natgillin/translations-raw huggingface dataset:
Urinary protein positive (> 1+)×
Valk uriinis (> 1+) x
Urinary incontinence Urinary urgency
Kusepidamatus
8% (15%) 8% (7%)
8% (15%)
20% (19%) 21% (17%)
20% (19%)
2% (1%) 4% (2%)
2% (1%)
2% (0%) 1% (2%)
Kusepakitsus
< 1% (< 1%) 9% (13%)
1% (1%)
6% (5%) 10% (8%)
8% (7%)
18% (11%) 17% (8%)
21% (17%)
2% (0%) 1% (0%)
4% (2%)
General disorders and administration site conditions Injection site reaction Λ § (various kinds) * °
Reproduktiivse süsteemi ja rinnanäärme häired Düsmenorröa
52% (11%)
2% (0%)
78% (20%)
< 1% (< 1%)
89% (37%)
6% (5%)
85% (37%)
18% (11%)
Injection site necrosis * ° & Λ
Menstruatsioonihäired *
1% (0%)
1% (2%)
5% (0%)
9% (13%)
6% (0%)
10% (8%)
5% (0%)
17% (8%)
Flu-like symptoms *° Fever Λ * °
Organsüsteemi klass
44% (18%) 13% (5%)
Üksik Sclerosis
61% (40%) 40% (13%)
Ägenemiste ja
43% (33%) 29% (24%)
multiplex’ ile
52% (48%) 59% (41%)
remissioonidega
9 SystemOrganClass
Kõrvaltoime
Single Event suggestive of
viitav episood
Secondary Secondary Progressive Progressive
Sclerosis Sclerosis
Multiple Multiple Sclerosis Sclerosis (European (North Study) American Study)
multiplex (Euroopa uuring)
Betaferon Betaferon 250 250
mikrogrammi (Platseebo) n=360 (n=358)
Betaferon 250 microgram
mikrogrammi (Platseebo) n=317 (n=308)
Betaferon 250
mikrogrammi (Platseebo) n=124 (n=123)
microgram microgram
Metrorraagia Impotentsus
(Placebo)
2% (0%) 1% (0%)
microgram
12% (6%) 7% (4%)
(Placebo) (Placebo)
10% (10%) 10% (11%)
n=317 (n=308)
15% (8%) 2% (1%)
(Placebo)
85% (37%)
n=292 (n=176)
5% (0%) 61% (40%)
n=360 (n=358)
6% (0%) 43% (33%)
n=124 (n=123)
5% (0%) 52% (48%)
Pain Chest pain ° Peripheral edema Asthenia * Chills Λ * ° Sweating * Malaise * × Laboratory abnormality Λ
Palavik ^ * ° Valu Valu rindkeres ° Perifeerne ödeem Asteenia * Külmavärinad ^ * ° Higistamine * Halb enesetunne * x
4% (4%) 1% (0%) 0% (0%) 22% (17%) 5% (1%) 2% (1%) 0% (1%)
13% (5%) 4% (4%) 1% (0%) 0% (0%) 22% (17%) 5% (1%) 2% (1%) 0% (1%)
31% (25%) 5% (4%) 7% (7%) 63% (58%) 23% (7%) 6% (6%) 8% (5%)
40% (13%) 31% (25%) 5% (4%) 7% (7%) 63% (58%) 23% (7%) 6% (6%) 8% (5%)
59% (59%) 15% (8%) 21% (18%) 64% (58%) 22% (12%) 10% (10%) 6% (2%)
29% (24%) 59% (59%) 15% (8%) 21% (18%) 64% (58%) 22% (12%) 10% (10%) 6% (2%)
52% (48%) 15% (15%) 7% (8%) 49% (35%) 46% (19%) 23% (11%) 15% (3%)
59% (41%) 52% (48%) 15% (15%) 7% (8%) 49% (35%) 46% (19%) 23% (11%) 15% (3%)
Significantly associated with Betaferon treatment for patients with first event suggestive of MS, p < 0.05 * Significantly associated with Betaferon treatment for RRMS, p < 0.05 ° Significantly associated with Betaferon treatment for SPMS, p < 0.05 § Injection site reaction (various kinds) comprises all adverse events occurring at the injection site, i. e. the following terms: injection site hemorrhage, injection site hypersensitivity, injection site inflammation, injection site mass, injection site necrosis, injection site pain, injection site reaction, injection site edema, and injection site atrophy & “ Flu-like symptom complex ” denotes flu syndrome and/ or a combination of at least two AEs from fever, chills, myalgia, malaise, sweating. # During the third year of the BENEFIT study, no change of the known risk profile of Betaferon was observed.
