Features and Progression of Potential Celiac Disease in Adults

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Features and Progression of Potential Celiac Disease in Adults Umberto Volta, Giacomo Caio, Fiorella Giancola, Kerry J. Rhoden, Eugenio Ruggeri, Elisa Boschetti, Vincenzo Stanghellini, Roberto De Giorgio  Clinical Gastroenterology and Hepatology  Volume 14, Issue 5, Pages 686-693.e1 (May 2016) DOI: 10.1016/j.cgh.2015.10.024 Copyright © 2016 AGA Institute Terms and Conditions

Figure 1 Management of 77 PCD patients enrolled in the study. Symptomatic PCD (n = 61) patients commenced a GFD, with clinical and serologic follow-up every 6 months to assess the response to GFD. Asymptomatic PCD (n = 16) patients were left on a GCD, with clinical and serologic follow-up every 6 months and histologic evaluation every 2 years to assess the progression to ACD. Clinical Gastroenterology and Hepatology 2016 14, 686-693.e1DOI: (10.1016/j.cgh.2015.10.024) Copyright © 2016 AGA Institute Terms and Conditions

Figure 2 Clinical features of PCD. Sixty-one of 77 patients (79%) with PCD were symptomatic, whereas the remaining 16 (21%) were asymptomatic. Of the symptomatic patients, only 16% showed the classic phenotype (diarrhea and weight loss), whereas the majority (84%) had the non-classic phenotype characterized by anemia, osteopenia, aphthous stomatitis, hypertransaminasemia, IBS-like symptoms, gastroesophageal reflux disease (GERD), and recurrent miscarriages. Clinical Gastroenterology and Hepatology 2016 14, 686-693.e1DOI: (10.1016/j.cgh.2015.10.024) Copyright © 2016 AGA Institute Terms and Conditions

Figure 3 Follow-up of 16 cases with asymptomatic PCD left on a GCD (3-year mean follow-up). One patient developed symptoms and raised antibody titers, with duodenal biopsy confirming ACD. The remaining 15 patients remained asymptomatic; 4 of them had antibody disappearance, 1 showed antibody fluctuation, and 10 had stable antibody positivity. Repeated duodenal biopsies, performed every 2 years in cases with antibody persistence and fluctuation, did not reveal any progression to ACD. Clinical Gastroenterology and Hepatology 2016 14, 686-693.e1DOI: (10.1016/j.cgh.2015.10.024) Copyright © 2016 AGA Institute Terms and Conditions

Figure 4 Variation of anti-EmA titer and anti-tTGA activity during mean follow-up of 3 years in 16 adults with PCD on GCD. Clinical Gastroenterology and Hepatology 2016 14, 686-693.e1DOI: (10.1016/j.cgh.2015.10.024) Copyright © 2016 AGA Institute Terms and Conditions

Figure 5 Representative photomicrographs illustrating IgA anti-TG2 intestinal deposits in 2 cases of asymptomatic PCD. Positivity of such deposits is indicated by white arrows in both pictures. Green arrows show the presence of TG2, and red arrows indicate positivity for IgA. Calibration bars = 50 μm. Clinical Gastroenterology and Hepatology 2016 14, 686-693.e1DOI: (10.1016/j.cgh.2015.10.024) Copyright © 2016 AGA Institute Terms and Conditions

Supplementary Figure 1 Other representative photomicrographs illustrating IgA anti-TG2 intestinal deposits (A, arrowheads), side-by-side with histologic (B) and immunohistochemical (C) findings of a patient with PCD. Note the dense CD3 immunostaining indicating an abundant lymphocytic infiltrate and increased IELs. Calibration bar for A–C = 25 μm. Clinical Gastroenterology and Hepatology 2016 14, 686-693.e1DOI: (10.1016/j.cgh.2015.10.024) Copyright © 2016 AGA Institute Terms and Conditions