
Plasma protein binding of atosiban is 46 to 48% in pregnant women.
Vezava atosibana na beljakovine v plazmi je pri nosečnicah od 46 do 48%.
6 Two metabolites were identified in the plasma and urine from human subjects.
Po infuziji 300 mikrogramov/ min zdravim nosečnicam ob roku je bilo razmerje med koncentracijo atosibana pri plodu in materi 0, 12.
The ratios of the main metabolite M1 (des-(Orn8, Gly-NH29)-[Mpa1, D-Tyr(Et)2, Thr4]-oxytocin) to atosiban concentrations in plasma were 1.4 and 2.8 at the second hour and at the end of the infusion respectively.
Razmerje med koncentracijo glavnega presnovka M1 (des - (Orn8, Gly- NH29) - [Mpa1, D- Tyr( Et) 2, Thr4] - oksitocin) in atosibana v plazmi je bilo po dveh urah 1, 4 in na koncu infundiranja 2, 8.
Atosiban is found in only small quantities in urine, its urinary concentration is about 50 times lower than that of M1.
Atosiban se v urinu pojavi le v majhni količini; njegova koncentracija v urinu je približno 50- krat manjša od koncentracijeM1.
Main metabolite M1 is apparently as potent as the parent compound in inhibiting oxytocin-induced uterine contractions in vitro.
Kaže, da glavni presnovek M1 in vitro zavira z oksitocinom izzvane kontrakcije maternice enako močno kot matična spojina.
Metabolite M1 is excreted in milk (see section 4.6).
Presnovek M1 se izloča v mleku (glejte poglavje 4. 6).
There is no experience with atosiban treatment in patients with impaired function of the liver or kidneys (see sections 4.2 and 4.4).
Izkušenj z uporabo atosibana pri bolnicah z okvarjenim delovanjem jeter ali ledvic ni (glejte poglavje 4. 2 in 4. 4).
It is unlikely that atosiban inhibits hepatic cytochrome P450 isoforms in humans (see section 4.5).
Ni verjetno, da bi atosiban pri človeku zaviral izooblike jetrnega citokroma P450 (glejte poglavje 4. 5).
No systemic toxic effects were observed during the two-week intravenous toxicity studies (in rats and dogs) at doses which are approximately 10 times higher than the human therapeutic dose, and during the three-months toxicity studies in rats and dogs (up to 20 mg/ kg/ day s. c.).
Dvotedenski intravenski raziskavi toksičnosti (pri podganah in psih) z odmerki, ki so bili približno 10 - krat večji kot terapevtski odmerek pri človeku, in trimesečni raziskavi na podganah in psih (do 20 mg/ kg/ dan s. c.) niso pokazale sistemskih toksičnih učinkov.
The highest atosiban subcutaneous dose not producing any adverse effects was approximately two times the therapeutic human dose.
Največji subkutani odmerek atosibana, ki ni povzročil nobenih neželenih učinkov, je bil približno dvakratnik terapevtskega odmerka pri človeku.
No studies were performed that covered fertility and early embryonic development.
Raziskave, ki bi obsegale vpliv na plodnost in zgodnji embrionalni razvoj niso bile izvedene.
Reproduction toxicity studies, with dosing from implantation up to late stage pregnancy, showed no effects on mothers and fetuses.
Raziskave reprodukcijske toksičnosti, z uporabo zdravila od oploditve do pozne nosečnosti, niso pokazale nobenih učinkov na matere in zarodke.
The exposure of the rat fetus was approximately four times that received by the human fetus during intravenous infusions in women.
Izpostavljenost podganjih plodov je bila približno 4 - krat večja od izpostavljenosti človeškega ploda med intravensko infuzijo pri materi.
Animal studies have shown inhibition of lactation as expected from the inhibition of action of oxytocin.
Raziskave na živalih so pokazale zavrtje sposobnosti za dojenje, kar je pričakovano glede na zaviranje delovanja oksitocina.
Atosiban was neither oncogenic nor mutagenic in in vitro and in vivo tests.
V raziskavah in vitro in in vivo atosiban ni bil onkogen ali mutagen.
Mannitol Hydrochloric acid 1M Water for injections
Manitol 1M klorovodikova kislina Voda za injekcije
In the absence of compatibility studies, this medicinal product must not be mixed with other medicinal products.
Ker raziskav kompatibilnosti ni, tega zdravila ne smemo mešati z drugimi zdravili.
6.3 Shelf life
6, 3 Rok uporabnosti
Once the vial has been opened, the product must be used immediately.
Ko je viala odprta, je treba zdravilo uporabiti takoj.
Store in a refrigerator (2°C - 8°C).
Shranjujte v hladilniku (2° C – 8 °C).
One vial of solution for injection contains 0.9 ml solution, corresponding to 6.75 mg atosiban.