Laboratoorsed kõrvalekalded ^ Oluliselt seotud Betaferon- raviga esimese sclerosis multiplex´ile viitava demüelinisatsiooniepisoodiga patsientidel, p < 0, 05  * Oluliselt seotud Betaferon- raviga ägenemiste ja remissioonidega kulgeva sclerosis multiplex´i patsientidel, p < 0, 05 ° Oluliselt seotud Betaferon- raviga sekundaarselt progresseeruva sclerosis multiplex´i patsientidel, p < 0, 05 § Süstekoha reaktsioonid (erinevat liiki) hõlmavad kõiki kõrvaltoimeid, mis esinevad süstekohal, st järgnevad terminid: verejooks süstekohal, süstekoha ülitundlikkus, süstekoha põletik, süstekoha paksenemine, süstekoha nekroos, valu süstekohal, süstekoha reaktsioon, süstekoha turse ja süstekoha atroofia. & “ Gripitaoliste sümptomite kompleks ” tähendab gripisündroomi ja/ või vähemalt kahe kõrvaltoime koosesinemist, mis hõlmavad palavikku, külmavärinaid, müalgiat, halba enesetunnet ja higistamist. # BENEFIT- uuringu kolmanda aasta jooksul ei täheldatud muutusi Betaferon' i riskiprofiilis.
10 Table 2 (reporting rates (very common ≥ 1/ 10, common ≥ 1/ 100 to < 1/ 10, uncommon ≥ 1/ 1,000 to < 1/ 100, rare ≥ 1/ 10,000 to < 1/ 1,000, very rare < 1/ 10,000) based on spontaneous adverse drug reaction reports).
Tabel 2 (kõrvaltoimete esinemissagedus (väga sage ≥1/ 10, sage ≥ 1/ 100 kuni < 1/ 10, aeg- ajalt ≥ 1/ 1000 kuni < 1/ 100, harv ≥ 1/ 10 000 kuni < 1/ 1000, väga harv < 1/ 10 000) baseerub spontaansetel kõrvaltoime teatistel).
Very common ≥ 1/ 10
≥ 1/ 10
Common ≥ 1/ 100 to < 1/ 10
≥ 1/ 100; < 1/ 10
Uncommon ≥ 1/ 1,000 to < 1/ 100
≥ 1/ 1, 000; < 1/ 100
Rare ≥ 1/ 10,000 to < 1/ 1,000
≥ 1/ 10, 000; < 1/ 1000
Blood and lymphatic system disorders
Vere ja lümfisüsteemi häired Immuunsüsteemi häired Endokriinsüsteemi häired
Anemia, Thrombocyto- penia, Leukopenia
aneemia, trombotsütopeenia, leukopeenia
Anaphylactic reactions Hyperthyroidism, Hypothyroidism, Thyroid disorder
lümfadenopaatia anafülaktilised reaktsioonid hüpertüreoos, hüpotüreoos, kilpnäärme häire
Blood triglycerides increased Anorexia
triglütseriidide taseme tõus veres, anoreksia
Depression (see also section 4.4)
depressioon (vt ka lõik 4. 4)
Confusion, Anxiety, Emotional lability, Suicide attempt (see also section 4.4)
segasusseisund, ärevus, emotsionaalne labiilsus, enesetapukatse (vt ka lõik 4. 4)
Cardiomyopathy, Tachycardia, Palpitation
kardiomüopaatia, tahhükardia, südamepekslemine
Hypertension
hüpertensioon
Respiratrory, thoracic and mediastinal disorders
Respiratoorsed, rindkere ja mediastiinumi häired
Bronchospasm, Dyspnea
bronhospasm, düspnoe
Vomiting, Nausea
oksendamine, iiveldus
Alanine amino- transferase increased, Aspartate amino- transferase increased
tõusnud alaniini aminotransferaas, tõusnud aspartaadi aminotransferaas
Blood bilirubin increased, Gamma-glutamyl- transferase increased, Hepatitis
tõusnud bilirubiini tase, tõusnud gamma- glutamüül - transferaas, hepatiit
Urticaria, Rash, Pruritus, Alopecia
urtikaaria, lööve, sügelus, alopeetsia
Skin discolouration
nahavärvuse muutus
Musculoskeletal, connective tissue and bone disorders
