최신연구결과(해외)

General studySerum pepsinogens can help to discriminate between H. pylori-induced and auto-immune atrophic gastritis: Results from a prospective multicenter study

관리자
2023-11-29
조회수 101

Dig Liver Dis. 2023 Oct;55(10):1345-1351. doi: 10.1016/j.dld.2023.03.015. 


1. Introduction

* 3 types of CAG (based on the origin and localization of the lesions in the stomach)

(1) Atrophic gastritis confined to the antrum, probably corresponding to the early phase of H. pylori-induced gastritis

(2) Atrophic gastritis confined to the corpus, most probably corresponding to AIG (upon clinical and biological confirmation of this diagnosis)

(3) Atrophic gastritis in both the antrum and the corpus (extensive gastritis), which may correspond to either the late stage H. pylori–induced gastritis, or mixed form of AIG and H. pylori gastritis


* PGI is secreted by chief cells and mucus neck cells of the corpus mucosa

* PGII is secreted throughout the stomach and proximal duodenum. 

* In case of CAG affecting the corpus, the level of PGI drops significantly, while the level of PGII remains usually unchanged, hence allowing to use the decreased levels of PGI and/or PGI/PGII ratios as potential biomarkers of corpus CAG.  


* the value of pepsinogen testing using ELISA (Enzyme linked immunoabsorbent assay) or CLEIA- (Chemiluminescent Immunoassay) for the detection of corpus gastric atrophy in the French population, with more than 70% sensitivity (Se) and 90% specificity (Sp) for both methods. 


2. Methods

* Diagnosis of AIG was based on the presence of typical histological lesions 

- Atrophic gastritis and/or intestinal metaplasia confined to the corpus with linear or nodular hyperplasia of enterochromaffin-like cells

* Serological anti-parietal cell antibodies and/or anti-intrinsic factor antibodies were also tested, but since they may be absent in AIG (sensitivity around 80% for APCA, 20% for anti-intrinsic factor), the only mandatory criterion was histology

* Two subgroups of patients with CAG

- patients with autoimmune gastritis (AIG

- patients with non-autoimmune atrophic gastritis (NAIG, H. pylori-related atrophic gastritis).

 

3. Results 

3.1. Description of the population

* 344 patients (156 males [45%]; mean age 58.8 [±14.2] years) : PG I, PGII, and H. pylori serology were assessed by ELISA 

* 356 patients (162 males (46%); mean age 58.6 (±14.2) years) : PGI and II levels were measured by CLEIA

* 44 patients with auto-immune gastritis (AIG) were identified, among whom 37 had an atrophic gastritis limited to the corpus, and 7 an extensive, antrum and corpus- involving gastritis. 

* H. pylori infection (past or present, diagnosed either by serology or histology)

: 14.9% of patients with AIG / 30.3% of patients with NAIG


3.2. Diagnostic performances of pepsinogens testing for the detection of corpus-limited atrophic gastritis (Table 1)

* PG testing yielded excellent diagnostic performances, with AUC of 0.971 and 0.942 for ELISA and CLEIA methods, respectively. 

* Diagnostic performances of PGI/PGII in these patients showed AUC of 0.946 and 0.941 for ELISA and CLEIA, respectively. 

* The comparison of both methods did not show significant differences.

Table 1. Diagnostic performances of Pepsinogens testing in patients with atrophic gastritis limited to the corpus, measured using ELISA and CLEIA methods. 


3.3. Comparison of serum pepsinogens levels between the patients with similar localization of CAG according to the origin (autoimmune or not)

* Patients with AIG (AI-corpus limited and AI-extensive) had significantly lower PGI level and PGI/PGII ratio than their NAIG (NAIG-corpus limited and NAIG-extensive) counterparts (Table 2)

Table 2. Comparison of serum pepsinogen I (PGI) levels (mean +/- SD) and PGI/PGII ratio (mean+/-SD), between the patients with auto-immune gastritis (AIG) and Non-auto-immune gastritis (NAIG) in ELISA and CLEIA study.

Fig. 1. Distribution of patients according to PGI and PGI/PGII ratio depending on the presence of atrophic gastritis.


3.4. Diagnostic performances of pepsinogen testing for the detection of AIG

* Focusing on patients with AIG, diagnostic performances still increased, with areas under curve up to 0.991 and 0.985, and 0.969 and 0.970 for PGI and PGI/PGII ratio, for ELISA and CLEIA methods, respectively (Table 3).

Table 3. Diagnostic performances of pepsinogen testing in patients with AIG, tested with ELISA and CLEIA.


* ROC curves for PG testing in patients with corpus limited gastric atrophy (AGC) and autoimmune (AI)-AGC.

Fig. 2. ROC curves for PG testing in corpus limited gastric atrophy (A) and AIG (B). CLEIA: Chemiluminescent Enzyme ImmunoAssay

Fig. 3. Cumulative distribution of the patients according to the PGI levels. 


<Conclusion>

The present study shows that patients with AIG present lower levels of PGI than those with H. pylori-induced atrophic gastritis, suggesting a deeper gastric atrophy in AIG. Accordingly, PGs testing is very accurate in predicting the presence of corpus-limited CAG and especially AIG. These results need to be confirmed in larger studies, and additional non-invasive markers are still to be identified for the detection of antral- or extensive H. pylori-related gastritis.


<Abstract>

Background: Serum pepsinogen (PG) testing is recommended by the European guidelines for diagnosis of chronic atrophic gastritis (CAG). However, wide variations in diagnostic performances are observed, due to the differences in the extent of gastric atrophy, and possibly in its origin (Helicobacter pylori-, autoimmune (AIG)). 

Aim: To analyze the diagnostic performances of PGs testing according to these different parameters, using enzyme-linked-immunosorbent serologic assay (ELISA) and chemiluminescent immunoassay (CLEIA). 

Methods: Serum samples from patients having undergone gastroscopy with biopsies in five French centers were collected prospectively. Sensitivity (Se), specificity (Sp), and Area Under Curve were analyzed according to the extent and origin of CAG. 

Results: Overall, 344 patients (156 males [45%]; mean age 58.8 [±14.2] years) were included, among whom 44 had AIG. Diagnostic performances of PG I for the detection of corpus CAG were excellent, with Se and Sp of 92.7% and 99.1% for ELISA and 90.5% and 98.2% for CLEIA, respectively. For AIG, corresponding values were 97.7% and 97.4% for ELISA, and 95.6% and 97.1% for CLEIA. In multivariate analysis, PG levels were associated with the auto-immune origin (p<0.001) but not with the extent of the atrophic gastritis.

Conclusions: Pepsinogens are highly efficient for the diagnosis of corpus-limited CAG and allow to discriminate AIG from H. pylori-induced gastritis

Keywords: Auto-immune gastritis, Pepsinogen, Atrophic gastritis, Gastric precancerous lesions.

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