Ena viala raztopine za injiciranje vsebuje 0, 9 ml raztopine, kar ustreza 6, 75 mg atosibana.
Colourless glass vials, clear borosilicated (type I) sealed with grey siliconised bromo-butyl rubber stopper, type I, and flip-off cap of polypropylene and aluminium.
Viala iz brezbarvnega, prozornega borosilikatnega stekla (tipa I), zaprta s sivim, silikoniziranim brombutilnim gumijastim zamaškom z odtržno zaporko iz polipropilena in aluminija.
Withdraw 0.9 ml of a 0.9 ml labelled vial of TRACTOCILE 7.5 mg/ ml, solution for injection and administer slowly as an intravenous bolus dose over one minute, under adequate medical supervision in an obstetric unit.
Izvlecite 0, 9 ml iz 0, 9- ml označene viale zdravila TRACTOCILE 7, 5 mg/ ml, raztopina za injiciranje in aplicirajte počasi v intravenskem bolusu eno minuto pod ustreznim zdravniškim nadzorstvom na porodnem oddelku.
The TRACTOCILE 7.5 mg/ ml, solution for injection should be used immediately.
TRACTOCILE 7, 5 mg/ ml, raztopino za injiciranje je treba uporabiti takoj.
In the absence of compatibility studies, this medicinal product must not be mixed with other medicinal products (see section 6.2).
Ker raziskav kompatibilnosti ni, tega zdravila ne smemo mešati z drugimi zdravili (glejte poglavje 6. 2).
Ferring Pharmaceuticals A/ S Kay Fiskers Plads 11 2300 København S Denmark
Ferring Pharmaceuticals A/ S Kay Fiskers Plads 11 2300 København S Danska
NUMBER IN THE COMMUNITY REGISTER OF MEDICINAL PRODUCTS
ŠTEVILKA (ŠTEVILKE) DOVOLJENJA (DOVOLJENJ) ZA PROMET
TRACTOCILE 7.5 mg/ ml concentrate for solution for infusion
TRACTOCILE 7, 5 mg/ ml koncentrat za pripravo raztopine za infundiranje
After dilution, the concentration of atosiban is 0.75 mg/ ml.
Po razredčenju je koncentracija atosibana 0, 75 mg/ ml.
Concentrate for solution for infusion Visual appearance: clear, colourless solution without particles.
Koncentrat za pripravo raztopine za infundiranje Videz: bistra, brezbarvna raztopina brez delcev.
TRACTOCILE is indicated to delay imminent pre-term birth in pregnant women with: − regular uterine contractions of at least 30 seconds duration at a rate of ≥ 4 per 30 minutes − a cervical dilation of 1 to 3 cm (0-3 for nulliparas) and effacement of ≥ 50% − age ≥ 18 years − a gestational age from 24 until 33 completed weeks − a normal fetal heart rate
TRACTOCILE je indiciran za odložitev iminentnega prezgodnjega poroda pri ženskah z: − rednimi kontrakcijami maternice, ki trajajo vsaj 30 sekund s pogostnostjo ≥ 4 na 30 minut, − odprtjem materničnega vratu od 1 do 3 cm (od 0 do 3 cm pri ženskah, ki še niso rodile) in stanjšanjem ≥ 50%, − starih ≥ 18 let, − gestacijsko starostjo od 24 do 33 dopolnjenih tednov, − normalno srčno frekvenco ploda.
TRACTOCILE is administered intravenously in three successive stages: an initial bolus dose (6.75 mg), performed with TRACTOCILE 7.5 mg/ ml solution for injection, immediately followed by a continuous high dose infusion (loading infusion 300 micrograms/ min) of TRACTOCILE 7.5 mg/ ml concentrate for solution for infusion during three hours, followed by a lower dose of TRACTOCILE 7.5 mg/ ml concentrate for solution for infusion (subsequent infusion 100 micrograms/ min) up to 45 hours.
TRACTOCILE se aplicira intravensko v treh zaporednih korakih: najprej bolusni odmerek (6, 75 mg) zdravila TRACTOCILE 7, 5 mg/ ml, raztopina za injiciranje, ki mu takoj sledi visokoodmerna triurna stalna infuzija (polnilna infuzija 300 mikrogramov/ min) zdravila TRACTOCILE 7, 5 mg/ ml, koncentrat za pripravo raztopine za injiciranje ter nato infuzija z manjšim odmerkom zdravila TRACTOCILE 7, 5 mg/ ml, koncentrat za pripravo raztopine za injiciranje (nadaljnja infuzija 100 mikrogramov/ min) do 45 ur.
Intravenous therapy using the initial bolus injection of TRACTOCILE 7.5 mg/ ml, solution for injection (see Summary of Product Characteristics of this product) should be started as soon as possible after diagnosis of pre-term labour.
