Oral lipoic acid as a treatment for acute optic neuritis: a blinded, placebo controlled randomized trial.

Multiple sclerosis intervention lipoic acid optic neuritis

Journal

Multiple sclerosis journal - experimental, translational and clinical
ISSN: 2055-2173
Titre abrégé: Mult Scler J Exp Transl Clin
Pays: United States
ID NLM: 101668877

Informations de publication

Date de publication:
Historique:
received: 08 01 2019
revised: 11 04 2019
accepted: 12 04 2019
entrez: 18 6 2019
pubmed: 18 6 2019
medline: 18 6 2019
Statut: epublish

Résumé

Lipoic acid, an antioxidant, has beneficial effects in experimental acute optic neuritis and autoimmune encephalomyelitis. Optical coherence tomography can detect retinal nerve fiber layer thinning, representing axonal degeneration, approximately 3-6 months after acute optic neuritis. To determine whether lipoic acid is neuroprotective in acute optic neuritis. A single-center, double-blind, randomized, placebo controlled, 24-week trial. Intervention included 6 weeks of once daily lipoic acid (1200 mg) or placebo within 14 days of acute optic neuritis diagnosis. The primary outcome was the mean difference in affected eye retinal nerve fiber layer (RNFL) thickness from baseline to 24 weeks. We enrolled 31 subjects (placebo n=16; lipoic acid n=15; average age 38.6 years (standard deviation (SD) 10.3)). Affected eye mean global RNFL thickness (µm) in the lipoic acid group decreased from 108.47 (SD 26.11) at baseline to 79.31 (SD 19.26) at 24 weeks. The affected eye RNFL in the placebo group decreased from 103.67 (SD 18.04) at baseline to 84.43 (SD 20.94) at 24 weeks. Unaffected eye RNFL thickness did not significantly change in either group over 24 weeks. Six weeks of oral lipoic acid supplementation after acute optic neuritis is safe and well tolerated; however, because of insufficient recruitment, we could not conclude that lipoic acid treatment was neuroprotective in acute optic neuritis.

Sections du résumé

BACKGROUND BACKGROUND
Lipoic acid, an antioxidant, has beneficial effects in experimental acute optic neuritis and autoimmune encephalomyelitis. Optical coherence tomography can detect retinal nerve fiber layer thinning, representing axonal degeneration, approximately 3-6 months after acute optic neuritis.
OBJECTIVE OBJECTIVE
To determine whether lipoic acid is neuroprotective in acute optic neuritis.
METHODS METHODS
A single-center, double-blind, randomized, placebo controlled, 24-week trial. Intervention included 6 weeks of once daily lipoic acid (1200 mg) or placebo within 14 days of acute optic neuritis diagnosis. The primary outcome was the mean difference in affected eye retinal nerve fiber layer (RNFL) thickness from baseline to 24 weeks.
RESULTS RESULTS
We enrolled 31 subjects (placebo n=16; lipoic acid n=15; average age 38.6 years (standard deviation (SD) 10.3)). Affected eye mean global RNFL thickness (µm) in the lipoic acid group decreased from 108.47 (SD 26.11) at baseline to 79.31 (SD 19.26) at 24 weeks. The affected eye RNFL in the placebo group decreased from 103.67 (SD 18.04) at baseline to 84.43 (SD 20.94) at 24 weeks. Unaffected eye RNFL thickness did not significantly change in either group over 24 weeks.
CONCLUSION CONCLUSIONS
Six weeks of oral lipoic acid supplementation after acute optic neuritis is safe and well tolerated; however, because of insufficient recruitment, we could not conclude that lipoic acid treatment was neuroprotective in acute optic neuritis.

Identifiants

pubmed: 31205740
doi: 10.1177/2055217319850193
pii: 10.1177_2055217319850193
pmc: PMC6537072
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2055217319850193

Références

Neurology. 1999 Apr 22;52(7):1479-84
pubmed: 10227638
Jpn J Ophthalmol. 1999 Mar-Apr;43(2):133-8
pubmed: 10340796
Mult Scler. 1999 Aug;5(4):244-50
pubmed: 10467383
J Neurol. 2004 Aug;251(8):996-1005
pubmed: 15316805
Ann Neurol. 2006 Jun;59(6):963-9
pubmed: 16718705
N Engl J Med. 1992 Feb 27;326(9):581-8
pubmed: 1734247
J Neuroimmunol. 2011 Apr;233(1-2):90-6
pubmed: 21215462
Lancet Neurol. 2014 Jan;13(1):83-99
pubmed: 24331795
Neurol Sci. 2015 Apr;36(4):617-20
pubmed: 25311917
Graefes Arch Clin Exp Ophthalmol. 2015 May;253(5):797-801
pubmed: 25605544
Lancet Neurol. 2016 Mar;15(3):259-69
pubmed: 26822749
Lancet Neurol. 2017 Mar;16(3):189-199
pubmed: 28229892
Neurol Neuroimmunol Neuroinflamm. 2017 Jun 28;4(5):e374
pubmed: 28680916
Mult Scler. 2019 Jan;25(1):55-62
pubmed: 29111873
Lancet. 1966 Nov 12;2(7472):1044-6
pubmed: 4162503
Lancet. 1969 Jul 26;2(7613):222
pubmed: 4183170
J Neurol Neurosurg Psychiatry. 1974 Aug;37(8):869-73
pubmed: 4371063
Neurology. 1983 Nov;33(11):1444-52
pubmed: 6685237
Surv Ophthalmol. 1994 Nov-Dec;39(3):262-3
pubmed: 7878526
Arch Ophthalmol. 1993 Jun;111(6):773-5
pubmed: 8512477
Neurology. 1998 Jan;50(1):230-7
pubmed: 9443485
Brain. 1998 Jan;121 ( Pt 1):3-24
pubmed: 9549485

Auteurs

Julie Falardeau (J)

Oregon Health and Science University, USA.

Allison Fryman (A)

Department of Veterans Affairs, MS Center of Excellence - West, USA.

Rohan Wanchu (R)

Oregon Health and Science University, USA.

Gail H Marracci (GH)

Oregon Health and Science University, USA.

Michele Mass (M)

Oregon Health and Science University, USA.

Lindsey Wooliscroft (L)

Oregon Health and Science University, USA.
Department of Veterans Affairs, MS Center of Excellence - West, USA.

Dennis N Bourdette (DN)

Oregon Health and Science University, USA.
Department of Veterans Affairs, MS Center of Excellence - West, USA.

Charles F Murchison (CF)

Department of Biostatistics, University of Alabama at Birmingham, USA.

William L Hills (WL)

Oregon Health and Science University, USA.

Vijayshree Yadav (V)

Oregon Health and Science University, USA.
Department of Veterans Affairs, MS Center of Excellence - West, USA.

Classifications MeSH