Pancreatic Disorders in Children with Inflammatory Bowel Disease

Abstract

Background and Objectives: Inflammatory bowel disease (IBD) is a chronic condition and mainly affects the intestines, however, the involvement of the other organs of the gastrointestinal tract (upper part, pancreas, and liver) have been observed. The coexistence of IBD with pancreatic pathology is rare, however, it has been diagnosed more frequently during recent years in the pediatric population. This article reviews the current literature on the most common pancreatic diseases associated with IBD in the pediatric population and their relationship with IBD activity and treatment. Materials and Methods: We performed a systematic review of data from published studies on pancreatic disorders, also reported as extraintestinal manifestations (EIMs), among children with IBD. We searched PubMed and Web of Science to identify eligible studies published prior to 25 April 2020. Results: Forty-four papers were chosen for analysis after a detailed inspection, which aimed to keep only the research studies (case control studies and cohort studies) or case reports on children and only those which were written in English. The manifestations of IBD-associated pancreatic disorders range from asymptomatic increase in pancreatic enzymes activity to severe disease such as acute pancreatitis. Acute pancreatitis (AP) induced by drugs, mainly thiopurine, seems to be the most- often-reported pancreatic disease associated with IBD in children. AP associated with other than drug etiologies, and chronic pancreatitis (CP), are rarely observed in the course of pediatric IBD. The pancreatic involvement can be strictly related to the activity of IBD and can also precede the diagnosis of IBD in some pediatric patients. The course of AP is mild in most cases and may occasionally lead to the development of CP, mainly in cases with a genetic predisposition. Conclusions: The involvement of the pancreas in the course of IBD may be considered as an EIM or a separate co-morbid disease, but it can also be a side effect of IBD therapy, therefore a differential diagnosis should always be performed. As the number of IBD incidences with concomitant pancreatic diseases is constantly increasing in the pediatric population, it is important to include pancreatic enzymes level measurement in the workup of IBD.

The course of acute pancreatitis in children and potential simple laboratory markers of severity – A single Centre retrospective study

“…Pancreatitis in children remains a poorly understood condition despite increasing incidence and risk of morbidity and mortality 8–10 . The aetiology of the disease is variable and management remains inconsistent among practitioners 9,11–13 . In most paediatric cases, AP resolves and patients have no further complications.…”

“…[8][9][10] The aetiology of the disease is variable and management remains inconsistent among practitioners. 9,[11][12][13] In most paediatric cases,…”

Pancreatic Associated Manifestations in Pediatric Inflammatory Bowel Diseases

“…It initiates antigen-specific mucosal immune responses against bacterial invasion into intestinal epithelial cells. Indeed, it has been demonstrated that GP2-deficient colitis mice present a more severe intestinal inflammation and an enhanced E. coli population than healthy mice, proving the role of GP2 in preventing E. Coli mucosal attachment and penetration [ 47 , 48 ]. By contrast, an increase of GP2 expression in the pancreas has been observed in a chemically induced colitis in mice, as a consequence of the production of pro-inflammatory cytokines such as TNF.…”

“…By contrast, an increase of GP2 expression in the pancreas has been observed in a chemically induced colitis in mice, as a consequence of the production of pro-inflammatory cytokines such as TNF. A rise in fecal GP2 concentration along with the presence of anti-GP2 antibodies has been also observed in CD patients, although the exact role of pancreatic GP2 and the pathogenetic role of anti-GP2 antibodies in IBD patients remains unclear [ 47 , 48 ].…”

“…All of the mentioned factors may therefore cooperate to the development of AP, which would furthermore explain the correlation between AP and the extent and severity of the flare-up [ 65 ]. As previously reported, some studies have focused on some genetic susceptibility loci which are shared by both pancreatitis and IBD, which may prove the link between these two conditions and make some forms of pancreatitis as true EIMs of IBD [ 47 , 48 ].…”