Pancreatic Dysfunction and Duodenal Inflammatory Responses Coordinate with Refractory Epigastric Pain Including Functional Dyspepsia: A Narrative Review

Abstract

Functional dyspepsia (FD) in the past, has been found to be associated with patients with pancreatic enzyme abnormalities and chronic pancreatitis in a certain population of patients who suffered from this disease. Since 2009, when the idea of early chronic pancreatitis (ECP) first emerged, the utility of endoscopic ultrasonography (EUS) has gained our attention as it may play an important role in distinguishing ECP from dyspepsia patients. Although the symptoms of patients with pancreatic enzyme abnormalities and pancreatic dysfunction overlap with those of dyspepsia, there are no available data to explain the direct relationships and linkages between pancreatic dysfunction and dyspeptic symptoms. The disturbance of exocrine pancreatic enzyme function and the reduction of pancreatic endocrine levels, such as insulin, may be associated with dyspeptic symptoms through impaired gastric emptying and duodenal inflammation. Recently, some studies have focused on the role of duodenal pathophysiology in gastric motility, bicarbonate secretion, and digestion. Since the reduction of bicarbonate secretion by pancreatic dysfunction fails to neutralize gastric acid in the proximal part of the duodenum, impaired bicarbonate secretion by pancreatic dysfunction in turn fails to protect the duodenal mucosa against gastric acid influx, thereby inducing duodenal inflammation. In addition, it has been suggested that elevated trypsin levels might be partly associated in part with duodenal inflammatory responses through PAR2-related immunomodulatory cells. This article offers a review on how duodenal inflammation may play a role in the etiology of FD and demonstrates whether pancreatic dysfunction may be associated with FD through intestinal inflammation.

Characterization of Duodenal Microbiota in Patients with Acute Pancreatitis and Healthy Controls

“…The response of acute pancreatitis to chemicals in the duodenum is facilitated by neuronal cross-talk between the duodenum and pancreas [ 12 ]. Additionally, when the pancreas is dysfunctional, it can cause a decrease in bicarbonate secretion, resulting in the inability of the proximal duodenum to neutralize gastric acid, thus inducing duodenal inflammation [ 13 ].…”

Comparison of pancreatic enzyme abnormalities and protease‐activated receptor‐2‐positive eosinophils in the duodenum of patients with functional dyspepsia‐irritable bowel syndrome overlap with functional dyspepsia alone in Asian populations

“…13 In addition, duodenal eosinophilia is increasingly recognized in FD. 12 Considering that pancreatic dysfunction could be associated with reduced bicarbonate secretion, resulting in loss of protection to the duodenal mucosa against gastric acid influx, thereby inducing duodenal inflammation, 14 we investigated the possibility of the association between pancreatic enzyme abnormalities and duodenal inflammation as a factor in FD-IBS overlap.…”