TY - JOUR
T1 - Association of body mass index with longitudinal rates of retinal atrophy in multiple sclerosis
AU - Filippatou, Angeliki G.
AU - Lambe, Jeffrey
AU - Sotirchos, Elias S.
AU - Fitzgerald, Kathryn C.
AU - Aston, Andrew
AU - Murphy, Olwen C.
AU - Pellegrini, Nicole
AU - Fioravante, Nicholas
AU - Risher, Hunter
AU - Ogbuokiri, Esther
AU - Kwakyi, Ohemaa
AU - Toliver, Brandon
AU - Davis, Simidele
AU - Luciano, Nicholas
AU - Crainiceanu, Ciprian
AU - Prince, Jerry L.
AU - Mowry, Ellen M.
AU - Calabresi, Peter A.
AU - Saidha, Shiv
N1 - Funding Information:
The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was funded by the National MS Society (RG-1606-08768 to S.S.), Race to Erase MS (to S.S.), and NIH/NINDS (R01NS082347 to P.A.C.).
Funding Information:
The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: A.G.F., J.L., A.A., O.C.M., N.P., N.F., H.R., E.O., O.K., and B.T. report no disclosures. K.C.F. is funded by a Career Transition Fellowship from the National MS Society (NMSS). E.S.S. has served on a scientific advisory board for Viela Bio and is funded by a Sylvia Lawry physician fellowship award from NMSS. J.L.P. is a founder of Sonovex, Inc. and serves on its Board of Directors. He has received consulting fees from JuneBrain LLC and is PI on research grants to Johns Hopkins from 12Sigma Technologies and Biogen. E.M.M. has grants from Biogen and Genzyme, is site PI for studies sponsored by Biogen, has received free medication for a clinical trial from Teva, and receives royalties for editorial duties from UpToDate. P.A.C. has received consulting fees from Disarm Therapeutics and Biogen and is PI on grants to JHU from Biogen and Annexon. S.S. has received consulting fees from Medical Logix for the development of CME programs in neurology and has served on scientific advisory boards for Biogen, Genzyme, Genentech Corporation, EMD Serono, and Celgene. He is the PI of investigator-initiated studies funded by Genentech Corporation and Biogen and received support from the Race to Erase MS foundation. He has received equity compensation for consulting from JuneBrain LLC, a retinal imaging device developer. He is also the site investigator of a trial sponsored by MedDay Pharmaceuticals.
Publisher Copyright:
© The Author(s), 2020.
PY - 2020/6/1
Y1 - 2020/6/1
N2 - Background: Studies evaluating associations between body mass index (BMI) and optical coherence tomography (OCT) measures in multiple sclerosis (MS) are lacking. Objective: To assess whether elevated BMI is associated with accelerated retinal atrophy. Methods: In this observational study, 513 MS patients were followed with serial spectral-domain OCT for a median of 4.4 years. Participants were categorized as normal weight (BMI: 18.5–24.9 kg/m2), overweight (BMI: 25–29.9 kg/m2), and obese (BMI: ⩾30 kg/m2). Participants with diabetes mellitus or uncontrolled hypertension and eyes with optic neuritis (ON) ⩽6 months prior to baseline OCT or during follow-up were excluded. Statistical analyses were performed with mixed-effects linear regression. Results: Obese patients (n = 146) exhibited accelerated rates of ganglion cell + inner plexiform layer (GCIPL) atrophy relative to normal weight patients (n = 214; –0.57%/year (95% confidence interval (CI): –0.65% to –0.48%) versus –0.42%/year (95% CI: –0.49% to –0.35%); p = 0.012). GCIPL atrophy rate did not differ between overweight (n = 153) and normal weight patients (–0.47%/year vs –0.42%/year; p = 0.41). Each 1 kg/m2 higher BMI was associated with accelerated GCIPL (–0.011%/year; 95% CI: –0.019% to –0.004%; p = 0.003) atrophy. Multivariable analyses accounting for age, sex, race, MS subtype, and ON history did not alter the above findings. Conclusions: Elevated BMI, in the absence of overt metabolic comorbidities, may be associated with accelerated GCIPL atrophy. Obesity, a modifiable risk factor, may be associated with accelerated neurodegeneration in MS.
AB - Background: Studies evaluating associations between body mass index (BMI) and optical coherence tomography (OCT) measures in multiple sclerosis (MS) are lacking. Objective: To assess whether elevated BMI is associated with accelerated retinal atrophy. Methods: In this observational study, 513 MS patients were followed with serial spectral-domain OCT for a median of 4.4 years. Participants were categorized as normal weight (BMI: 18.5–24.9 kg/m2), overweight (BMI: 25–29.9 kg/m2), and obese (BMI: ⩾30 kg/m2). Participants with diabetes mellitus or uncontrolled hypertension and eyes with optic neuritis (ON) ⩽6 months prior to baseline OCT or during follow-up were excluded. Statistical analyses were performed with mixed-effects linear regression. Results: Obese patients (n = 146) exhibited accelerated rates of ganglion cell + inner plexiform layer (GCIPL) atrophy relative to normal weight patients (n = 214; –0.57%/year (95% confidence interval (CI): –0.65% to –0.48%) versus –0.42%/year (95% CI: –0.49% to –0.35%); p = 0.012). GCIPL atrophy rate did not differ between overweight (n = 153) and normal weight patients (–0.47%/year vs –0.42%/year; p = 0.41). Each 1 kg/m2 higher BMI was associated with accelerated GCIPL (–0.011%/year; 95% CI: –0.019% to –0.004%; p = 0.003) atrophy. Multivariable analyses accounting for age, sex, race, MS subtype, and ON history did not alter the above findings. Conclusions: Elevated BMI, in the absence of overt metabolic comorbidities, may be associated with accelerated GCIPL atrophy. Obesity, a modifiable risk factor, may be associated with accelerated neurodegeneration in MS.
KW - Multiple sclerosis
KW - body mass index
KW - optical coherence tomography
KW - retina
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U2 - 10.1177/1352458519900942
DO - 10.1177/1352458519900942
M3 - Article
C2 - 32297826
AN - SCOPUS:85083577036
SN - 1352-4585
VL - 26
SP - 843
EP - 854
JO - Multiple Sclerosis Journal
JF - Multiple Sclerosis Journal
IS - 7
ER -