Preneoplastic Conditions in the Stomach: Always a Point of No Return

Abstract

Gastric atrophy (GA) and intestinal metaplasia are defined preneoplastic conditions of the stomach, whereas Helicobacter pylori gastritis by itself represents a risk condition for gastric cancer (GC) development. After H. pylori eradication, an overall reduction of GC incidence has been shown. However, this effect is lost once H. pylori gastritis has evolved to severe GA. On the other hand, only up to 5% of patients with severe GA may develop intestinal-type GC, and therefore the so-called ‘point of no return' may not be appropriate to define the condition of all patients carrying preneoplastic changes in the gastric mucosa. Patients with the highest risk for GC are those who have already had GC that was cured by endoscopic resection. Prospective trials on the effect of H. pylori eradication in this high-risk group of patients showed inconsistent results, probably because of the inclusion of patients with and without baseline severe GA. Severe fundic GA determined by means of histology or serology represents the condition with the highest risk for metachronous neoplastic lesions in the stomach. In the present review, we focus on the effects of H. pylori eradication in patients with severe atrophy in terms of GC prevention.

Helicobacter pylori Infection, Gastric Cancer and Gastropanel

“…In 2009, in Padova, Italy, Venerito M and his team [4] showed that gastric corpus mucosal atrophy is associated with reduced PGI levels (< 25 µg/dL), reduced PGI/PGII ratio (< 3) and increased G17 (> 10 pmol/L) with a high sensitivity (80-90%) and specificity (90-100%).…”

“…Around 10% of patients with H. pylori induced chronic active gastritis progress to severe atrophic changes of the gastric mucosa. Around 5% of those with severe atrophic gastritis develop intestinal-type gastric cancer [4]. The first study indicating that H. pylori eradication is beneficial in reducing the incidence of gastric cancer (GC) only in subjects without precancerous conditions of the gastric mucosa was published in 2004 by Wong et al [5].…”

Oxyntic gastric atrophy inHelicobacter pylorigastritis is distinct from autoimmune gastritis

“…According to the updated Sydney system classification, GA can be scored as absent, mild, moderate or severe 2. GA can involve pyloric glands (gastric antrum), oxyntic glands (gastric corpus) or both (extensive atrophy) 3. According to the current evidence, the causes of oxyntic gastric atrophy (OGA) are (1) H. pylori infection (environmental aetiology), (2) AIG (primary autoimmunity) and (3) combined H. pylori -autoimmune aetiology 4–6.…”

Autoimmune gastritis in autoimmune thyroid disease

“…Helicobacter pylori infection, together with AIG, is the major etiologic factor for OGA . In around 10% of patients, H. pylori gastritis progresses to severe atrophic changes of gastric mucosa over time, often many decades, with an annual incidence of 1–3% .…”

“…6 Helicobacter pylori infection, together with AIG, is the major etiologic factor for OGA. 7 In around 10% of patients, H. pylori gastritis progresses to severe atrophic changes of gastric mucosa over time, often many decades, with an annual incidence of 1-3%. 8,9 Studies from the nineties reported gastric autoantibodies in patients with H. pylori gastritis 10-12 but whether H. pylori infection is the cause of AIG or rather an innocent bystander is still a matter of debate.…”