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 e157
Material and methods: The biopsy proven celiac patient undergone
gluten-free diet (GFD) for 5 years, with moderate benefits. Two
years ago she presented anaphylaxis, after eating a salty wheat
pancake, that was granted to be gluten-free. Subsequently, she
presented Food Dependent Exercise Induced Anaphylaxis (FDEIA),
commonly found in adults, diagnosed by an exercise challenge test
following wheat ingestion: the most severe response is attributed
to one w gliadin that is a relative of the protein that causes celiac
disease. We performed skin prick tests (mm) that were positive for
Parietaria judaica (20), grass pollen (5), peach containing uniquely
lipid transfer protein (Pru p3, 30 mg/mL; ALK-Abelló, Denmark) (5),
kiwi (5), wheat (10), zucchini (5), corn (5), rye (10). Prick-prick tests
were positive for wheat flour (5), crude corn (7) [3].
Results: Blood cell count, biochemistry, and Ig determinations
were normal. Total serum IgE was 215 kU/l. Values for specific IgE
(Phadia-CAP, Uppsala, Sweden) in kUA/L were as follows: wheat
gluten (16.4), rye (11.3), barley (11.0), corn (0.46), rPru p3 (0.38), Phl
p2 (0.58), wheat (27.5). rTri a 19 w-5 gliadin was found negative, r tri
a 14 (Ltp of wheat) 19.3 was positive.
Despite the daily administration of high-dose of inhaled combined
fluticasone/salmeterol (2000/200 lg) and montelukast tablet (10
mg), the patient suffered constantly from respiratory symptoms.
The patient has allergy to pollen and dust mites. Because of celiac
disease has not been carried food challenge either at rest or after
exercise. She is still following a dietary regime for celiac patients.
We gradually reduced the restriction on wheat consumption for
gluten-free products.
Conclusions: In both cereal allergy and celiac disease (CD),
the reaction to gluten is mediated by T-cell activation in the
gastrointestinal mucosa. However, in cereal allergy it is the cross-
linking of immunoglobulin (Ig)E by repeat sequences in gluten
peptides (for example, serine-glutamine-glutamine -glutamine-
(glutamine-) proline-proline-phenylalanine) that triggers the
release of chemical mediators, such as histamine, from basophils
and mast cells [1]. In contrast, CD is an autoimmune disorder, as
demonstrated by specific serologic autoantibodies. anti TG and EMA.
The diagnosis of IgE-mediated allergy is based on the clinical history
and presence of IgE-antibodies (IgE-Ab) in skin or blood, and the
result of an oral food challenge. In our knowledge, the coexistence
in the same patient of both these wheat related disease is very rare.
P.07 IBD 1
P.07.1
GUT MICROBIOTA MOLECULAR SPECTRUM IN HEALTHY
CONTROLS, DIVERTICULAR DISEASE, IBS AND IBD PATIENTS:
TIME FOR MICROBIAL MARKER OF GASTROINTESTINAL
DISORDERS?
Lopetuso L.R.*1, Petito V.1, Schiavoni E.1, Zambrano D.1,
Paroni Sterbini F.2 , Gaetani E.1, Franceschi F.1, Cammarota G.1,
Sanguinetti M.2, Masucci L.2, Scaldaferri F.1, Gasbarrini A.1
1Internal Medicine, Gastroenterology Division, Catholic University
of Sacred Heart, Roma, Italy, 2Institute of Microbiology, Catholic
University of Sacred Heart of Rome, Roma, Italy
Background and aim: Increasing evidences have emerged on
the analysis of bacterial species making up the gastrointestinal
microbiota. However few data exist on differences in gut microbiota
composition in GI diseases, such as IBD, IBS and diverticular disease
compared to healthy controls.
