Helicobacter pylori (H. pylori), a bacterium implicated in the development of peptic ulcer and gastric cancer, is estimated to infect around half the world's population. Its prevalence in Australia is unclear. This scoping review aimed to evaluate all Australian literature providing estimates of the prevalence of H. pylori.

Australian studies examining H. pylori prevalence from 1982 onwards were eligible for inclusion. Medline, Embase and Scopus databases, and grey literature sources, were searched. Two independent reviewers undertook a two-stage screening process. Data were extracted by two independent reviewers using a pre-specified template.

Of 444 identified studies, 75 were included in the review. H. pylori prevalence in Australian population-based studies (n = 8) ranged from 38.0% in 1991 to 15.1% in 2002; however, estimated prevalence across all non-clinical population studies in diverse sub-groups (n = 29) has varied dramatically. Decreased prevalence has been more marked in populations with gastrointestinal symptoms and conditions compared to non-clinical populations. Data on H. pyloriprevalence in vulnerable populations are lacking.

This is the first scoping review of Australian studies reporting H. pylori prevalence. A wide range of study designs, population groups, geographic regions, and diagnostic methods was included, involving data collected over a 50-year period (1969 to 2018). The summary of H. pylori prevalence estimates over time in this review points to a decrease in prevalence in Australia, particularly among populations with gastrointestinal symptoms and illnesses; however, it is unknown whether there is inequity in prevalence trends across vulnerable sub-groups of the Australian population. Future research and interventions supporting the health and wellbeing of vulnerable populations is required to ensure equitable health gains are made for all.

Multiple endocrine neoplasia type 1 (MEN1) is a rare inherited endocrine cancer syndrome. Multiple gastro-entero-pancreatic neuroendocrine tumors (GEP-NETs) affect 30% to 80% of MEN1 patients, with the most common functioning GEP-NET being gastrinoma. Biochemical identification of hypergastrinemia may help to recognize the presence of gastrinomas before they are detectable by instrumental screening, enabling early diagnosis and start of therapy, preferably before tumor progression and metastases occurrence.

Evaluate the effectiveness of secretin stimulation test to precociously diagnose the presence of gastrin-secreting tumors.

Results of secretin stimulation tests, performed between 1991 and February 2020, were retrospectively analyzed, as aggregate, in a cohort of MEN1 patients with GEP-NETs.

Data were extracted from the MEN1 Florentine database.

The study included 72 MEN1 patients with GEP-NETs who underwent a secretin stimulation test for the evaluation of gastrin secretion.

A positive secretin stimulation test was assumed with a difference between basal fasting serum gastrin (FSG) and the maximum stimulated value of gastrin over 120 pg/mL.

The secretin stimulation test showed a secretin-induced hypergastrinemia in 27.8% (20/72) of patients with GEP-NETs, and a positive test in 18 cases. The test allowed the identification of a positively stimulated hypergastrinemia in 75.0% (3/4) of patients who presented a basal FSG within the normal range.

Diagnosis of gastrinoma is complex, difficult, and controversial. Results of this study confirm that a positive secretin stimulation test allows early diagnosis of gastrinomas, even in the presence of borderline or normal levels of nonstimulated FSG.

Multiple endocrine neoplasia type 1 (MEN1), a rare tumor syndrome that is inherited in an autosomal dominant pattern, is continuing to raise great interest for endocrinology, gastroenterology, surgery, radiology, genetics, and molecular biology specialists. There have been 2 major clinical practice guidance papers published in the past 2 decades, with the most recent published 8 years ago. Since then, several new insights on the basic biology and clinical features of MEN1 have appeared in the literature, and those data are discussed in this review. The genetic and molecular interactions of the MEN1-encoded protein menin with transcription factors and chromatin-modifying proteins in cell signaling pathways mediated by transforming growth factor β/bone morphogenetic protein, a few nuclear receptors, Wnt/β-catenin, and Hedgehog, and preclinical studies in mouse models have facilitated the understanding of the pathogenesis of MEN1-associated tumors and potential pharmacological interventions. The advancements in genetic diagnosis have offered a chance to recognize MEN1-related conditions in germline MEN1 mutation-negative patients. There is rapidly accumulating knowledge about clinical presentation in children, adolescents, and pregnancy that is translatable into the management of these very fragile patients. The discoveries about the genetic and molecular signatures of sporadic neuroendocrine tumors support the development of clinical trials with novel targeted therapies, along with advancements in diagnostic tools and surgical approaches. Finally, quality of life studies in patients affected by MEN1 and related conditions represent an effort necessary to develop a pharmacoeconomic interpretation of the problem. Because advances are being made both broadly and in focused areas, this timely review presents and discusses those studies collectively.