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= GIP, Gluten inmunogenic peptides = GIP are fragments of the peptides from gluten that are retentive to degradation in the digestive process. These peptides start a series of immunogenic reactions in the celiac patient. The resistance of GIP to digestion ensures that a relevant part of them will be excreted by any person that ingest gluten. Due to this fact, the recovery of this amounts of GIP in urine and stool samples shows if there has been gluten ingestion. This diagnostic method is non-invasive because it doesn´t need any biopsy or blood extraction.

The benefits are the following: an improvement in the general monitoring of the disease and sensitivity to gluten without celiac, improving the quality of life and well-being of these patients to avoid the consequences of gluten intake. This also translates into a reduction of costs for the health system that is carried out in cases of persistence of symptoms and complications.

The detection of GIP in stool and urine samples is a direct, objective, non-invasive and precise method for the monitoring and monitoring of DSG in the short and long term. GIP are useful in patients with negative serology:

o 71% of the population with transgressions to the DSG (GIP +) are negative in anti-TTG.

o 87% of the population with transgressions to the DSG (GIP +) are negative in anti-DGP.

Regarding the urine samples in the clinical trial Moreno ML., Et al. Gut 2017 [ref. 9) has been created that there is a better correlation between presence and absence of GIP in urine samples and persistence / absence of atrophy in the intestinal mucosa of celiac patients of the existence with other markers such as tissue anti-transglutaminase antibodies.

To establish a correlation between GIP in the urine of adults with CD and the appearance of mucosal damage, a histological study of 25 intestinal biopsies of adults with CD who had undergone a DSG for at least 2 years was performed.

Correlation between the presence of GIP in the urine and the histology of the small intestine in adult patients with CD. Histological aspect determined by the Marsh scale of the severity of the mucosal lesion (Marsh I-III). GIP- (white bar), absence of GIP in the urine; GIP + (gray bar), visual presence of non-quantifiable GIP in the urine (> LDT  QL). p = 0.0007 (Fisher's exact test). The values ​​are expressed as a percentage of patients. CD, celiac disease; GIP, immunogenic gluten peptides; LDT, limit of detection of the technique; QL, limit of quantification.

Only 13 of the 25 patients with GIP- (52%) and none of them had histological damage to the mucosa (ie, all were Marsh 0-I). Of the 13 GIP- individuals, 5 had Marsh 0 (normal mucosa) and 8 had Marsh I (elevated IEL without structural changes). All patients with GIP- were TTG / AGA - also. In contrast, six out of seven adults with CD with clear histological abnormalities (crypt hyperplasia - Marsh II and mucosal atrophy - Marsh III) had detectable levels of GIP in the urine (86%), and only one subject with Marsh III had detectable but not quantifiable levels of GIP in the urine.

A difference of the excellent GIP correlation with histology, serological data had no correlation with mucosal damage. We found positivity in anti-TTG and / or AGA in only four individuals, two with Marsh and the other two with Marsh II. Five patients with severe mucosal injury were not positive in either TTG or AGA (71.4%).

Therefore, this study indicated that only the detection of GIP in urine correlated with the compliance of DSGGFD and with mucosal function in patients with CDRS in a GFDDSG.

Regarding stool samples in the clinical trial Comino I., et al. 2016 the results have been obtained in the laboratory tests for the correction between the different antibodies of the gluten and the GIP as those that can be observed in the following graph:

a) Correlation between anti-tTG-IgA and fecal GIP.

b) Correlation between anti-DGP-IgA and fecal GIP.

The positivity for both anti-tTG IgA and for GIP was selected in 14 patients. However, anti-tTG IgA was negative in 40 of the 56 patients with positive stool for GIP. Therefore, there was no association between fecal GIP and anti-tTG IgA (P = 0.230). In contrast, there is an association between the levels of GIP and anti-DGP IgA (P = 0.044). Elevated amounts of anti-DGP IgA were found in 11 patients, 6 of which were also positive for GIP in faeces. The negative levels of anti-DGP IgA were manifested in 160, and of these, 114 had undetectable levels of GIP in feces.