Material and methods: Aim of our study was to evaluate the
differences in gut microbiota composition between IBD, IBS and
diverticular disease (DD) patients. 10 Crohn’s Disease (CD), 5
Ulcerative Colitis (UC), 4 DD, 3 IBS patients, and 8 controls (CD)
were enrolled and fecal samples collected from each. Microbiota
composition was assessed by a metagenomic gene-targeted
approach (16S rRNA) using the Roche 454 GS Junior, following DNA
isolation from stool samples stored at –80 °C. Data were analyzed in
Qiime. Individual species richness was estimated using Chao1 alpha-
diversity index. We also explored the differential relative abundance
of several taxa of interest, selected according to literature.
Results: Bacteria amplicons were detected in all samples. Prevalent
classes of bacteria were: Bacteroidia (min 13,06% - max 91,55%),
Firmicutes (min 7,48% - max 86,10%) and Proteobacteria (min 0,48% -
max 46,48%). Fusobacteria were found only in CD and DD patients
(min 0,67%- max 50,71%). IBD microbiota composition differed
significantly compared to all other. In particular, UC patients showed
a reduced concentration in Bacteroidetes and an increased presence
of Firmicutes vs. CT, DD and IBS. On the other side, Bacteroidetes and
Firmicutes composition varied among CD patients, being increased
or reduced when compared to the other groups. Proteobacteria
were increased in all diseased group compared to CT, being more
represented in CD and IBS-D. Moreover, Actinobacteria were
increased in IBD and DD vs. IBS and CT. The most represented
species in IBD and DD vs. other groups was Collinsella Aerofaciens.
Rikenellaceae were suppressed in IBD patients, as well as
Fecalibacterium Prausnitzii. Akkermansia Muciniphila was present
only in IBS patients. Enterobacteriaceae were increased only in CD
patients vs. other groups. Finally, while chao1 score was similar
between CT, IBS and DD, it was deeply reduced in IBD patients.
Conclusions: These preliminary data show that starting from
microbiota, GI disease can be a continuous pathological spectrum
where IBD display one extreme in gut microbiota composition while
controls display the other. Furthermore, GI diseases share some
microbial patterns, sharing perhaps common pathophysiological
pathways. New analyses are needed to confirm this hypothesis and
evaluate therapeutical implications.
P.07.2
BEYOND MUCOSAL HEALING: TRANSMURAL AND EXTRAMURAL
HEALING AFTER ONE-YEAR ANTI-TNFA THERAPY IN CROHN’S
DISEASE
Serio M.*1, Efthymakis K.1, Milano A.1, Pierro A.2, Laterza F.1,
Maselli G.2, Bonitatibus A.1, Sallustio G.2, Neri M.1
1Medicine and Aging Sciences and CESI, Universita` “G. D’Annunzio”,
Chieti, Italy, 2Radiology Department, Fondazione di Ricerca e
Cura ‘‘Giovanni Paolo II’’, Universita` Cattolica del Sacro Cuore,
Campobasso, Italy
Background and aim: Crohn’s disease (CD) is characterized by
transmural (full-thickness) inflammation, frequently with extra­
mural complications beyond to the mesentery and adjacent organs.
The capability of anti-TNFa therapies in achieving and maintaining
both clinical remission and mucosal healing (MH) has repeatedly
been described, while only one study was designed to assess
prospectively their role in transmural healing. Aim of this study
was to analyze transmural healing (TH) in consecutive CD patients
after a 1-year treatment with anti-TNFa and to correlate TH with
endoscopic and clinical activity as well as biological markers.
Material and methods: 13 patients with moderate to severe
ileocolic CD were enrolled. All underwent ileocolonoscopy and MRI-
enterography before and after 1-year treatment with anti-TNFa;
clinical remission was defined as CDAI<150, response as a 70-point
reduction from baseline. CRP and fecal calprotectin (FC) (positivity
cut-off respectively>0,50 mg/dl and >150 μg/gr) were also measured.
Endoscopic activity was assessed by SES-CD, range 0-40, with
mucosal healing defined as score <3 and response as a 50% decrease