It remains unknown if a proportion of these peptides is also reabsorbed and then metabolized or excreted using alternative pathways. Thus, they demonstrated that gluten-derived peptides enter the kidneys, and after the ultrafiltration process they are partially or totally excreted in the urine.
Several authors have reported the detection of GIP in the urine of patients with CD and healthy individuals using mass spectrometry and antibody-based methods. Furthermore, it has been described that a fraction of longer peptides resistant to the action of the peptidases can also cross the basolateral membrane of the enterocytes and reach portal circulation. As a dietary protein, gluten hydrolyzation occurs mainly in the small intestine by pancreatic enzymes, which break polypeptides into small peptides and amino acids that are transported through the intestinal barrier. There is limited evidence regarding gluten digestion, metabolism, and excretion mechanisms. The pathogenesis of CD involves structural changes in the small intestinal mucosa and intraepithelial lymphocyte infiltration when gluten immunogenic peptides (GIP) resistant to digestive enzymes cross the epithelial barrier to the lamina propria, leading to the activation of both innate and adaptive immune responses.
Importantly, extraintestinal symptoms comprise a substantial proportion of the clinical manifestations of CD such as dermatitis herpetiformis, arthritis, neurological symptoms, anaemia, osteopenia, osteoporosis, tooth enamel defects, aphthous stomatitis, hypertransaminasemia, etc. The clinical presentation of CD is extremely variable, ranging from typical gastrointestinal symptomatology to extraintestinal symptoms or have no symptoms at all. The use of the LFIA test in three urine samples collected at different times may show a sensitivity of 19.6% for a gluten ingestion like 50 mg, increasing to 93% after 2 g consumption.Ĭeliac disease (CD) is a chronic systemic immune-mediated disease triggered by the ingestion of dietary gluten in genetically predisposed individuals with the human leukocyte antigen, HLA-DQ2, and/or HLA-DQ8 haplotypes. Conclusions: An increase in the frequency of urine tests may be a suitable approach to avoid false negative results. The ranges of detection were 3–12 h (50 mg) and 0–15 h (2 g). The higher frequency and concentration of GIP was found between 6 and 9 h after both gluten ingestions. Results: GIP were detected in 15% and 95% of participants after 50 mg and 2 g gluten intakes, respectively. GIP were analyzed by lateral flow immunoassay (LFIA) tests and quantified using an LFIA reader. Methods: 20 healthy participants followed the same diet for 12 days in which 50 mg and 2 g of gluten were ingested and all the urinations were collected. The aim of this study was to determine the range of time and the amount of gluten immunogenic peptides (GIP) excreted in urine after specific gluten ingestions. Background: A lifelong strict gluten-free diet is the only available treatment for celiac disease, but total exclusion of gluten is difficult to achieve.
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