Association Between Helicobacter pylori Infection and the Risk of Pancreatic Cancer: A Systematic Review Based on Observational Studies

Abstract

Helicobacter pylori (H. pylori) bacterial infection has long been scrutinized as one of the potential risk factors for the development of pancreatic cancer with quite inconsistent and unequivocal data. Little is known about the risk factors involved with this malignancy. In this systematic review, we aimed to examine the relationship between H. pylori infection and pancreatic cancer based on the evidence from the existing observational studies across the world. We searched major electronic databases such as PubMed, MEDLINE, Science Direct, and Cochrane Library. After a careful and thorough screening process, we selected 15 observation studies for this systematic review. Six of 15 studies found a significant association between H. pylori infection and pancreatic cancer. Additionally, four of these studies found a significant relationship between the cytotoxin-associated gene A strain of H. pylori and pancreatic cancer. Based on the evidence from the selected studies, a weak association was observed between H. pylori infection and cancer of the pancreas, especially in European and Asian populations compared to the North American population. The cross-sectional evidence from the case-control studies only suggests the existence of an association but does not provide substantial evidence of the causative relationship. Further large-scale, prospective cohort studies are warranted in the future to understand this contradictory relationship better.

Is Helicobacter pylori infection associated with pancreatic cancer? A systematic review and meta-analysis of observational studies

“…This causes the unstrained release of duodenal secretin, which is then followed by an increased basal pancreatic bicarbonate output and DNA synthesis, further leading to pancreatic ductal hyperplasia. 56 , 57 Third, it was also assumed that the colonization of H. pylori in the gastric antrum leads to decreased gastric acid production and hypergastrinemia. The resulting low acidity promotes the excessive proliferation of bacteria and secretion of N-nitroso compounds, which could be activated in the ductal epithelium and transported to the pancreas through the bloodstream.…”

“…The resulting low acidity promotes the excessive proliferation of bacteria and secretion of N-nitroso compounds, which could be activated in the ductal epithelium and transported to the pancreas through the bloodstream. 57 , 58 In addition, a recent study 59 has shown a link between mucin 4 (MUC4) and H. pylori infection, proposing that MUC4 may be a cytokine involved in the pathogenesis of pancreatic cancer. All in all, to gain a better understanding of the relationship between H. pylori and pancreatic cancer, it is essential to conduct comprehensive studies that consider the influence of environmental and genetic susceptibility factors.…”

“…This causes the unstrained release of duodenal secretin, which is then followed by an increased basal pancreatic bicarbonate output and DNA synthesis, further leading to pancreatic ductal hyperplasia. 56,57 Third, it was also assumed that the colonization of H. pylori in the gastric antrum leads to decreased gastric acid production and hypergastrinemia.…”

Artificial Intelligence in the Diagnosis and Treatment of Pancreatic Cystic Lesions and Adenocarcinoma

“…Risk factors for pancreatic cancer include cigarette smoking, obesity, chronic pancreatitis, advanced age, family history, and hereditary cancer syndromes [28][29][30]. Other patient characteristics such as diet, medication use, and infections have been investigated as possible contributors to PDAC development [31][32][33]. Despite extensive research into novel predictors and effect sizes of known risk factors, there is currently no unified recommendation on a high-risk population (outside of those with hereditary cancer syndromes) that may benefit from dedicated screening [34].…”