Lihas- skeleti ja sidekoe kahjustused Reproduktiivse süsteemi ja rinnanäärme häired
Myalgia, Hypertonia
müalgia, hüpertoonia
Reproductive system and breast disorders
menstruaaltsükli häired
Menstrual disorder
Organsüsteemi
11 System Organ Class
Aeg- ajalt
Flu-like symptoms*, Chills*, Fever *, Injection site reaction*, Injection site inflammation*, Injection site pain
gripitaolised sümptomid * külmavärinad *, palavik *, süstekoha reaktsioon *, süstekoha põletik *, valu süstekohal
Injection site necrosis*
süstekoha nekroos *
Chest pain, Malaise, Sweating
valu rindkeres, halb enesetunne, higistamine
Weight decrease
kehakaalu langus
The most appropriate MedDRA term is used to describe a certain reaction and its synonyms and related conditions.
* esinemissagedus baseerub kliinilistel uuringutel Teatud reaktsiooni ja selle sünonüümide ning sellega seotud haigusseisundite kirjeldamiseks kasutatakse kõige sobivamaid MedDRA termineid.
Interferon beta-1b has been given without serious adverse events compromising vital functions to adult cancer patients at individual doses as high as 5,500 microgram (176 million IU) intravenously three times a week.
RÜ) kolmel korral nädalas, ilma et oleks tekkinud elulisi funktsioone mõjustavaid kõrvaltoimeid.
Cytokines, Interferons, ATC Code:
Farmakoterapeutiline grupp: tsütokiinid, interferoonid ATC- kood:
Interferons have molecular weights ranging from 15,000 to 21,000 Daltons.
Interferoonide molekulkaal on vahemikus 15 000… 21 000 daltonit.
Interferon alpha, interferon beta, and interferon gamma have overlapping yet distinct biologic activities.
Eristatakse kolme interferoonide klassi: alfa -, beeta - ja gammainterferoon, mille omadused kattuvad osaliselt, kuid kõigil on erinev bioloogiline aktiivsus.
The activities of interferon beta-1b are species-restricted and therefore, the most pertinent pharmacological information on interferon beta-1b is derived from studies of human cells in culture or in human in vivo studies.
Beeta- 1b interferooni aktiivsus on liigiti erinev ning seetõttu saab kõige tõepärasema info selle kohta uuringutes inimrakkudel in vitro või inimesel in vivo.
Interferon beta-1b has been shown to possess both antiviral and immunoregulatory activities.
Beeta- 1b interferoon omab nii viirusvastast kui ka immunoregulatoorset toimet.
The mechanisms by which interferon beta-1b exerts its actions in multiple sclerosis are not clearly understood.
Beeta- 1b interferooni toimemehhanismid sclerosis multiplex’ i ravi korral pole veel täielikult selgunud.
However, it is known that the biologic response-modifying properties of interferon beta-1b are mediated through its interactions with specific cell receptors found on the surface of human cells.
On teada, et beeta- 1b interferooni bioloogilist vastust modifitseerivaid omadusi vahendavad spetsiaalsed retseptorid, mida on leitud inimese rakkude pinnalt.
The binding of interferon beta-1b to these receptors induces the expression of a number of gene products that are believed to be the mediators of the biological actions of interferon beta-1b.