Intravensko zdravljenje z uvodno bolusno injekcijo zdravila TRACTOCILE 7, 5 mg/ ml, raztopina za injiciranje (glejte povzetek glavnih značilnosti za to zdravilo) je treba začeti čim prej po diagnozi prezgodnjega porajanja.
9 The following table shows the full posology of the bolus injection followed by the infusion:
9 Naslednja tabela prikazuje celotno odmerno shemo z bolusno injekcijo in infuzijo, ki sledi:
TRACTOCILE should not be used in the following conditions:
TRACTOCILA se ne sme uporabljati v naslednjih primerih:
11 The undesirable effects in the women were the following:
11 Neželeni učinki pri ženskah so bili:
Metabolism and nutrition disorders: hyperglycaemia Nervous system disorders: headache, dizziness Cardiac disorders: tachycardia, Vascular disorders: hot flush, hypotension Gastrointestinal disorders: vomiting General disorders and administration site conditions: injection site reaction
Bolezni živčevja: glavobol, omotica.
Uncommon (> 1/ 1,000, < 1/ 100)
Bolezni prebavil: bruhanje.
Psychiatric disorders: insomnia Skin and subcutaneous tissue disorders: pruritis, rash General disorders and administration site conditions: pyrexia
Splošne težave in spremembe na mestu aplikacije: reakcija na injekcijskem mestu.
Rare (> 1/ 10,000, < 1/ 1,000)
(> 1/ 1. 000, < 1/ 100) Bolezni kože in podkožja: srbenje, izpuščaj.
Incidental cases of uterine haemorrhage/ uterine atony were reported.
Redki Opisani so bili posamezni primeri maternične krvavitve oz. atonije (> 1/ 10. 000, < 1/ 1. 000)
TRACTOCILE contains atosiban (INN), a synthetic peptide ([Mpa1, D-Tyr(Et)2, Thr4, Orn8]-oxytocin) which is a competitive antagonist of human oxytocin at receptor level.
TRACTOCILE vsebuje atosiban (INN), sintetičen peptid ([Mpa1, D- Tyr( Et) 2, Thr4, Orn8] - oksitocin), ki je kompetitiven antagonist človeškega oksitocina na receptorski ravni.
Primary endpoint: the primary efficacy outcome was the proportion of women remaining undelivered and not requiring alternative tocolysis within 7 days of treatment initiation.
Glavno merilo učinkovitosti je bil delež žensk, ki niso rodile in v 7 dneh od začetka zdravljenja niso potrebovale alternativne tokolize.
The data show that 59.6% (n=201) and 47.7% (n=163) of atosiban- and β -agonist-treated women (p=0.0004), respectively, were undelivered and did not require alternative tocolysis within 7 days of starting treatment.
Podatki kažejo, da ni rodilo in v 7 dneh po začetku zdravljenja ni potrebovalo drugačne tokolize 59, 6% (n = 201) žensk, ki so dobivale atosiban, in 47, 7% (n = 163) žensk, ki so dobivale β- agonist (p = 0, 0004).
Most of the treatment failures in CAP-001 were caused by poor tolerability.
Večino neuspehov zdravljenja je v CAP- 001 povzročilo slabo prenašanje.
12 insufficient efficacy were significantly (p=0.0003) more frequent in atosiban (n=48, 14.2%) than in the β -agonist-treated women (n=20, 5.8%).
Neuspešno zdravljenje zaradi nezadostne učinkovitosti je bilo značilno pogostejše (p = 0, 0003) med ženskami, ki so dobivale atosiban (n = 48, 14, 2%), kot med tistimi, ki so dobivale β- agonist (n = 20, 5, 8%).
Fetal and maternal outcome did apparently not differ between the atosiban and the β -agonist group, but the clinical studies were not powered enough to rule out a possible difference.
Izid za plod in mater se v skupini z atosibanom po vsem sodeč ni razlikoval od izida v skupini z β - agonistom, toda moč kliničnih raziskav ni bila tolikšna, da bi izključila možno razliko.
Of the 361 women who received atosiban treatment in the phase III studies, 73 received at least one re- treatment, 8 received at least 2 re-treatments and 2 received 3 re-treatments (see section 4.4).
Od 361 žensk, zdravljenih s atosibanom v raziskavi III. faze, je bilo 73 deležnih vsaj enega ponovnega zdravljenja, 8 vsaj dveh, 2 pa sta bili ponovno zdravljeni trikrat (glejte poglavje 4. 4).
In healthy non-pregnant subjects receiving atosiban infusions (10 to 300 micrograms/ min over 12 hours), the steady state plasma concentrations increased proportionally to the dose.
Pri zdravih, nenosečih preiskovankah, ki so dobile infuzijo atosibana (od 10 do 300 mikrogramov/ min v 12 urah), je ravnotežna koncentracija v plazmi naraščala sorazmerno odmerku.