Essential fatty acids and disease activity in patients with Sjögren’s syndrome Original paper

Sjögren’s syndrome (SS) is an autoimmune disease that mainly affects tear ducts and salivary glands, causing dry eyes, dry mouth, and difficulty swallowing. Previous research in an animal model for SS showed that aspirin could raise the levels of anti-inflammatory resolvin D1, thereby increasing saliva secretion and reducing mouth dryness.

There are two kinds of essential fatty acids (EFAs): omega−3 (ω−3) and omega−6 (ω−6). EPA and DHA (two ω−3 EFAs) are substrates for resolvin synthesis, so there is a potential link between ω−3 levels and SS. The present study examined EFA intake by SS patients and healthy controls and looked for associations between clinical symptoms and disease activity.

This cross-sectional study included 108 patients with SS and 100 healthy controls. EFA intake was assessed via questionnaire. Blood levels of EFAs were measured in the SS patients to search for a correlation between EFAs, cytokines, and indices of disease activity. In a subsample of the SS patients, ocular disease activity and cytokine levels in tears were also assessed.

Median EFA intake was lower in the SS patients, according to the food-intake questionnaire, and the SS patients with the highest disease activity score also tended to have the lowest ω−3 levels. Saliva levels of DHA, α-linolenic acid, and total ω−3 were negatively correlated with the cytokine CCl2, a chemotactic factor implicated in the pathogenesis of SS. Levels of arachidonic acid (an ω−6 EFA) correlated with levels of the cytokine CXCL9 in tears, whereas there was a negative correlation between IL-21 and total ω−6. Although IL-21 plays a role in both anti- and pro-inflammatory activities, it is elevated in SS.

EFA intake was assessed by questionnaire in both SS patients and healthy controls, but EFA levels were only measured in SS patients, so we can’t rule out the possibility that lipid metabolism could be altered in SS patients (relative to healthy controls) independent of dietary intake. It would explain why, although EFA intake was lower in the SS patients, the difference didn’t correlate with serum measurements.