The Challenge of Treatment in Potential Celiac Disease

Table 1

A short history of the most important findings concerning PCD.

Study	Year	Conclusions
Holm et al. [29]	1992	A healthy person who initially has a normal biopsy, but who also has an increased density of γδ T-cells, may later develop mucosal atrophy compatible with CD.
Iltanen et al. [30]	1999	39 of 79 (49%) children with normal jejunal mucosa had an increased density of intraepithelial γδ T-cells.
Jarvinen et al. [28]	2003	An increase especially in γδ T-cells strengthens the probability of CD.
Korponay-Szabo et al. [20]	2004	TG2-related IgA deposits in the morphologically normal jejunum were predictive of forthcoming overt coeliac disease with villous atrophy.
Jarvinen et al. [27]	2004	The villous tip intraepithelial lymphocyte count was statistically significantly higher in patients with early-stage coeliac disease than in nonceliac controls (sensitivity, 0.84; specificity, 0.88).
Paparo et al. [17]	2005	Increased number of lamina CD25+ and/or enhanced expression of ICAM 1 and crypt HLA DR.
Salmi et al. [23]	2006	Intestinal coeliac autoantibody deposit had a sensitivity and specificity of 93% and 93%, respectively, in detecting subsequent coeliac disease.
Koskinen et al. [21]	2010	Mucosal transglutaminase 2-specific autoantibody deposits proved to be accurate gluten-dependent markers of celiac disease.
Tosco et al. [25]	2011	In most positive cases a patchy distribution of the deposits was observed with areas of clear positivity and areas with absent signal.
Bernini et al. [35]	2011	Potential CD largely shares the metabolomic signature of overt CD. Results prove that metabolic alterations may precede the development of small intestinal villous atrophy.
Biagi et al. [31]	2013	In PCD, the intestinal mucosa is maintained architecturally normal thanks to an increased enterocytic proliferation.
Borrelli et al. [32]	2013	Potential CD patients show a low grade of inflammation that could likely be due to active regulatory mechanism preventing the progression toward a mucosal damage.
Borrelli et al. [33]	2016	In potential CD, IL-21 is less expressed than that in active CD.
Borrelli et al. [22]	2018	In CD, the intestinal deposits of anti-tTG2 are a constant presence and appear very early in the natural history of the disease.