Introduction
In autoimmune atrophic gastritis (AAG), immune-mediated morpho-functional changes in gastric mucosa lead to hypo-achlorhydria and subsequent hypergastrinemia. This stimulates gastric enterochromaffin-like (ECL) cell proliferation, escalating the risk of type I gastric neuroendocrine neoplasms (gNENs). Yet, longitudinal studies on the AAG-type I gNENs association are still scanty.
Aims & Methods
Our study aims to assess in a multicentric cohort of AAG patients, the frequency and the characteristics of type I gNENs.
We conducted a multicentric, cross-sectional study from January to June 2023, prospectively enrolling consecutive patients diagnosed with AAG, from January 2000 to June 2023, who underwent at least one endoscopy. Data on demographics, clinical history, biochemical profiles, serological data, and endoscopic and histopathological findings were collected.
Results
The study included 612 patients with AAG [444 (75.2%) female, median age 66 (IQR 54-73) years]. At enrollment, 355 (58.1%) patients had ECL cell hyperplasia. Over a median follow-up of 4 (IQR 2-7) years, and after a median number of two upper GI endoscopies per patient, and a median disease duration of 7 (IQR 3-8) years, 108 patients showed 125 gNENs, corresponding to an incidence rate of 0.051 person-years. All the gNENs were well-differentiated. In 22 (18%) cases Ki 67 was not available; of the remaining 103, 86 (68.8%) cases were G1, 17 (13.6%) were G2, all of which with a Ki-67 < 10%; no G3 lesions were observed. 119 (95.2%) gNENs were located in the body/fundus. The median size was 5 (IQR 3-10) mm. 79 (73.1%) patients underwent endoscopic removal, 10 (9.2%) gastrectomy, 12 (11.1%) somatostatin analog therapy due to multifocal/recurrent disease, and 7 (6.5%) were only monitored. Patients with AAG and gNENs had significantly higher gastrin levels compared to patients without gNENs [median 874 pg/mL (IQR 362.5-1335) vs 581.5 pg/mL (IQR 281.8-1071.5), p=0.014]. However, there were no significant differences in proton-pump inhibitor use, OLGA and OLGIM stages, H. pylori status, and notably, circulating chromogranin A levels.
| AAG patients with gNENs (#108)
|
Sex, female (%)
| 78 (72.2)
|
Age (years), median (IQR)
| 68 (57-75.8)
|
APCA positivity, n (%)
| 76 (70.4)
|
Current smokers, n/n available (%)
| 19/57 (33%)
|
PPI treatment, n/n available (%)
| 10/41 (24.4%)
|
OLGIM, n (%)
| II: 60 (56)
|
OLGA, n (%)
| II: 76 (70)
|
Chromogranin A (ng/mL), median (IQR)
| 160 (86.9-251.5)
|
Gastrin (pg/mL), median (IQR)
| 874 (362.5-1335)
|
Conclusion
Type I gNENs are a relevant complication in patients with AAG. Elevated circulating gastrin levels are linked to their occurrence, with hypergastrinemia acting as a driver for abnormal proliferation of gastric ECL cells. Regular endoscopic surveillance and thorough histopathological examination are crucial in patients with AAG, serving as a key strategy for early diagnosis and treatment of gNENs.
References
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2. Köseoğlu H, Duzenli T, Sezikli M. Gastric neuroendocrine neoplasms: A review. World J Clin Cases 2021;9(27):7973–85.
3. Sheikh-Ahmad M, Saiegh L, Shalata A, et al. Factors Predicting Type I Gastric Neuroendocrine Neoplasia Recurrence: A Single-Center Study. Biomedicines 2023;11(3):828.
4. Pachuashvili NV, Nagornaya DP, Tertychnyi AS. [Metachronous tumors of the stomach in a patient with autoimmune gastritis]. Arkh Patol 2023;85(1):57–61.
