OBJECTIVE: The Escala Study evidenced that the administration of glatiramer acetate for relapsing-remitting multiple sclerosis improved the spasticity of patients previously treated with interferon-β. However, whether such an improvement was translated into cost savings remained unclear. We therefore conducted a cost analysis of glatiramer acetate versus interferon-β in these patients with multiple sclerosis and spasticity.
METHODS: This cost analysis encompassed data from the observational Escala Study, which included patients with relapsing-remitting multiple sclerosis and spasticity whose treatment had been switched from interferon-β to glatiramer acetate. Costs prior to starting glatiramer acetate (interferon-β period) were compared to the subsequent six months on glatiramer acetate (glatiramer acetate period). The analysis was carried out following the recommendations for conducting pharmacoeconomic studies and from the Spanish National Health System perspective. Costs associated with multiple sclerosis treatment, spasticity treatment and relapse management were expressed in 2014 euros (€); a 7.5 % discount was applied-when needed-as stipulated in Spanish law.
RESULTS: The management of relapsing-remitting multiple sclerosis, spasticity and relapses accounted for a 6-month cost per patient of 7,078.02€ when using interferon-β and 4,671.31€ when using glatiramer acetate. Switching from interferon-β to glatiramer acetate therefore represented a cost saving of 2,406.72€ per patient in favour of glatiramer acetate, which resulted from savings in treatment costs, relapse management and spasticity treatment of 1,890.02€, 430.48€ and 86.21€, respectively. The ratio of the costs during interferon-β was 1.5 times the costs during glatiramer acetate; thus, a fixed budget of 5,000,000€ would enable 1,070 patients to be treated with glatiramer acetate and only 706 patients with interferon-β.
CONCLUSIONS: The treatment of relapsing-remitting multiple sclerosis with glatiramer acetate entailed cost savings when compared to interferon-β in patients with spasticity, which not only resulted from its lower costs of therapy and relapse management but also from its favourable effect on reducing spasticity. Thus, glatiramer acetate may be regarded as a more efficient alternative than interferon-β from the perspective of the Spanish National Health System
I was taken to task when commenting on
Meca-Lallana JE, Hernández-Clares R, Carreón-Guarnizo E.Spasticity in multiple sclerosis and role of glatiramer acetate treatment. Brain Behav. 2015 ;5(9):e00367. doi: 10.1002/brb3.367. Epub 2015 Jul 14.
DrK said “Increased spasticity is a well-known adverse effect of beta-interferons, and I usually explain this to pwMS as well as myself as part of Uhthoff’s phenomenon ” ( This s the worsening of neurologic symptoms in multiple sclerosis (MS) and other neurological, demyelinating conditions when the body gets overheated from hot weather, exercise, fever, or saunas and hot tubs. It is possibly due to the effect of increased temperature on nerve conduction. With an increased body temperature, nerve impulses are either blocked or slowed down in a damaged nerve but once the body temperature is normalized, signs and symptoms may disappear or improve) “triggered by the drug. Beta-IFN causes temperature to rise as part of the flu-like syndrome, that unmasks or exacerbates pre-existing symptoms. Some pwMS don’t have fever and yet get increased spasticity, perhaps cytokine release does not reach the threshold to cause temperature but is sufficient to exacerbate symptom, I don’t know, may be others do. It may well depend on the degree of damage to motor fibres due to MS and the severity of spasticity. In people who whilst taking b-IFN developed SPMS the experience of stopping the drug is often a relief with lesser spasticity playing a key role. To suggest Glatiramer is actively improving spasticity is more difficult to prove beyond reasonable doubt, and in my view is has not. There are obviously sponsored papers trying to suggest there is an effect of Drug C whilst it is actually stopping Drug B that explains the difference.”