Abstracts of the 23rd National Congress of Digestive Diseases / Digestive and Liver Disease 49S2 (2017) e73–e223
postprandial inflammation. Therefore, our aim was the evaluation
of postprandial modification of both inflammatory and antioxidant
markers in a group of HV after administration of different oral
gluten loads.
Material and methods: 20 non-smoking, normal-weighted HV
were enrolled. After an overnight fast, all the subjects underwent
an evaluation of serum levels of proinflammatory cytokines (IL1β,
IL6 and TNFα), endogenous antioxidant system (uric acid), glucose
and insulin while fasting and after an oral gluten load of 2g (in
10 HV) or 20g (in 10 HV) every 30 minutes for a 4-hour period.
Moreover, serum lipopolysaccharide (LPS) was measured as a pu-
tative factor responsible for inflammatory response. The presence
and severity of gastrointestinal symptoms were monitored by VAL
while fasting and in the postprandial period.
Results: After the ingestion of the 2g oral load of gluten none
of the measured paramether showed a significant increase in
the postprandial period. On the contrary, after the ingestion of
the 20 gr oral load mean values of TNFα and IL1β showed a
significant increase (2.45±1.75pg/ml and 0.65±0.31pg/ml) as com-
pared to mean fasting values (1.17±1.49pg/ml and 0.29±0.15pg/ml;
p<0.05). Moreover, only in the 20gr group, mean postprandial
values of uric acid were significantly higher (74.98±33.02nmol/ml)
than in fasting condition (45.34±10.08nmol/ml; p<0.05). IL6, glu-
cose, insulin and LPS did not show any significant difference after
the ingestion of the 20 gr gluten oral load. Symptoms were generally
absent after both oral loads and, when present, they were sporadic
and negligible.
Conclusions: Our results show that in HV the ingestion of a high,
but not a low, oral load of gluten induces an important postprandial
inflammatory response causing the activation of the main endoge-
nous antioxidant system. However, in HV a symptomatic response
did not accompany these activations. Further studies are needed to
investigate inflammatory and antioxidant postprandial response in
patients with gluten-related disorders.
P.03.14
THE ROLE OF SMALL INTESTINAL BACTERIAL OVERGROWTH IN
CYSTIC FIBROSIS: A RANDOMIZED CASE-CONTROLLED CLINICAL
TRIAL WITH RIFAXIMIN
A. De Alessandri 1 , M. Furnari ∗,2 , M. Bassi 1 , M. Haupt 1 , R. Haupt 3 ,
P. Gandullia 4 , A. Calvi 4 , F. Bagnasco 3 , G. Romanisio 1 , V. Savarino 2 ,
L. Minicucci 1
1 Cystic
Fibrosis Center, IRCCS G. Gaslini Institute, University of Genoa,
Genoa, Italy; 2 Department of Internal Medicine, Gastroenterology Unit,
IRCCS Azienda Ospedaliera Universitaria San Martino-IST, University of
Genoa, Genoa, Italy; 3 Epidemiology and Biostatistic Service, IRCCS G.
Gaslini Institute, Genoa, Italy; 4 Gastroenterology and Pediatric
Endoscopy Unit, IRCCS G. Gaslini Institute, Genoa, Italy
Background and aim: Scientific literature shows a high prevalence
of Small Intestinal Bacterial Overgrowth (SIBO) in patients with
Cystic Fibrosis (CF). The role of SIBO in nutritional status and
gastrointestinal symptoms in CF is not known. Our aim was to study
SIBO epidemiology and clinical impact and to assess the efficacy of
rifaximin in eradicating SIBO in CF patients.
Material and methods: A symptoms questionnaire and Glucose
Breath Test (GBT) were given to 79 patients (median age 19.6 years;
9.2–36.9) attending an Italian CF Centre. Subjects with a positive
GBT were enrolled in a randomized controlled trial and received
rifaximin 1200mg for 14 days or no treatment. Patients repeated
GBT and questionnaire 1 month after withdrawal of therapy or 45
days after the first negative GBT.
Results: Twenty-five patients resulted affected by SIBO (31.6%)
with a significant correlation with lower SDS-BMI (p<0.01) and
e151
serum albumin levels (p<0.05), independently from pancreas in-
sufficiency. Twenty-three patients took part in the randomized trial,
13 patients (56.5%) in rifaximin group and 10 patients (43.5%) in
control group. Some patients dropped out for lung exacerbations.
Eradication rate of SIBO was 9/10 (90%) in rifaximin group and 2/6
(33.3%) in control group (p<0.05). In the rifaximin-group gastroin-
testinal symptom improvement was observed in 4/5 patients aged
≤14 years and in 0/5 patients aged >14 years (p<0.05); in 2/6
patients in the control group.
Conclusions: CF patients show a high prevalence of SIBO, related to
a poorer nutritional status. Rifaximin therapy is well tolerated and
the results are promising in terms of efficacy in eradicating small
intestinal bacterial overgrowth in Cystic Fibrosis.
P.03.15
LACTOBACILLUS CASEI DG AND ITS POSTBIOTIC REDUCE THE
INFLAMMATORY MUCOSAL RESPONSE: AN EX-VIVO ORGAN
CULTURE MODEL OF POST-INFECTIOUS IRRITABLE BOWEL
SYNDROME
D. Compare, A. Martino ∗ , D. Angrisani, C. Sgamato, B. Iovine,
U. Salvatore, P. Coccoli, A. Rocco, G. Nardone
University Federico II, Naples, Italy
Background and aim: The evidence on the role of gut microbiota
in post-infectious irritable bowel syndrome (PI-IBS) is convincing.
Based on the assumption that IBS develops in up to 30% of indi-
viduals recovering from acute gastroenteritis, the pathogenetic role
of gut microbiota was well established mainly for PI-IBS, diarrhea
(D) predominant subtype. As a consequence, the manipulation of
the microbiota is becoming an attractive therapeutic option for this
disease. Lactobacillus spp. positively affect IBS symptoms, although
the mechanisms through which probiotics exert their beneficial
effects are largely unknown.
Aim of this study was to evaluate the role of Lactobacillus
casei DG (LC-DG) and its postbiotic (PB) in modulating the
inflammatory/immune-response in PI-IBS in an ex-vivo organ cul-
ture model.
Material and methods: Ex-vivo organ cultures of ileal and colonic
mucosa from 10 PI-IBS D patients, and 10 healthy controls (HC)
were treated with LPS, LC-DG and PB. IL-1α, IL-6, IL-8 and IL-10
mRNA levels were assessed by real-time PCR and Toll like receptor
4 (TLR-4) protein expression by Western blotting.
Results: At baseline, IL-1α, IL-6 and IL-8 mRNA levels were signifi-
cantly higher while IL-10 mRNA levels were lower in post-infectious
IBS-D then in HC in both ileum and colon (p<0.0001). TLR-4 protein
expression was significantly higher in post-infectious IBS-D patients
in respect to HC, particularly in colonic mucosa (p<0.0001). LC-DG
and PB significantly reduced the mRNA levels of pro-inflammatory
cytokines while increased that of IL-10 after LPS stimulation
(p<0.0001). The protective effect was more pronounced for PB then
LC-DG treatment, in all cases. TLR-4 protein expression, increased
by LPS treatment, was attenuated by LC-DG and PB in both groups
particularly in ileal mucosa (p<0.0001).
Conclusions: LC-DG and its PB attenuate the inflammatory mucosal
response in an ex-vivo organ culture model of PI-IBS D, thus
providing biological plausibility to the therapeutically usefulness of
this probiotic strain in this clinical setting.