Beeta- 1b interferooni sidumine nendele retseptoritele käivitab mitmete geeniproduktide ekspressiooni, mida loetakse beeta- 1b interferooni bioloogilise aktiivsuse mediaatoriteks.
A number of these products have been measured in the serum and cellular fractions of blood collected from patients treated with interferon beta-1b.
Mitmeid selliseid aineid on leitud Betaferon´iga ravitud patsientide seerumis ja vere rakufraktsioonides.
Interferon beta-1b both decreases the binding affinity and enhances the internalisation and degradation of the interferon-gamma receptor.
Beeta- 1b interferoon alandab gammainterferooni retseptorite sidumisvõimet ja põhjustab nende internalisatsiooni ja degradatsiooni.
Interferon beta-1b also enhances the suppressor activity of peripheral blood mononuclear cells.
Beeta- 1b interferoon suurendab ka perifeerse vere mononukleaarsete rakkude supressiooniaktiivsust.
No separate investigations were performed regarding the influence of Betaferon on the cardiovascular system, respiratory system and the function of endocrine organs.
Eraldi uuringuid Betaferon´i toime kohta südame- veresoonkonnale, hingamissüsteemile ja endokriinorganite funktsioonile pole teostatud.
12 Clinical trials:
Kliinilised uuringud:
RR-MS:
RR- MS:
One controlled clinical trial with Betaferon in patients with relapsing remitting multiple sclerosis and able to walk unaided (baseline EDSS 0 to 5.5) was performed.
Kontrollitud kliiniline uuring Betaferon´iga viidi läbi ägenemiste ja remissioonidega kulgeva sclerosis multiplex´iga patsientidel, kes olid võimelised kõndima ilma kõrvalise abita (EDSS algtase 0 kuni 5, 5).
Patients receiving Betaferon showed a reduction in frequency (30%) and severity of clinical relapses, as well as the number of hospitalisations due to disease.
Patsientidel, kellele manustati Betaferon´i, ilmnes kliiniliste ägenemiste raskuse ning esinemissageduse (30%) langus ning samuti ka haigusest tulenevate hospitaliseerimiste arvu langus.
There is no evidence of an effect of Betaferon on the duration of relapses or on symptoms in between relapses, and no significant effect was seen on the progression of the disease in relapsing remitting multiple sclerosis.
Puuduvad andmed Betaferon´i mõjust ägenemiste kestusele või sümptomitele ägenemiste vahelisel perioodil ning märkimisväärset mõju pole täheldatud haiguse progressioonile ägenemiste ja remissioonidega kulgeva sclerosis multiplex´i puhul.
SP-MS:
SP- MS:
Two controlled clinical trials with Betaferon involving a total of 1657 patients with secondary progressive multiple sclerosis (baseline EDSS 3 to 6.5, i. e. patients were able to walk) were performed.
Viidi läbi kaks kontrollitud kliinilist uuringut Betaferon´iga, kokku 1657 sekundaarselt progresseeruva sclerosis multiplex´iga patsiendil (EDSS algtase 3 kuni 6, 5, st patsiendid olid võimelised kõndima).
One of the two studies demonstrated a statistically significant delay in the time to disability progression (Hazard Ratio = 0.69, 95% confidence interval (0.55, 0.86), p=0.0010, corresponding to a 31% risk reduction due to Betaferon) and in the time to becoming wheelchair bound (Hazard Ratio = 0.61, 95% confidence interval (0.44, 0.85), p=0.0036, corresponding to a 39% risk reduction due to Betaferon) in patients who received Betaferon.
Üks kahest uuringust näitas statistiliselt märkimisväärset invaliidsuse arengu edasilükkumist (riskisuhe = 0, 69, 95% usaldusvahemik (0, 55, 0, 86), p=0, 0010, mis vastab 31% riski vähenemisele Betaferon´i tõttu) ning ratastooli jäämise aja edasilükkumist (riskisuhe = 0, 61, 95% usaldusvahemik (0, 44, 0, 85), p=0, 0036, mis vastab 39% riski vähenemisele Betaferon´i tõttu).
This effect continued over the observation period of up to 33 months.
