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e92
Abstracts of the 22
nd
National Congress of Digestive Diseases / Digestive and Liver Disease 48S2 (2016) e67–e231
Material and methods:
L. rhamnosus GG (ATCC 53103 strain)
was grown in MRS medium at 37°C and samples were collected in
exponential, early, middle and late stationary phases. Supernatants
were recovered by centrifugation, filtered and stored at -20°C. The
SMC culture was exposed for 24h to purified LPS (1μg/ml) of a
pathogen strain of E.coli (O111:B4) with and without supernatants.
Postbiotics effects were evaluated on morphofunctional alterations
and IL-6 production. Data are expressed as mean±SE (p<0.05
significant).
Results:
LPS induced persistent significant 20.5%±0.7 cell shortening
and 34.5%±2.2 decrease in acetylcholine-induced contraction of
human SMC. These morphofunctional alterations were paralleled to
a 365.65%±203.13 increase in IL-6 production. All these effects were
dose-dependently reduced in the presence of LGG-supernatants.
Supernatants of the middle exponential phase already partially
restored LPS-induced cell shortening by 57.34%±12.7 and IL6
increase by 145.8%±4.3 but had no effect on inhibition of contraction.
Maximal protective effects were instead obtained with supernatants
of the late stationary phase with LPS-induced cell shortening
restored by 84.1%±4.7, inhibition of contraction by 85.5%±6.4 and IL6
basal production by 92.7%±1.2.
Conclusions:
Byproducts produced by LGG are able to directly
protect human colonic smooth muscle from LPS-induced myogenic
damage. Novel insights are provided about the possibility that LGG-
derived products could reduce the risk of progression of a bacterial
gastroenteritis to post-infective motor disorders.
OC.06.4
THE OCCURRENCE OF POSTPRANDIAL SYMPTOMS IN IRRITABLE
BOWEL SYNDROME IS ASSOCIATED WITH A REDUCTION OF
POSTPRANDIAL SENSITIVITY THRESHOLDS
Di Stefano M., Bergonzi M.*, Valvo B., Saputo E., Craviotto V.,
Bresciani M., Pagani E., Miceli E., Corazza G.R.
1st Department of Internal Medicine, IRCCS S. Matteo Hospital
Foundation, Pavia, Italy
Background and aim:
Irritable bowel syndrome (IBS) is a chronic
condition with recurrent abdominal discomfort or pain associated
with an alteration of bowel habits (Longstreth, Gastroenterology
2006). The pathophysiology is partially known and alterations of
intestinal motility, visceral sensitivity and psycho-emotional aspects
have been described, causing alterations of the activity of the
brain-gut axis. Patients with IBS very frequently report abdominal
symptoms after the ingestion of a meal (Bohn, Am J Gastroenterol
2013), unrelated to functional dyspepsia. Therefore, the aim of this
study was the evaluation of visceral sensitivity in fasting condition
and after the administration of a meal in a subgroup of IBS patients
with postprandial exacerbation of symptoms in comparison with
healthy volunteers (HV).
Material and methods:
Thirty IBS patients (range 22-63), diagnosed
according to Rome III criteria and a group of 10 age- and sex-matched
HV were enrolled. In 15 IBS patients postprandial exacerbation of
symptom was present, while in the other 15 patients this problem
was not present. All subjects underwent the recto-sigmoid barostat
test (Di Stefano, Gut 2006). A double lumen polyvinyl tube with
an adherent, infinitely compliant plastic balloon was positioned at
the recto-sigmoid junction. Basal and postprandial recto-sigmoid
sensitivity thresholds were determined by sequential ramp
distensions with patients reporting their sensation on a 0-6 scale.
The modifications in balloon volume were monitored for 30 minutes
during fasting and 60 minutes postprandially (200 Kcal, 200 ml
liquid meal). The presence and severity of abdominal symptoms
were evaluated by VAL both during fasting and in the postprandial
period.
Results:
In comparison with HV, both mean fasting and postprandial
perception thresholds in IBS patients with or without postprandial
exacerbation of symptoms did not show any significant difference
(ANOVA=NS). As expected, the mean fasting discomfort threshold
was significantly lower in IBS patients than in HV (IBS with
postprandial symptoms 13.6±4.5 mmHg, IBS without postprandial
symptoms 14.6±4.2 mmHg; HV 20.2±2.3 mmHg, ANOVA p<0.001),
but between the two subgroups of IBS there were no differences.
On the contrary, the postprandial discomfort threshold was
significantly lower than fasting values only in the subgroup of IBS
with postprandial symptoms (IBS with postprandial symptoms
8.1±5.6 mmHg, IBS without postprandial symptoms 12.9±5.9
mmHg; HV 19.0±2.5 mmHg, ANOVA p<0.001). Finally, in IBS patients
with meal-related symptoms there was a significant increase of
abdominal discomfort and bloating during the test. None of the
patients suffered from dyspeptic symptoms.
Conclusions:
In IBS patients, a further reduction of the
discomfort threshold in the postprandial period may represent
a pathophysiological mechanism explaining the postprandial
occurrence of abdominal symptoms.
OC.06.5
ASSESSING THE RATE OF INCORRECT DIAGNOSIS OF CELIAC
DISEASE: DATA FROM A TERTIARY REFERRAL CENTER
Branchi F.*, Ferretti F., Roncoroni L., Bravo M., Bardella M.T.,
Conte D., Elli L.
Center for the Prevention and Diagnosis of Celiac Disease -
Gastroenterology and Endoscopy Unit, Fondazione IRCCS Ca’ Granda -
Ospedale Maggiore Policlinico, Milano, Italy
Background and aim:
It is not uncommon in clinical practice to
deal with patients with a diagnosis of celiac disease (CD) who do
not actually fulfill the criteria, in spite of the availability of updated
international guidelines. The aim of this study was to identify
incorrect diagnostic approaches to patients with suspected CD
among referrals to our tertiary center.
Material and methods:
The clinical records of all consecutive
patients referred for the first clinical evaluation to our outpatient
clinic between January 1st 2014 and October 31st, 2015 were
evaluated. Patients with known or suspected CD were included. Data
on symptoms, serology, duodenal histology were collected, as well
as HLA class II profile when available. The current recommendations
of the Italian Ministry of Health were used as a reference standard
for the diagnosis of CD.
Results:
During the study period, 340 patients with a recent or
suspected diagnosis of CD were referred for a first evaluation to our
outpatient service. An incorrect diagnostic approach was identified
in 33 patients (9,7%, 28 females/5 males, median age 33 years, range
24-78) of whom 28 already possessed the medical indemnity for CD
despite not fulfilling criteria for CD. The most common diagnostic
mistake was the lack of HLA genetic testing and exclusion of other
causes in presence of seronegative villous atrophy (n=15), followed
by the absence of duodenal histology (n=6) and by tests performed
already on a gluten-free diet (GFD, n=6). Five patients had been given
a diagnosis of CD even in presence of negative serology and normal
duodenal histology and one patient was actually allergic to wheat.
The correct completion of the diagnostic work-up was programmed
with a median delay of 3 years (range 6 months-9 years), with
three patients receiving a final diagnosis of CD, two re-classified as
potential CD, 15 in whom CD was ruled out and 12 still waiting for a
definite diagnosis.
Conclusions:
Despite the presence of established diagnostic criteria
for CD, the rate of incorrect diagnosis was surprisingly high in our
series, mainly as a consequence of preventable mistakes in the
diagnostic process. These results may reflect a relevant burden on