Symptoms are not a good indicator of gluten exposure in either patients with coeliac disease (CD) or noncoeliac gluten sensitivity (NCGS), suggests a study. Production of serum interleukin (IL)-2 signals a rapid-onset gluten-induced T-cell activation in CD despite long-standing treatment.
“The effector site is unknown, given no increased intestinal permeability after gluten,” the authors said.
Sixty participants (n=20 treated, healed CD; n=20 treated NCGS; n=20 controls) were randomized to a single, double-blind sham (rice flour) or 3-g gluten challenge with 72-hours follow-up to determine whether blinded gluten exposure induced symptoms, patients accurately identified gluten exposure, and serum IL-2 levels distinguished CD from NCGS patients after gluten exposure.
The authors collected 12 serial questionnaires (100-mm visual analogue scale; pain, bloating, nausea, and fatigue) and 10 serial plasma samples. They used both urinary lactulose-13C mannitol ratios and endoscopic mucosal impedance to assess mucosal permeability.
Of the 40 patients with CD and NCGS, 35 (83 percent) reported symptoms with gluten (eight CD and nine NCGS) and sham (nine CD and nine NCGS) compared with nine of 20 (45 percent) controls after gluten (n=6) and sham (n=3). No significant between-group difference in symptoms was noted.
Only two of 10 patients with CD and four of 10 NCGS identified gluten, while eight of 10 participants with CD and five of 10 NCGS identified sham.
Furthermore, there was a marked plasma IL-2 increase in patients with CD after gluten, which peaked at 3 hours and normalized within 24 hours postchallenge despite no significant intestinal permeability change from baseline.