This Is MS Multiple Sclerosis Knowledge & Support Community

Hi, I have been on Rebif for 2 months after being diagnosed with RRMS. I was told I am allergic to Rebif and need to try a new med. Can anyone tell me what differences they have found from Rebif to one of the other's?

Thanks,

Samantha

Sammy76 wrote:Hi, I have been on Rebif for 2 months after being diagnosed with RRMS. I was told I am allergic to Rebif and need to try a new med.

Hi Sammy,
What reaction did you have that led to the conclusion that you are allergic to Rebif?

My wife was originally on Rebif and seemed to tolerate it well but during the titration process, one injection before the full dose, her neuro told her to stop because her liver enzyme levels were too high.

Some weeks later she was told that her levels had lowered enough to start the titration process again, but she had become interested in the Tovaxin IIb clinical trial at that point.

I'm admittedly not real familiar with allergies to the interferons. Rebif and Avonex are Interferon 1a, Betaseron is Interferon 1b and Copaxone is Glatimer Acetate. Possibly a genuine allergy to Interferon means that Copaxone is your only other choice within the crabs?

Bob

Hi Samantha

I was on Rebif 4 years before my neuros finally admitted that it was making me very ill - I had been telling them that for 3 years! After 4 years I had hardly any white blood cells left, high liver enzymes, and I was very ill every 3-4 weeks, as well as having 4 MS relapses a year as well. It was just awful, a really bleak time when I look back at it. I never lost the extreme flu-like reactions, it just kept happening at every injection.

What kind of reaction did you have?
Well done to your docs to spot it so soon, hopefully they are right, and you will do better on another med.

I switched to Copaxone. It seemed to take about 6 months to have a full effect. I think (!) I'm on it 4.5 years now, and I have only had 3 relapses in those years. This is a huge improvement for me. The relapses I had were not severe and a lot of my energy has come back.
I am off Copaxone at the moment as I'm pregnant, but I'm going right back on it afterwards.
Good luck with everything.

Hi Samantha,
I don't know if this will be relevant to your situation as I don't know the specifics of your allergic reaction to Rebif. However, here's a paper where that discusses some of the differences between Betaseron, Rebif, and Avonex with respect to neutralizing antibodies (NAB). It was found that NAB production was highest for people on Betaseron but after a 1 to 2 month washout period, people could switch over to Avonex without reoccurrence of NAB production.

Interferon-beta (INF-beta) antibodies in interferon-beta1a- and interferon-beta1b-treated multiple sclerosis patients. Prevalence, kinetics, cross-reactivity, and factors enhancing interferon-beta immunogenicity in vivo. Eur Cytokine Netw. 2001 Mar;12(1):56-61.

• We analysed the role of dosage, route and frequency of administration of clinical grade interferon-beta (IFN-beta) preparations in inducing anti-IFN-beta antibodies (IFN-beta-Abs) in 5 groups of relapsing-remitting multiple sclerosis (RRMS) patients who were respectively treated as follows: 1) weekly intramuscular (i.m.) injections of 30 mg of recombinant IFN-beta1a (Avonex), 2) subcutis (s.c.) injections of 250 mg IFN-beta1b (Betaferon) every other day, 3) weekly i.m. injections of 250 mg IFN-beta1b (Betaferon), 4) s.c. injections of 22 mg of IFN-beta1a (Rebif) three times a week, and 5) i.m. injections of 22 mg of IFN-beta1a (Rebif) twice a week. IFN-beta-Abs were determined by ELISA. IFN-beta1b was more immunogenic than IFN-beta1a not only when administered s.c. every other day, but also when administered i.m. at a lower weekly dose; i.m. injection, however, significantly delayed the appearance, and induced lower serum levels of IFN-beta-Abs. In patients treated with s.c. IFN-beta1b, Ab levels peaked 3 to 9 months after therapy initiation, and then slowly, but progressively, declined to pre-therapy levels that in some patients were reached after three years. Patients treated with i.m. or s.c. IFN-beta1a only rarely developed IFN-beta-Abs, and then at very low titers. Overall, the i.m. weekly administration of IFN-beta1a was the less immunogenic treatment. In IFN-beta1b-treated patients, a wash-out period of two/three months was sufficient to bring the IFN-beta-Ab levels below the cut-off. Our findings suggest that the immunogenicity of IFN-beta1a is low, regardless of the route of administration and the dosage, while that of IFN-beta1b is high, and is significantly, but not completely reduced by i.m. administration. As IFN-beta-Abs are cross-reactive, a wash-out period is suggested when the preparation is changed from IFN-beta1b to IFN-beta1a in order to maintain the clinical benefits of the therapy

NHE

would that count?