Selline mõju jätkus kogu 33- kuulise jälgimisperioodi ulatuses.
In the second trial of Betaferon in secondary progressive multiple sclerosis, no delay in the time to disability progression was observed.
Teises Betaferon´i uuringus sekundaarselt progresseeruva sclerosis multiplex´i korral invaliidsuse arengu edasilükkumist ei täheldatud.
In retrospective meta-analyses including the data of both studies, an overall treatment effect was found which was statistically significant (p=0.0076; 8 million IU Betaferon versus all placebo patients).
RÜ Betaferon vs platseebo- grupp) raviefekti saavutamist.
Retrospective analyses in subgroups showed that a treatment effect on disability progression is most likely in patients with active disease before treatment commences (Hazard Ratio 0.72, 95% confidence interval (0.59, 0.88), p=0.0011, corresponding to a 28% risk reduction due to Betaferon in patients with relapses or pronounced EDSS progression, 8 million IU Betaferon versus all placebo patients).
RÜ Betaferon vs platseebo- grupp).
From these retrospective subgroup analyses there was evidence to suggest that relapses as well as pronounced EDSS progression (EDSS > 1 point or > 0.5 point for EDSS > =6 in the previous two years) can help to identify patients with active disease.
Nende alagruppide retrospektiivsete analüüside põhjal võis järeldada, et haiguse ägenemised, nagu ka väljendunud EDSS progressioon (EDSS > 1 punkt või > 0, 5 kuni EDSS > =6 eelneva 2 aasta jooksul) on abiks aktiivse haigusega patsientide kindlakstegemisel.
In both trials secondary progressive multiple sclerosis patients receiving Betaferon showed a reduction in frequency (30%) of clinical relapses.
Mõlemas uuringus täheldati sekundaarselt progresseeruva sclerosis multiplex´iga patsientidel, kellele manustati Betaferon´i, kliiniliste ägenemiste esinemissageduse langust (30%).
There is no evidence of Betaferon having an effect on the duration of relapses.
Puuduvad andmed Betaferon´i mõjust ägenemiste kestusele.
Single clinical event suggestive of MS:
Üksik sclerosis multiplex’ ile viitav demüelinisatsiooniepisood:
One controlled clinical trial with Betaferon was performed in patients with a single clinical event and MRI features suggestive of multiple sclerosis (at least two clinically silent lesions on the T2-weighted MRI).
Üks kontrollitud kliiniline uuring Betaferon’ iga viidi läbi üksiku kliinilise episoodiga ja sclerosis multiplex’ ile viitava MRI- leiuga patsientidel (vähemalt kaks kliiniliselt tumma kollet T2- kaalutud MRI kujutisel).
Patients with monofocal or multifocal onset of the disease were included (i. e. patients with clinical evidence for a single or at least two lesions, respectively, of the central nervous system).
Uuringusse hõlmati patsiendid, kellel haiguse alguses esines üks või mitu kollet (st patsiendid, kellel kesknärvisüsteemis esineb vastavalt üks või vähemalt kaks kliiniliselt kinnitatud kollet).
Any disease other than multiple sclerosis that could better explain signs and symptoms of the patient had to be excluded.
Välistada tuli igasugune muu haigus peale sclerosis multiplex’ i, mis seletaks paremini patsiendil esinevaid nähte ja sümptomeid.
After the placebo-controlled phase, patient entered a pre-planned follow-up phase with Betaferon to evaluate the effects of immediate versus delayed start of Betaferon-treatment, comparing patients initially randomized to Betaferon ("immediate treatment group") or to placebo ("delayed treatment group").
Omavahel võrreldi patsiente, kes esmalt randomiseeriti Betaferon- gruppi („ kiire ravi grupp “) ja platseebogruppi („ hilisema algusega ravigrupp “).
13 In the placebo-controlled phase, Betaferon delayed the progression from the first clinical event to clinically definite multiple sclerosis (CDMS) in a statistically significant and clinically meaningful manner, corresponding to a risk reduction of 47% (Hazard Ratio = 0.53, 95% confidence interval (0.39, 0.73), p < 0.0001).
