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

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e98 Abstracts of the 22nd National Congress of Digestive Diseases / Digestive and Liver Disease 48S2 (2016) e67–e231
epithelial cells. The aim of this study was to evaluate the role of
hyperinsulinemia in EAC onset related to GERD, in a murine model
of surgically-induced EAC.
Material and methods: We used the transgenic MKR+/+ murine
model characterized by marked hyperinsulinemia and a mild
dysglycemia, without showing obesity and/or a diabetic phenotype.
Twenty-nine wild type and twenty-nine MKR+/+ mice underwent
duodenum/jejunum-esophageal anastomosis in order to induce
reflux. Thirty weeks after surgery the mice were sacrificed, the
esophagus was explanted and the blood was recovered. Serum
concentrations of glucose, insulin, C-peptide and leptin were
measured by Luminex-XMap-Technology. Histological and insulin
signal analysis were performed in the esophageal tissue. Non-
operated wild type and MKR+/+ mice were used as controls.
Results: Hyperinsulinemic mice developed very high percentages
of EAC (75,9%) compared with normo-insulinemic wild type mice
(34,5%). The higher insulin concentration in MKR+/+ mice compared
to wild type mice (2474,3 pg/mL and 697,3 pg/mL, respectively; p=
0.038) corresponded to insulin signal pathway increase in murine
esophageal tissue. Insulin signal amplification leads to downstream
proteins activation, such as AkT and p70S6K, that are involved on
cell survival and proliferation mechanisms. Insulin signal increase in
pre-neoplastic lesion suggests an involvement of hyperinsulinemia
along disease progression.
Conclusions: Taken together our results suggest a key role of insulin
for promoting both, pre-cancerous and cancerous lesions, in chronic
duodenum-esophageal reflux condition. Monitoring of serum
metabolic parameters in hyperinsulinemic GERD and BE patients
and to improve their metabolic status and insulin sensitivity with a
correct diet and physical activity could have strong implications for
EAC prevention.
OC.07.8
COMBINED USE OF SERUM MARKERS AND MORPHOLOGICAL
EVALUATION IN EARLY CHRONIC ATROPHIC GASTRITIS
DETECTION: PRELIMINARY RESULTS
Panozzo M.P.*1, Franceschi M. 2, Baldassarre G.2, Morini A.3,
Visonà A.3, Antico A.1
11 Department of Clinical Pathology, ULSS 4 Alto Vicentino, Santorso
(VI), Italy, 22 Endoscopic Unit, Department of Surgery, ULSS 4 Alto
Vicentino, Santorso (VI), Italy, 33 Department of Pathological Anatomy,
ULSS 4 Alto Vicentino, Santorso (VI), Italy
Background and aim: Chronic atrophic gastritis (CAG) is one of the
key steps in developing gastric malignancy. Its early diagnosis may
be focused by gastric biochemical markers (pepsinogens and gastrin
17); the aetiology may be established by Helicobacter pylori (Hp),
parietal cell (PCA) and Intrinsic Factor (IF) antibodies.
The aim of the study was to establish the predictive value of serum
biomarkers in early detection of chronic atrophic gastritis either
infective and/or autoimmune patterns.
Material and methods: From April 2013 to July 2015 in the sera of
1844 subjects (M=641, F=1203, age 44 years, means 6-87), selected
on the basis of the presence of dyspeptic (but not alarm) symptoms,
microcitic anemia iron therapy resistant or macrocitemia, risk factor
for CAG (family, autoimmune thyroid disease, autoimmune multiple
syndrome), Pepsinogen I (PGI) and II (PGII), Gastrin 17 (G17) and HP
(Biohit, Plc, Finlandia) were detected. PCA (IFA/FEIA methods) and IF
(Dot Blot/FEIA methods) were assayed only in patients serologically
individuated as CAG which were also submitted to endoscopy
(EGDS) and histological evaluation (OLGA System).
Results: 54/1844 patients (2,9%) showed a serum pattern compatible
with CAG (8 M, 46 F). 46/54 (85,2%) and 18/54 (33,3%) subjects
were PCA and IF positive, respectively; 49/54 (90,7%) CAG were
histologically confirmed, while 5 patients who presented slight
low PGI and PGI/II ratio and slight increase of G17 were classified
as OLGA 0. HP were found in 40%, 25%, 15.4% and 11.7% of patients
from OLGA 0 to OLGA III; PCA positivity was detected in I-IV OLGA
patients but not in 0 group, while IF was present only in OLGA II and
III but not in the other groups.
Conclusions: Low PGI levels and PGI/II ratio can early indicate a
functional CGA. The progression of functional impairment showed
by increased G17 levels is well correlated with the atrophy grade.
Hp infection seems to be the most relevant aetiological factor in
pre-atrophic stages, while autoimmune picture better characterizes
the degree of CGA. PCA and IF autoantibodies are suggestive for the
presence of atrophy.
OC.07.9
POTENTIAL AUTOIMMUNE ATROPHIC GASTRITIS
Lenti M.V.*, Padula D., Dequarti A., Miceli E., Alvisi C., Luinetti O.,
Di Sabatino A., Di Stefano M., Corazza G.R.
Fondazione IRCCS Policlinico San Matteo, Pavia, Italy
Background and aim: Autoimmune atrophic gastritis (AAG) is an
organ specific autoimmune disease characterized by gastric body-
fundus atrophy with antrum sparing. AAG diagnosis is based on
distinctive features according to the updated Sydney system. Some
serological markers, such as parietal cells autoantibodies (PCA),
fasting gastrin, vitamin B12, complete blood count and chromogranin
A may be useful in the early diagnosis of AAG. The natural history
of PCA positive patients is still unknown; in particular in high-risk
patients (history of autoimmune diseases, patients with subtle
histological alterations). Aim of the present study is to define a
risk group of subjects that may develop AAG, therefore defining a
potential AAG.
Material and methods: All outpatients referred to our gastro­
enterological unit, over a 3-year period, screened for AAG (PCA status
and gastric bioptic samples) were enrolled. Among them, patients
showing only PCA positivity and those with subtle histological
alterations, i.e. gastrin cells hyperplasia, enterochromaffine-like cell
(ECL) hyperplasia, low grade atrophy) were evaluated after a year
through an upper endoscopy.
Results: Among 2147 patients undergoing upper endoscopy over
a 3-yr period, AAG was identified in 202 patients (ratio F:M=2.5:1,
mean age 60±18.6 years, range 15-82 years). Fourteen patients (ratio
F:M 1:1, mean age 56±16.5) had no or low grade corpus atrophy;
all of them had gastrin cell hyperplasia and/or ECL hyperplasia and
were PCA positive. All of them underwent upper endoscopy after a
year and only one had a total regression of the lesions described,
whereas the others developed a frank corpus atrophy
Conclusions: AAG may onset only with scanty histological
alterations and PCA positivity may predict the development of the
disease. Up to now, natural history of AAG has never been studied.
A better characterization of patients may facilitate early detection,
identifying a subset of individuals at risk. Finally, patients showing
subtle histological alterations should undergo an endoscopic follow-
up, as well as those with PCA positivity.