From DG News, April 20, 2016:
Link Between Disease Activity and Food Allergies in Patients With Multiple Sclerosis
By Jill Stein
VANCOUVER -- New data demonstrate increased disease activity in patients with multiple sclerosis (MS) and a history of food allergies, according to a study presented here at the 68th Annual Meeting of the American Academy of Neurology (AAN).
Camilo Diaz-Cruz, MD, Brigham and Women’s Hospital, Boston, Massachusetts, and associates presented their data on April 17.
The findings are from a study that explored the association between a history of allergies and MS in patients participating in the Comprehensive Longitudinal Investigation of Multiple Sclerosis at the Brigham and Women’s Hospital (CLIMB) who completed a self-administered questionnaire.
CLIMB is an ongoing prospective cohort study that began in 2000 in which information about MS attacks, neurological examinations, and treatment is prospectively entered into a database. Patients undergo a comprehensive neurological examination every 6 months.
The primary outcome measure in the study was the adjusted annualised relapse rate (ARR) since disease onset.
Patients were classified into 2 groups: allergic (at least 1 known allergy) or never allergic (NA) (no allergies reported). Overall, 922 allergic patients and 427 NA patients were included in the study. A history of food, environmental, and drug allergies was reported in 238 (26%), 586 (64%), and 574 (62%) of patients, respectively.
The adjusted ARR was higher in the allergic group than in the NA group, but this difference was not significant. When stratified by allergy type, patients citing a history of any food allergy had a higher ARR than NA patients (0.08 vs 0.063; P = .0305). No significant differences in the ARR were seen when comparing the environmental or drug allergy groups with the NA group.
The findings suggest that patients with food allergies have more active MS than patients without allergies, concluded the researchers.
They further noted that evidence increasingly points to mast cells as mediators of this association, partly because of their ability to disrupt blood-brain barrier permeability and to release cytokines that activate T cells and macrophages. Also, mast cell-deficient mice develop a less severe experimental autoimmune encephalomyelitis, and inhibitors of mast cell degranulation decrease the severity of EAE. Finally, the use of sedating histamine 1 receptor blockers has been associated with a decreased risk of MS.