ECTRIMS eLearning

Increase in serum levels of uric acid under treatment with Dimethyl fumarate for multiple sclerosis
Author(s):
G. Mallucci
,
G. Mallucci
Affiliations:
V. D'Ambrosio
,
V. D'Ambrosio
Affiliations:
E. Zardini
,
E. Zardini
Affiliations:
A. Romani
,
A. Romani
Affiliations:
D. Franciotta
,
D. Franciotta
Affiliations:
R. Bergamaschi
R. Bergamaschi
Affiliations:
ECTRIMS Learn. Mallucci G. 09/14/16; 145598; EP1503
Giulia Mallucci
Giulia Mallucci
Contributions
Abstract

Abstract: EP1503

Type: ePoster

Abstract Category: Therapy - disease modifying - Neuroprotection

Objectives: Aim of this pilot study is to investigate serum uric acid (UA) changes during open-label treatment of relapsing-remitting MS with Dimethyl fumarate (DMF).

Material and methods: We enrolled eight-teen MS patients receiving DMF in the MS Centre of Neurological Institute Mondino, Italy. Patients were prospectively followed, collecting demographic and clinical data as well as laboratory assessment. UA evaluation was performed at baseline visit, at 6- and 12-month follow-up. The patients did not report any dietary modification during the DMF course and were not on drugs known to affect UA levels. Patients previously treated with glatiramer acetate were excluded.

Results: Eight-teen patients (55% F, mean age: 38.0+10.4 years; mean disease duration: 8.6+6.3 years) completed 6 months of DMF. Mean annual relapse rate (ARR) in the two years before DMF was 0.73+0.7, median baseline EDSS was 1.5 (range 1.5-5). Eight patients (50%) were treatment naïve, eight (50%) switched to DMF from interferons. Of the enrolled patients, eight patients completed 12 months of DMF (no statistical difference in clinical and demographical data).

At baseline, one male and one female had UA levels below the lower limit of the normal (normal: 2.4-5.7 mg/dl for women, 3.4-7 mg/dl for men). After 6 months on DMF, serum UA increased in eleven patients and marginally decreased (4.3 to 4.1 mg/dl) in a single patient. Mean UA increased from 3.3+0.81 to 3.9+0.84 mg/dl. At 12 months, UA levels were higher than at baseline and at 6 months in each patient. At 12 months, mean UA significantly increased compared to baseline (3.4+0.83 vs 4.2+0.66, p=0.04). None of the patients had levels outside the normal range after 6 or 12 months of treatment.

Clinically, there was stability in the relapse rate in DMF-treated patients in the first year of treatment. Out of seven patients in whom information is available, the number of T2- weighted MRI lesions remained stable, and no gadolinium-enhancing lesion was reported.

Conclusion and discussion: This is the first study showing a progressive increase of UA levels during DMF treatment, suggesting a progressive increase of antioxidant reserves. To understand if UA could represent a mechanism of action of DMF in MS, we are increasing our patients" cohort.

Disclosure: G. Mallucci received support to travel to scientific meetings from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva.

V. D"Ambrosio has nothing to disclose.

E. Zardini has nothing to disclose.

D. Franciotta has nothing to disclose.

R. Bergamaschi received research grants from Bayer Schering, Biogen Idec, Merck Serono, Novartis, Sanofi-Aventis, Teva received lecture honoraria from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva; and received support to travel to scientific meetings from Almirall, Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva.

Abstract: EP1503

Type: ePoster

Abstract Category: Therapy - disease modifying - Neuroprotection

Objectives: Aim of this pilot study is to investigate serum uric acid (UA) changes during open-label treatment of relapsing-remitting MS with Dimethyl fumarate (DMF).

Material and methods: We enrolled eight-teen MS patients receiving DMF in the MS Centre of Neurological Institute Mondino, Italy. Patients were prospectively followed, collecting demographic and clinical data as well as laboratory assessment. UA evaluation was performed at baseline visit, at 6- and 12-month follow-up. The patients did not report any dietary modification during the DMF course and were not on drugs known to affect UA levels. Patients previously treated with glatiramer acetate were excluded.

Results: Eight-teen patients (55% F, mean age: 38.0+10.4 years; mean disease duration: 8.6+6.3 years) completed 6 months of DMF. Mean annual relapse rate (ARR) in the two years before DMF was 0.73+0.7, median baseline EDSS was 1.5 (range 1.5-5). Eight patients (50%) were treatment naïve, eight (50%) switched to DMF from interferons. Of the enrolled patients, eight patients completed 12 months of DMF (no statistical difference in clinical and demographical data).

At baseline, one male and one female had UA levels below the lower limit of the normal (normal: 2.4-5.7 mg/dl for women, 3.4-7 mg/dl for men). After 6 months on DMF, serum UA increased in eleven patients and marginally decreased (4.3 to 4.1 mg/dl) in a single patient. Mean UA increased from 3.3+0.81 to 3.9+0.84 mg/dl. At 12 months, UA levels were higher than at baseline and at 6 months in each patient. At 12 months, mean UA significantly increased compared to baseline (3.4+0.83 vs 4.2+0.66, p=0.04). None of the patients had levels outside the normal range after 6 or 12 months of treatment.

Clinically, there was stability in the relapse rate in DMF-treated patients in the first year of treatment. Out of seven patients in whom information is available, the number of T2- weighted MRI lesions remained stable, and no gadolinium-enhancing lesion was reported.

Conclusion and discussion: This is the first study showing a progressive increase of UA levels during DMF treatment, suggesting a progressive increase of antioxidant reserves. To understand if UA could represent a mechanism of action of DMF in MS, we are increasing our patients" cohort.

Disclosure: G. Mallucci received support to travel to scientific meetings from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva.

V. D"Ambrosio has nothing to disclose.

E. Zardini has nothing to disclose.

D. Franciotta has nothing to disclose.

R. Bergamaschi received research grants from Bayer Schering, Biogen Idec, Merck Serono, Novartis, Sanofi-Aventis, Teva received lecture honoraria from Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva; and received support to travel to scientific meetings from Almirall, Bayer Schering, Biogen Idec, Genzyme, Merck Serono, Novartis, Sanofi-Aventis, Teva.

By clicking “Accept Terms & all Cookies” or by continuing to browse, you agree to the storing of third-party cookies on your device to enhance your user experience and agree to the user terms and conditions of this learning management system (LMS).

Cookie Settings
Accept Terms & all Cookies