SC12
Protective Environmental Risk Factors for Neuromyelitis Optica

Thursday, May 29, 2014
Trinity Exhibit Hall
Jennifer Graves, MD, PhD , UCSF Pediatric MS Center, San Francisco, CA
Sirisha Grandhe, BA , UCSF Pediatric MS Center, San Francisco, CA
Kelley M Weinfurtner, B.A. , UCSF Pediatric MS Center, San Francisco, CA
Lauren Krupp, MD , Department of Neurology, SUNY Stony Brook, Stony Brook, NY
Tanuja Chitnis, MD , Massachusetts General Hospital for Children, Boston, MA
Jayne Ness, MD , Alabama Pediatric MS Center, Birmingham, AL
Moses Rodriguez, MD , Department of Neurology, Mayo Clinic, Rochester, MN
Tim Lotze, MD, PhD , Texas Children's Hospital, Houston, TX
Mark Gorman, MD , Massachusetts General Hospital, Partners Pediatric MS Center, Boston, MA
Ellen Mowry, MD, MCR , Neurology, Johns Hopkins Hospital, Baltimore, MD
Maria Milazzo, NP , Neurology, Stony Brook University Medical Center, Stony Brook, NY
Judith A James, MD , Rheumatology, Oklahoma Medical Research Foundation, University of Oklahoma, Oklahoma City, OK
T. Charles Casper, PhD , Department of Pediatrics, University of Utah, Salt Lake City, UT
Emmanuelle Waubant, MD, PhD , UCSF Pediatric MS Center, San Francisco, CA



Background:

Risk factors for neuromyelitis optica (NMO) are largely unknown.

Objectives:

To determine if environmental factors known to modify multiple sclerosis (MS) risk are associated with the risk of neuromyelitis optica (NMO) in children. 

Methods:

This is a case-control study of prospectively enrolled pediatric NMO, MS and healthy subjects. Early life exposures were obtained by standardized questionnaire. Serum 25(OH) vitamin D levels were measured by chemoluminescence assay.  EBV, CMV, HSV-1, and HSV-2 antibody responses were determined by ELISA. Multivariate logistic regression models were used to determine risk factor associations with NMO including adjustments for age at sampling, sex, race and ethnicity.

Results:

Early life exposures were obtained from 36 pediatric subjects with NMO, 491 with MS and 224 healthy controls. Daycare (OR 0.33 95% CI 0.14, 0.80, p=0.01) and breastfeeding (OR 0.41 95%CI 0.18,0.96; p=0.04) were associated with lower odds of having NMO compared to healthy subjects. C-section tended to be associated with a two-fold higher odds of NMO. Parental smoking was not meaningfully associated with NMO risk. A subgroup of the subjects had serotyping (34 NMO, 189 MS, 94 controls). Compared to MS patients, EBV exposure tended to be associated with lower odds to have NMO (EBNA1 OR 0.156, 95% CI 0.022, 1.089, p=0.06).  HSV-1 exposure (OR 0.147, 95%CI: 0.025 to 0.862, p=0.034) and being DRB1*15 positive (OR 0.18, 95%CI: 0.035, 0.93, p=0.040) were also associated with lower odds to have NMO. 

Conclusions:

Early exposure to other young children may be a protective factor against the development of NMO, as previously reported for MS, suggesting that viral infections may contribute to disease risk modification.  Unlike MS, pediatric NMO does not appear to be associated with exposures to common herpes viruses.