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Determination of gluten consumption in celiac disease patients on a gluten-free diet
- Syage, Jack A, Kelly, Ciarán P, Dickason, Matthew A, Ramirez, Angel Cebolla, Leon, Francisco, Dominguez, Remedios, Sealey-Voyksner, Jennifer A
- TheAmerican journal of clinical nutrition 2018 v.107 no.2 pp. 201-207
- biomarkers, calibration, celiac disease, enzymes, gluten, gluten-free diet, histology, intestines, meta-analysis, patients, placebos, protein intake, therapeutics, urine
- Celiac disease (CD) patients adhering to a gluten-free diet (GFD) are exposed frequently to low levels of gluten that contribute to symptoms and persistent intestinal histologic damage. We analyzed prior clinical data to determine how much gluten is accidentally consumed while on a GFD. The aim was to understand the range of gluten consumption for a wide distribution of CD patients. A meta-analysis was conducted on data from 2 different clinical programs: 1) measurements of gluten in stool and urine in CD and non-CD populations; and 2) analysis of data from trials for the investigational therapeutic latiglutenase. The stool and urine studies included controlled gluten challenges. A calibration factor was applied that allowed normal ingestion of gluten to be computed from the urine and stool measurements. From the latiglutenase trial data, a determination of gluten consumption was made by estimating how much gluten was eliminated from patients’ diets due to a trial effect that led to improved histology even in the placebo group. The average inadvertent exposure to gluten by CD individuals on a GFD was estimated to be ∼150–400 (mean) and ∼100–150 (median) mg/d using the stool test and ∼300–400 (mean) and ∼150 (median) mg/d using the urine test. The analyses of the latiglutenase data for CD individuals with moderate to severe symptoms indicate that patients ingested significantly >200 mg/d of gluten. These surrogate biomarkers of gluten ingestion indicate that many individuals following a GFD regularly consume sufficient gluten to trigger symptoms and perpetuate intestinal histologic damage.