Platseeboga kontrollitud faasis aeglustas Betaferon haiguse progresseerumist esimesest kliinilisest episoodist CDMS- iks statistiliselt ja kliiniliselt olulisel viisil, vastav risk vähenes 47% (riskisuhe = 0, 53; 95% usaldusintervall (0, 39, 0, 73; p < 0, 0001).
Within the study period of two years, CDMS occurred in 45% of the placebo group compared to 28% of the Betaferon group (Kaplan-Meier estimates).
Kahe aasta jooksul esines CDMS- i platseeborühmas 45% võrreldes 28% Betaferon’ i rühmas (Kaplan- Meieri hinnang).
Betaferon prolonged the time to CDMS by 363 days, from 255 days in the placebo group to 618 days in the Betaferon group (based on the 25th percentiles).
Betaferon pikendas aega CDMS- ini 363 päeva võrra, 255- lt päevalt platseeborühmas kuni 618 päevani Betaferon’ i manustavas rühmas (põhinedes 25. protsentiilil).
This treatment effect was still evident after the additional year of follow-up at which stage the risk reduction was 41% (Hazard Ratio = 0.59, 95% confidence interval (0.42, 0.83), p = 0.0011). Within the study period of three years, CDMS occurred in 51% of the delayed treatment group compared to 37% of the immediate treatment group (Kaplan-Meier estimates).
Kolmeaastase uuringu perioodil esines CDMS- i 51% - l hilisema ravialgusega grupi patsientidest ja 37% - l kiire algusega ravigrupi patsientidest (Kaplan- Meieri arvutuste põhjal).
The persistence of the treatment effect was observed although the majority of patients from the placebo-group was treated with Betaferon in the third year of the study.
Raviefekti püsimist täheldati, kuigi enamikku platseebogrupi patsientidest raviti uuringu kolmandal aastal Betaferon' iga.
The robustness of the treatment effect was also shown by the delay of progression to multiple sclerosis according to the McDonald criteria.
Ravitoime tugevust näitas ka haiguse sclerosis multiplex’ iks progresseerumise aeglustumine vastavalt McDonaldi kriteeriumitele.
In two years, the risk in the placebo group was 85% and 69% in the Betaferon group (Hazard Ratio = 0.57, 95% confidence interval (0.46, 0.71), p < 0.00001).
Kahe aasta jooksul oli risk platseeborühmas 85% ja Betaferon’ i rühmas 69% (riskisuhe = 0, 57; 95% usaldusintervall (0, 46, 0, 71; p < 0, 00001).
After 3 years, a pre-planned interim analysis showed EDSS progression (confirmed increase in EDSS of greater than or equal 1.0 compared to baseline) occurred in 24% of the patients in the delayed treatment group compared to 16% in the immediate treatment group [Hazard ratio=0.6, 95% confidence interval (0.39, 0.92), p=0.022].
Pärast 3 aasta möödumist näitas planeeritud vahe- analüüs, et EDSS progresseerus (kinnitatud kõrgem EDSS 1, 0 või suurem võrreldes algtasemega) 24% - l hilisema ravialgusega grupi patsientidest võrrelduna 16% - ga ravi varem alustanute rühmast (riskide suhe = 0, 60; 95%, usaldusintervall 0, 39 – 0, 92, p = 0, 022).
There is no evidence for benefit in terms of confirmed disability progression in the majority of patients receiving'immediate 'treatment.
Puuduvad tõendid, mis näitaksid soodsat toimet kinnitatud puude progressioonile enamusel varem ravi alustanud patsientidest.
No benefit, attributable to Betaferon, in quality of life (as measured by FAMS - Functional Assessment of MS:
Elukvaliteedis (mõõdetuna FAMS’ iga (Functional Assessment of Multiple Sclerosis) - Sclerosis multiplex’ i funktsionaalne hindamine:
Treatment Outcomes Index) was seen.
Ravivastuse indeks) ei täheldatud kasu, mida võiks omistada Betaferoni’ le.
