SEROLOGICAL DIAGNOSIS OF CHRONIC ATROPHIC GASTRITIS RELATED TO

HISTOLOGICAL EVALUATION:A CLINICAL STUDY ON 10,000 PATIENTS

IN PRIMARY CARE SETTING

Barchi AlbertoCapasso MarioCesario Silvia

MoreMED, 10 aprile 2018

ChronicAtrophic Gastritis

Atrophy with Fibrosis Atrophy with Intestinal Metaplasia

Normal Gastric Mucosa

Chronic Gastritis

Atrophic Gastritis

Intestinal Metaplasia

Dysplasia

Gastric Adenocarcinoma

The Multi-step of gastric carcinogenesis: “ Correa’s cascade”

H. pylori

Gastric Cancer: Epidemiology

• Gastric Cancer is a relevant medical

issue worldwide.

951.594 diagnosis of GC

723.073 deaths

• In Italy 13.001 new cases, with 9.917 deaths.

584 cases of gastric cancer (M=318, mean age 78ys, range 36-105ys) from 2010 to 2016

early gastric cancer: 44/584 (7.53%) (M=24, mean age 75.68ys, range 47-92ys). advanced gastric cancer was established in 540 pts (M=318, F=222, mean age 78.20ys, range 36-105ys). (92.47%)

The Parma area

Eearly

8%

Advanced

early advanced

The Modena/Reggio Emilia Area

CAG and OLGA STAGING SYSTEM

Gastropanel®(Biohit, Finland).

PG I 30-120 μg/L

PG II 2-15 μg/L

G-17 1-9 pmol/L

Hp-IgG <30 EIU

Normal Values

PG I PG II

G-17 Hp-IgG

OLGA I-II (25 pts T1; 26 pts T2) PG I-II RATIO >3

OLGA III-IV (10 pts T1; 13 pts T2)PGI-II RATIO<3

T1 12 years follow-up T2

Vanoi Valley (Italy)

1994-2006

93 subjects

Gastropanel Gastropanel

OLGA staging OLGA staging

• Low-grade

IEN: 2 pts

T1; 1 pts T2

• High-grade

IEN: 0 pts

T1; 1 pts T2

• Invasive

GC: 0 pts

T1; 2 pts T2

P = 0.001

The aim of the present study is to investigate the frequency of CAG in a study

population in primary care setting by means of a non-invasive test, compared

with histology as a gold standard.

Aim of the study

Material and Methods

Material and Methods

In every patient were performed:

➢ Upper G.I. endoscopy with biopsy samplingevaluated according to Sydney classification and/or O.L.G.A. Staging System

➢ Gastropanel®

The normal values: PGI: 30-120 µg/L, PGII: 2-15 µg/L, G-17: 1-9 pmol/L, Hp-IgG: < 30 U/L.

SEROLOGICAL DIAGNOSIS OF BODY CAG WAS MADE BY:

Low levels of PGI (PGI < 25 µg/L) as well as high levels ofG-17 (G-17 > 14 pmol/L) were considered diagnostic forCAG

➢ PG I serum levels < 25 µg/L

➢ G-17 concentrations > 14 pmol/L

Material and Methods

Group A (7,400 pts) – Padova - Group B (2,600 pts) – Treviso -

8%

32%

12%

48 %

CAG(m.a. 57 yrs)

Not atrophicgastritis H.p.+(m.a.54 yrs)

Normal(m.a. 44yrs)

GERD

Body chronic atrophic gastritis was diagnosed by serology in 716 out of 10,000 (7.2%)Results

4%

26%

29%

42%

CAG(m.a.58 yrs)

Not atrophicgastritisH.p.+(m.a. 59yrs)Normal(m.a. 47yrs)

GERD

p < 0.05

PGI

Controllo H. pylorii positivi GERD CAGNormal H. Pylori + GERD CAG

G-17

Controllo H. pylorii positivi GERD Normal H. Pylori + GERD CAG

p < 0.05

Group B: 1.900 out of 2.600 pts suitablefor histological evaluation by OLGA

M= 769; F=1131mean age = 56.4 ysrange= 29-78 ys.

Exclusion criteria: upper GI surgery, alarm symptoms.

Results: 1900 in Group B

4%

26%

29%

42%

CAG(m.a.58 yrs)

Not atrophicgastritisH.p.+(m.a. 59yrs)Normal(m.a. 47yrs)

GERD

4 %

SEX [Male] Mean Age Range

44 61 49-82

19%

57%

24%

N patients = 83

OLGA 2 OLGA 3 OLGA 4

OLGA % PZ

2 19.2 %

3 56.6%

4 24.2%

The great majority of 83 pts in which the

diagnosis was CAG showed a picture of OLGA

3 or OLGA 4 .

83 out of 1.900 investigated patients showed CAG

The relationship between PGI levels and OLGA stage shows a statistically significant difference between the stages OLGA 0, 1, 2 and the stages 3 and 4.

OLGA STAGING PGI mean values (pmol/L)

OLGA 0 72.45

OLGA 1 85.95

OLGA 2 47.38

OLGA 3 16.00

OLGA 4 10.10p< 0.001

Results

ResultsThe relationship between OLGA stages and G-17 serum levels shows a statistically significant difference.

OLGA STAGING G-17 mean values (µg/L)

OLGA 0 4.6

OLGA 1 5.2

OLGA 2 26.5

OLGA 3 44.6

OLGA 4 38.5p< 0.01

By comparing OLGA 0-1 against OLGA 2-4 → p<0.02

CONCLUSION: Relationship between OLGA and Gastropanel®420 PATIENTS

In a primary care setting a picture of CAG was found in above 7.2% of patients inagreement with previous studies

The higher frequency in Group A could be explained by different referenceevaluation of Centers. First Level (Treviso) vs Third Level (Padova)

Subjects affected by CAG show higher mean age in comparison with bothpatients with H.p. related non atrophic gastritis and normal population in bothsettings

Statistically significant relationship (p<0.02) was found between atrophichistological damage according with OLGA staging and serological values byGastropanel.

CONCLUSIONS

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