Peer Reviewed

Case in Point

Chronic Pancreatitis in an Elderly Woman With Inflammatory Bowel Disease: Extraintestinal Manifestation or Physiologic Aging?

Marie L. Borum, MD, EdD, MPH, and Gayatri Patel, MD

Elderly patients with inflammatory bowel disease (IBD) can have normal age-related alterations of the GI tract, which can obscure identification of IBD extraintestinal manifestations. One well-documented association with IBD is pancreatitis, commonly occurring secondary to drug treatment and structure-related changes.1 However, there are cases of chronic pancreatitis in patients without a history of acute pancreatitis that are identified by histologic or radiologic evidence.2,3 These cases are thought to be an insidious extraintestinal manifestation of IBD. In the elderly patients with IBD, however, the aging process can cause structural changes that mimic chronic pancreatitis on imaging, and detection of these differences requires understanding of the nuances. Pancreatic exocrine insufficiency is a potentially important prognostic factor that can differentiate between normal pancreatic changes in the elderly from idiopathic chronic pancreatitis. Thus, geriatricians should have an increased awareness of the association of subclinical chronic pancreatitis in patients suffering with IBD, as it can mistakenly be attributed to normal aging. This is even more important as the prevalence of IBD in North America is increasing, and the population of people over the age of 65 is increasing concomintantly.4,5 Lack of awareness can lead to inadequate and suboptimal management of the patient. This case report describes an elderly patient with Crohn’s disease who presented with an unusual case of chronic pancreatitis found on imaging.


A 67-year-old woman with a history of colonic Crohn’s disease presented to the emergency department reporting new onset bilateral flank pain and hematuria. Her Crohn’s disease was in remission after it was diagnosed 12 years earlier via colonoscopy. Biopsies at that time showed noncaseating granulomas, cecal erythema, and ulcerations consistent with both acute and chronic inflammation. She was subsequently treated with mesalamine, and her symptoms completely resolved without complications. Her remaining medical history was significant for controlled hypertension and gastroesophageal reflux. Her family history was noncontributory.

Laboratory Testing

An abdominal CT scan showed bilateral, nonobstructing nephrolithiasis and an incidental finding of pancreatic volume loss and calcifications. The patient was further queried regarding any history of pancreatitis or risk factors for precipitation, both of which were negative. She reported alterations in bowel movements with steatorrhea for the past 1 to 2 months. She said the bowel movements were noticeably different from her diarrhea associated with Crohn’s disease. This warranted further pancreatic studies, which revealed increased fecal fat and low serum trypsin with normal levels of amylase, lipase, and immunoglobulin G4 (IgG4). 

The patient was started on pancreatic enzyme supplements with notable improvement in frequency and consistency of her stools. 


Pancreatitis associated with IBD is often attributed to known factors, such as adverse drug effects (ie, 5-aminosal icyclic acid [ASA] or azathioprine), cholelithiasis, ileal or duodenal involvement in Crohn’s disease or primary sclerosing cholangitis associated with ulcerative colitis.1,6 There is a higher incidence of pancreatitis in patients with Crohn’s disease compared to ulcerative colitis.7 While most cases have an identifiable etiology, there are a number of acute, and even more rarely, chronic pancreatitis cases with unexplained pathogenesis and thus labeled idiopathic. The rate of idiopathic pancreatitis in Crohn’s disease varies in the literature, from 1.2% to 1.5% with 1 series showing 8%.1,8,9 True incidence is hard to estimate as many have a subclinical/asymptomatic disease course or the symptoms of IBD mask the diagnosis of pancreatitis.6,9 

The earliest evidence of association between subclinical pancreatitis and IBD patients is in a postmortem study by Ball and colleagues,2 who found either gross or histological pancreatic lesions in 53% of ulcerative colitis patients with no history of pancreatitis. This is supported by a more recent study by Toda and colleagues,3 who  found 16% of ulcerative colitis patients, who had no history or risk factors for pancreatitis, with pancreatic duct changes on magnetic resonance cholangiopancreatography. 

Emerging evidence suggests that some cases of chronic pancreatitis have an underlying mechanism similar to autoimmune pancreatitis based on similarities in histology and pancreatic duct abnormalities.10 The autoimmune serological marker, IgG4, which is associated with autoimmune pancreatitis, has been found in a number of idiopathic chronic pancreatitis cases suggesting an underlying autoimmune mechanism; however, evidence has not been consistent to deem it as a useful marker.10,11 Additionally, it has been suggested that chronic pancreatitis is due to autoantibodies against the exocrine pancreas. Most evidence of this has been found in Crohn’s disease patients, but there is little correlation with pancreatic insufficiency or pancreatic duct changes, making evidence inconclusive.11,12 

While the underlying mechanism of IBD-related chronic pancreatitis is unclear, its features are evident on CT imaging. Findings can include increased inhomogeneous density of parenchyma, pseudocysts, intraparenchymal or ductal calcifications, irregular dilatations and strictures of the duct, and overall decrease in size if in advanced stages.13 The patient’s age, however, should be accounted for since aging incites degenerative changes of the pancreas and leads to changes on CT as well.13 

Common features that contrast chronic pancreatitis findings on CT include increased homogenous density of parenchyma, patchy fibrosis, lipomatosis, diffuse ductal homogenous enlargement, and overall homogenous reduction in size with preservation of the shape.13 The patient presented in this case report had evidence of pancreatic loss, which can be attributed to both aging or chronic pancreatitis. The findings of calcifications, however, are more consistent with chronic pancreatitis. Additionally, evidence of exocrine pancreatic insufficiency in our case patient, determined by the fecal elastase test, may be the most common feature of IBD-related chronic pancreatitis found to date.11,14 

Again, however, functional changes due to physiologic aging need to be considered during the evaluation. A number of older studies that evaluate exocrine insufficiency in the elderly15-18 show inconsistent results, which may be partially attributed to each study utilizing different pancreatic exocrine tests with varying sensitivities. 

A recent study by Herzig and colleagues19 evaluated levels of fecal pancreatic elastase-1 in older individuals who had no known history of GI disease or surgery, diabetes, or alcohol abuse. Findings indicative of pancreatic exocrine insufficiency (<200 µg/g) were found in 23 (21.7%) of 106 individuals over 60 years of age. This study suggests that a small fraction of healthy older individuals may have functional pancreatic changes. However, this study was limited as there may have been undiagnosed cases of diabetes, which increases the risk of exocrine insufficiency. More studies are needed to better characterize this association.

Chronic pancreatitis with unclear pathogenesis may be an extraintestinal manifestation of IBD. It can present in patients with GI alterations that are consistent with symptoms of pancreatic exocrine insufficiency and can be identified on CT imaging. While more evidence is needed to evaluate pancreatic exocrine insufficiency in the healthy elderly population, it is important to recognize that the combination of chronic pancreatitis changes on imaging with features of pancreatic insufficiency suggest an IBD-related process in a patient with Crohn’s disease or ulcerative colitis. Clinicians caring for elderly patients with IBD should maintain a heightened awareness of the different morphological and functional pancreatic changes that can occur due to IBD manifestations versus physiological changes of aging. This ensures that patients are receiving appropriate assessment and care in order to reduce morbidity and mortality.  

Marie L. Borum, MD, EdD, MPH, is a professor of medicine and director of the division of gastroenterology and liver diseases at George Washington University in Washington, DC.

Gayatri Patel, MD. is an internal medicine resident.


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