Significant effects were also obtained in patients with less disseminated and less active disease at the time of the first event, the risk in two years for progression to CDMS in patients with monofocal onset was 47% for placebo and 24% for Betaferon, without gadolinium (Gd-) enhancement 41% and 20%, with less than 9 T2 lesions 39% and 18%.
Olulisi toimeid täheldati ka patsientidel, kellel haigus esimese episoodi ajal oli vähem levinud ja vähem aktiivne, CDMS- iks progresseerumise risk kahe aasta jooksul oli patsientidel, kellel alguses oli üks kolle, platseeborühmas 47% ja Betaferon’ i rühmas 24%, ilma gadoliiniumiga (Gd) võimendamata 41% ja 20%, vähema kui 9 T2- lesiooniga 39% ja 18%.
Further subgroup analyses indicated a high risk for progression to CDMS within 2 years in monofocal patients with at least 9 T2- lesions (55% risk for placebo, 26% for Betaferon) or Gd-enhancement (63% versus 33%).
Alarühmade edasine analüüsimine näitas haiguse CDMS- iks progresseerumise suurt riski kahe aasta jooksul ühe koldega vähemalt 9 T2- lesiooniga patsientidel (55% risk platseeborühmas, 26% Betaferon’ i rühmas) või Gd- ga võimendatult (63% vs 33%).
In multifocal patients, the risk for CDMS was independent from MRI findings at baseline, indicating a high risk for CDMS because of the dissemination of the disease based on clinical findings.
Mitme koldega patsientidel ei sõltunud CDMS- i risk esialgsetest MRI leidudest, viidates suurele CDMS- i riskile, sest haiguse levik on kliiniliste analüüside põhjal kindlaks tehtud.
However, the long-term impact of early treatment with Betaferon is unknown even in these high risk subgroups as this study was mainly designed to assess the time to CDMS rather than the long term evolution of the disease.
Siiski on varajase Betaferon- ravi pika- ajaline mõju teadmata isegi nendes suure riskiga patsientide alarühmades, sest see uuring oli kavandatud peamiselt selleks, et hinnata pigem aega haiguse CDMS- iks progresseerumiseni kui haiguse pikaajalist arengut.
Therapy with Betaferon was well accepted in the study of patients with a single clinical event as indicated by a high rate of trial completion (92.8% in the Betaferon group).
Üksiku kliinilise episoodiga patsientide uuringus võeti Betaferon- ravi hästi vastu, mida näitas ka uuringu lõpetajate suur määr (92, 8% Betaferon’ i saavas rühmas).
To increase tolerability of Betaferon in the study of patients with a first clinical event, a dose titration was applied and non- steroidal anti-inflammatory drugs were administered at start of therapy.
Suurendamaks Betaferon’ i talutavust esimese kliinilise episoodiga patsientide uuringus, tiitriti annust ja manustati ravi alguses mittesteroidseid põletikuvastaseid ravimeid.
RR-MS, SP-MS and single clinical event suggestive of MS:
RR- MS, SP- MS ja üksik sclerosis multiplex’ ile viitav demüelinisatsiooniepisood
Betaferon was effective in all multiple sclerosis studies to reduce disease activity (acute inflammation in the central nervous system and permanent tissue alterations) as measured by magnetic resonance imaging (MRI).
Magnetresonantstomograafilised uuringud (MRI) näitasid, et Betaferon vähendas haiguse aktiivsust (äge põletik kesknärvisüsteemis ning püsivad koekahjustused) kõigis sclerosis multiplex´i uuringutes.
14 5.2 Pharmacokinetic properties
5. 2 Farmakokineetilised omadused
Betaferon serum levels were followed in patients and volunteers by means of a not completely specific bioassay.
Patsientidel ja vabatahtlikel uuriti Betaferon’ i seerumitaset mitte täiesti spetsiifilise meetodi abil.
Maximum serum levels of about 40 IU/ ml were found 1-8 hours after subcutaneous injection of 500 microgram (16.0 million IU) interferon beta-1b.
500 mikrogrammi (16, 0 miljonit RÜ) beeta- 1b interferooni subkutaansel manustamisel saavutati maksimaalne seerumitase ca 40 RÜ/ ml 1… 8 tunni pärast.