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SUMMARY BackgroundBreath tests represent a valid and non-invasive diagnostic tool in many gastroenterological conditions. The rationale of hydrogen-breath tests is based on the concept that part of the gas produced by colonic bacterial fermentation diffuses into the blood and is excreted by breath, where it can be quantified easily. There are many differences in the methodology, and the tests are increasingly popular.

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Background: Autoimmune atrophic gastritis (AAG) is characterised by a wide clinical spectrum that could delay its diagnosis.Aims: To quantify the diagnostic delay in patients suffering from AAG and to explore possible risk factors for longer diagnostic delay. Methods:Consecutive patients with AAG evaluated at our gastroenterological outpatient clinic between 2009 and 2018 were included. Diagnostic delay was estimated as the time lapse occurring between the appearance of the first likely symptoms, laboratory alterations, and other clues indicative of AAG and the final diagnosis.Patient-dependent and physician-dependent diagnostic delays were also assessed.Multivariable regression models were fitted.Results: 291 patients with AAG (mean age at diagnosis 61 ± 15 years; F:M ratio = 2.3:1) were included. The median overall diagnostic delay was 14 months (interquartile range [IQR] 4-41). Factors associated with longer median overall diagnostic delay were female sex (17 months, IQR 5-48), having a previous misdiagnosis (36 months, IQR 17-125) and a history of infertility/miscarriages (33 months, IQR 8-120), whereas a higher level of education was associated with longer patient-dependent diagnostic delay (4 months, IQR 1-12). First evaluation by a gastroenterologist was associated with a median longer diagnostic delay (6 months, IQR 2-15) compared to an internist (3 months, IQR 3-31) and a haematologist (1 month, IQR 0-2). Age, socioeconomic or marital status did not affect the diagnostic delay.Conclusions: AAG is burdened by substantial diagnostic delay, especially in female patients, and due to lack of awareness, particularly among gastroenterologists.Uncommon vitamin B12 deficiency-related manifestations are overlooked and may prolong the diagnostic delay.

Background: Gastric neuroendocrine neoplasms (NENs) are very heterogeneous, ranging from mostly indolent, atrophic gastritis-associated, type I neuroendocrine tumors (NETs), through highly malignant, poorly differentiated neuroendocrine carcinomas (pdNECs), to sporadic type III NETs with intermediate prognosis, and various rare tumor types. Histologic differentiation, proliferative grade, size, level of gastric wall invasion, and local or distant metastases are used as prognostic markers. However, their value remains to be tailored to specific gastric NENs. Methods: Series of type I NETs (n = 123 cases), type III NETs (n = 34 cases), and pdNECs (n = 43 cases) were retrospectively collected from four pathology centers specializing in endocrine pathology. All cases were characterized clinically and histopathologically. During follow-up (median 93 months) data were recorded to assess disease-specific patient survival. Results: Type I NETs, type III NETs, and pdNECs differed markedly in terms of tumor size, grade, invasive and metastatic power, as well as patient outcome. Size was used to stratify type I NETs into subgroups with significantly different invasive and metastatic behavior. All 70 type I NETs < 0.5 cm (micro-NETs) were uneventful. Ki67-based grading proved efficient for the prognostic stratification of type III NETs; however, grade 2 (G2) was not associated with tumor behavior in type I NETs. Although G3 NETs (2 type I and 9 type III) had a very poor prognosis, it was found that patient survival was longer with type III G3 NETs compared to pdNECs. Conclusions: Given the marked, tumor type-related behavior differences, evaluation of gastric NEN prognostic parameters should be tailored to the type of neoplastic disease.

Summary Background Autoimmune atrophic gastritis (AAG) is an immune‐mediated disorder characterised by destruction of gastric oxyntic mucosa Aim To explore gastric histopathological evolution in a cohort of AAG patients over a prolonged follow‐up Methods Single centre prospective study enrolling consecutive patients with histologically confirmed AAG between 2000 and 2018. All AAG patients undergoing endoscopic follow‐up every 1‐3 years were classified as having stages 1, 2 or 3 according to atrophy severity (mild, moderate and severe). AAG patients with either glandular or neuroendocrine dysplasia/neoplasia were classified as having stage 4. Disease stage progression, and changes in serum anti‐parietal cell antibody (PCA), chromogranin A and gastrin‐17 were assessed. Results In total, 282 AAG patients (mean age 60.3 years; F:M ratio 2.4:1; median follow‐up 3 years, interquartile range 1‐7) were enrolled. All patients with stages 1 or 2 progressed to stage 2 or 3 over time with a steady trend (P = .243) and regression from a severe to a milder stage was never noticed. Disease progression of patients with stages 1 or 2 occurred within the first 3 years. PCA positivity rate did not change over time. Stage 3 patients had higher gastrin‐17 levels compared to patients with stages 1 and 2 (median 606 vs 295 pg/mL; P < .001). In stage 3, the hazard ratio for the risk of developing stage 4 was 6.6 (95% CI 1.5‐29; P = .001). Conclusions AAG is a steadily progressive disease, in which stages 1 and 2 always progress to stage 3. The risk of developing a complicated disease stage is greater in patients with more severe gastric lesions.

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