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Vol. 66, No. 4 2015
Northeast Florida Medicine
DCMS online
. org
Inflammatory Bowel Disease
atic autoantibodies, and pancreatic cancer.
14
Due to the
ominous IBD-pancreas association, periodic assessment
of the pancreatic function in suspected IBD patients is
prudent, as pancreatic involvement may also precede the
onset of IBD.
Pancreatitis
Pancreatitis is a rare extraintestinal manifestation of
IBD. The risk of developing acute
15
or chronic pancre-
atitis
16
in adults and children with IBD has proven to
be augmented. New data also suggests that autoimmune
pancreatitis, which is less common, arises more often
among this subgroup.
17
In IBD patients, pancreatitis is usually clinically silent
18
and holds an incidence rate that ranges from 4.8 to 38
in 100,000 inside the U.S.
19
Recently, the incidence of
acute pancreatitis (AP) in CD has been reported to vary
from 1 to 1.4 percent during a period of 10 years.
15
Con-
currently, Bermejo et al described a 1.6 percent incidence
of AP in IBD patients, with 63.4 percent of the etiology
attributable to medical treatment.
20
Furthermore, evidence reveals that AP may denote the
onset of IBD in children and in adults. The prevalence
of AP as a debuting symptom of IBD is 0.06 percent
in adults and 3.6 percent in children.
21
Other previous
studies have shown a maximum prevalence of 27 percent
of AP preceding IBD.
22,23
Additionally, AP in adults has
been commonly described in CD rather than in UC, but
its severity is similar to that in the general population.
15
Idiopathic Chronic Pancreatitis (ICP)
The association of IBD with idiopathic chronic pan-
creatitis has been sporadically reported predominantly in
pediatrics.
24-26
Although some patients present with irregu-
lar pancreatograms indicative of chronic pancreatitis, they
are usually asymptomatic even when significant exocrine
insufficiency coexists.
27
Therefore, it is not surprising to
find pancreatic fibrosis, acinar regression, and granulomas
in patients with IBD, especially in CD.
16,28
On the other
hand, pancreatic duct changes (stenosis) and weight loss
are more likely to happen in UC.
29
Exocrine Pancreatic Insufficiency (EPI)
EPI is an extraintestinal manifestation of IBD charac-
terized by deficiency of the exocrine pancreatic enzymes
(amylase, protease, and lipase), resulting in maldigestion.
30
Normally, lipase breaks triglycerides into fatty acids and
monoglycerides. Those are solubilized by bile salts, and
ultimately turned into micelles for lipid absorption.
31
Detection of EPI is often delayed since fat digestion is
not markedly impaired until lipase output falls below 10
percent and/or maldigestion of fat is clinically perceived as
steatorrhea.
32
This is why fat malabsorption precedes that
of proteins and carbohydrates.
33
Steatorrhea is also caused
due to bile salt pool reduction (owed to precipitation and
subsequent adsorption to undigested food)
34
and due to
neurohormonal disturbances (that result in gall bladder
hypomotility and accelerated gastrointestinal transit).
35
The etiology of exocrinopathy in IBD includes pan-
creatic and nonpancreatic causes.
36
Pancreatic causes of
EPI include ICP (primary cause) and pancreatic duct
obstructions (like gallstones, pancreatic cancer, or ana-
tomic abnormalities) that thwart pancreatic excretions
from reaching the duodenum. Nonpancreatic causes of
EPI comprise autoimmune pancreatitis
37
, and surgical
procedures in the gastrointestinal and pancreatic terri-
tories, leading to loss of pancreatic parenchyma and/or
postprandial asynchrony.
38
Pancreatic insufficiency is associated to IBD’s activity
and extent, and can be observed in patients with or with-
out a history of pancreatitis.
27,39,40
It has been reported in
approximately 18 percent of IBD patients; some studies
even show a 21-80 percent rate of inadequate levels of
pancreatic exocrine secretions in IBD patients.
41,42
Hence,
due to its silent insidious nature, fecal elastase-1 levels
should be assessed to determine presence and severity of
exocrinopathy.
43
EPI’s management primarily consists of pancreatic
enzyme replacement therapy (PERT), however it also
includes fat-soluble vitamin supplementation, and life-
style adjustments.
Autoimmune Pancreatitis (AIP)
Patients with IBD present up to a 15X increased risk
of AIP compared to the general population. The presence
of IgG4-positive cells on the colon’s mucosa of afflicted
patients may imply that IBD embodies an extrapancre-
atic manifestation of autoimmune pancreatitis; for that
reason almost 6 percent of patients diagnosed with AIP,
also hold a diagnosis of IBD.
44