Digestive and Liver Disease - Volume 48 - Supplement 2 - February 2016

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Abstracts of the 22nd National Congress of Digestive Diseases / Digestive and Liver Disease 48S2 (2016) e67–e231 e155
Results: Results. Smad7 protein, but not RNA, expression was
increased in RCD samples compared to normal controls, while there
was no difference between ACD or ICD and normal controls. In RCD
duodenal mucosa, Smad7-positive cells were abundant in both the
epithelial and lamina propria compartments. TGFb1 protein content
did not differ among groups. However, TGFb1-associated Smad2/3
phosphorylation was less pronounced in RCD as compared to
controls. Knockdown of Smad7 in RCD biopsy samples reduced RNA
expression of interleukin (IL)-15, IL-6 and TNFa, all cytokines that
are over-produced in RCD mucosa.
Conclusions: Conclusions. High Smad7 associates with defective
TGFb1 signalling in RCD, thus suggesting a novel mechanism
by which the ongoing mucosal inflammation is sustained and
perpetuated in this disorder.
P.06.6
SUBTYPES OF CHRONIC GASTRITIS IN PATIENTS WITH COELIAC
DISEASE BEFORE AND AFTER GLUTEN-FREE DIET
Gabrieli D.*, Valerii G., Ciccone F., Di Ruscio M., Serva D.,
Capannolo A., Viscido A., Melideo D., Frieri G., Necozione S.,
Latella G.
Università degli studi dell’Aquila, L’Aquila, Italy
Background and aim: Chronic gastritis appears to be more common
in patients with coeliac disease (CD). Aim of this study is to evaluate
the frequency of lymphocytic gastritis (LG), chronic active gastritis
(CAG) and chronic inactive gastritis (CIG) in a cohort of patients with
CD, and their histological changes after treatment with a gluten-free
diet.
Material and methods: A five-year prospective study including all
consecutive patients with a new diagnosis of CD performed at our
GI Unit, in the period between January 2010 and January 2015. All
gastric and duodenal biopsy specimens at the time of the diagnosis of
CD and at the first endoscopic control after 18-24 months on gluten
free diet were analyzed. CD diagnosis was made in the presence of
anti-tissue transglutaminases and/or anti-endomisial antibodies
associated with specific alterations at histological evaluation of
duodenal biopsies, according to the modified Marsh-Oberhuber
classification. Gastric lesions were classified according to the
Updated Sydney System. Giemsa staining was used for histological
diagnosis of Helicobacter pylori infection and immunohistochemical
staining for the diagnosis of LG, defined as a dense proliferation of
intraepithelial lymphocytes (more than 25 lymphocytes per 100
epithelial cells). Anti-gastric parietal cell antibodies were assayed
by enzyme-linked immunosorbent assay (ELISA). Demographic,
clinical, and laboratory data were collected.
Results: 250 patients with CD were enrolled (191 F, 59 M, mean age
34 years at the diagnosis). At the time of CD diagnosis, histological
examination showed normal gastric mucosa in 78 patients (31.2%),
LG in 32 (12.8%), CAG in 74 (29.6%), and CIG in 66 (26.4%).
Out of 32 patients with LG, 20 (62.5%) were H. pylori negative and all
of them showed an improvement of gastritis after gluten free diet.
Out of 74 patients with CAG, 30 (40.5%) were H. pylori negative and
one third of them showed an improvement of gastritis after gluten
free diet.
Out of 66 patients with CIG, 63 (95.4%) patients were H. pylori
negative.
LG is significantly associated to histological improvement after
gluten-free diet compared to other types of gastritis (p= 0.0039).
Conclusions: Subtypes of gastritis have different probability to be
influenced by the gluten-free diet. LG is present in a significant
number (13%) of CD patients and seems to improve as well as
duodenal lesions after gluten free diet. Two thirds of LG are not
associated with H. pylori infection. Both CAG and CIG are also
significantly associated with coeliac disease, despite less influenced
by gluten free diet.
P.06.7
GLIADIN EFFECT ON THE OXIDATIVE BALANCE AND DNA DAMAGE
IN CACO-2 CELL LINE
Monguzzi E.*2, Marabini L.1, Roncoroni L. 3, Doneda L.3, Conte D.2,
Elli L.3
1Department of Pharmacological and Biomolecular Sciences, Università
degli Studi di Milano, Milano, Italy, 2Department of Pathophysiology
and Transplantation, Università degli Studi di MIlano, Milano, Italy,
3Gastroenterology and Endoscopy Unit and Center for Prevention and
Diagnosis of Celiac Disease, Fondazione IRCCS Cà Granda - Ospedale
Maggiore Policlinico - Milan, Milano, Italy
Background and aim: Wheat has been identified as a key
environmental factor in different human disorders (celiac disease,
food allergies and non-celiac gluten sensitivity). As its components
(gliadins) can induce different cellular and biological noxious
alterations, present study was aimed at evaluating the gliadin effect
on oxidative/reductive balance and assessing the possible oxidative/
genotoxic damage.
Material and methods: Caco-2 cells were exposed for 12-24 h to
increasing concentrations (from 250 to 1000μg/mL) of digested
gliadin, then investigating : i) cytotoxicity (MTT test); ii) oxidative
balance (DCFDA ROS evaluation); iii) DNA damage by means of
comet assay (Alkaline and with ENDO III e Fpg enzymes) to identify
single and double strand DNA breaks; iv) transglutaminase type 2
(TG2) activity in different cellular compartments (including nucleus,
cytoskeleton, membranes and cytoplasm) with ELISA assay.
Results: Gliadin treatment did not significantly reduce cell viability
after 24h at different concentration (250µg/mL-1000μg/mL).
Conversely, gliadin induced a significant increase of ROS production
after 12h of exposition at the concentrations of 500μg/ml and
1000μg/mL. Alkaline comet analysis revealed a DNA damage in all
of the analyzed parameters (Tail length, Tail moment and % DNA),
the damage being particularly evident at the dose of 1000μg/mL.
Moreover, comet analysis with enzymes showed an increase in
the delta tail moment at 1000μg/mL, consist of oxidative origin of
the damage. After gliadin treatment, TG2 activity increased from
191% to 310% into the cytoskeleton and from 117% to 153% into the
nucleus. The analysis of cellular compartments evidenced a TG2
translocation from the cytoplasm to the nucleus and cytoskeleton
suggesting a proapoptotic process.
Conclusions: Present findings demonstrated with a gliadin-induced
genotoxic damage associated to both an oxidative imbalance and an
apoptotic process.
P.06.8
SERUM 25-HYDROXYCHOLECALCIFEROL LEVELS AT CELIAC
DISEASE DIAGNOSIS PREDICT BONE MINERAL DENSITY
RECOVERY AFTER GLUTEN EXCLUSION
Efthymakis K.*, Serio M., Sanelli R., Milano A., Laterza F.,
Bonitatibus A., Neri M.
Department of Medicine and Ageing Sciences, “G. D’Annunzio”
University and Foundation, Chieti, Italy
Background and aim: Celiac disease (CD) patients at presentation
variably show reduced bone mineral density (BMD) and altered
bone-related serology, including serum 25-hydroxycholecalciferol
(25[OH)]VitD). Gluten-free diet (GFD) has been shown to promote
repair in children and to a smaller extent in adults. However,
complete bone mineral recovery is uncertain and predictive markers
are lacking.