A Clinical and Pathophysiological Overview of Intestinal and Systemic Diseases Associated with Pancreatic Disorders: Causality or Casualty?

Abstract

The relationship between chronic intestinal disease, including inflammatory bowel disease (IBD) and celiac disease (CelD), and pancreatic disorders has been little investigated. Although an increased risk of acute pancreatitis (AP), exocrine pancreatic insufficiency with or without chronic pancreatitis, and chronic asymptomatic pancreatic hyperenzymemia have been described in these patients, the pathogenetic link remains unclear. It may potentially involve drugs, altered microcirculation, gut permeability/motility with disruption of enteric-mediated hormone secretion, bacterial translocation, and activation of the gut-associated lymphoid tissue related to chronic inflammation. In addition, the risk of pancreatic cancer seems to be increased in both IBD and CelD patients with unknown pathogenesis. Finally, other systemic conditions (e.g., IgG4-related disease, sarcoidosis, vasculitides) might affect pancreatic gland and the intestinal tract with various clinical manifestations. This review includes the current understandings of this enigmatic association, reporting a clinical and pathophysiological overview about this topic.

Prophylactic Coloprotective Effect of Urtica dioica Leaves against Dextran Sulfate Sodium (DSS)-Induced Ulcerative Colitis in Rats

“…These findings demonstrated that pretreatment with AEUD or MESA reduced hyperamylasemia in DSS-treated rats. Increased permeability of the inflamed mucosa may be the cause of the pancreatic enzyme rise found in more severe or active disease; this is a mechanism previously suggested in persons with intestinal infarction who also have elevated serum amylase levels [54].…”

The Impact of Chronic Pancreatitis on the Occurrences of Human Cancers: Real-World Data

“…Chronic pancreatitis (CP) is a chronic inflammatory disease of the pancreas that could lead to irreversible damage to the pancreatic tissues and to associated exocrine and endocrine insufficiency [1][2][3][4][5]. The diagnosis of CP relies on a combination of image findings that indicate irreversible damage to the pancreas, such as calcification, stones, and duct stricture or dilation, along with manifested exocrine and endocrine dysfunctions [6].…”

“…Emerging evidence suggested that CP is not a localized disease confined to the pancreas [2]. CP is associated with elevated systemic levels of inflammatory mediators such as interleukin-6, tumor necrosis factor-α, interleukin-8, and members of the interleukin-1 family [7].…”

“…CP can often be attributed to several prevalent risk factors, including excessive alcohol consumption, smoking, and genetic mutation [2,[11][12][13]. Notably, alcohol use and smoking are well-established risk factors for various types of cancer.…”