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134 E. D. Ehrenpreis
Fig. 15.3 Fat wrapping association with skip areas in a surgically resected portion of the small
intestine from a patient with Crohn’s disease. Fat wrapping is seen adjacent to an area of inflamed
and narrowed small intestine (arrows) and also is seen in adjacent to a second affected area or skip
lesion(arrowheads) with a small area of normal small intestine in between the two affected areas.
Photographs courtesy of Dr. J Calvin Coffey
fibroblast differentiation may produce an “outside in” phenomenon that are asso-
ciated with both inflammation and fibrosis of the intestine. B cells and innate
lymphocytes infiltrate mesenteric lymphatics in areas of fat wrapping. Bacterial
translocation and lymphaticslymphatics infiltration from the inflamed bowel wall
may initiate these events.
Imaging Studies of the Mesentery in Crohn’s Disease
Imaging studies demonstrate the relationship between the mesenteric and intestinal
activity in patients with Crohn’s disease. CT imaging in patients with Crohn’s
disease may demonstrate mesenteric edema with hypervascularity and stretching of
the mesenteric vessels, known as the Comb sign (Fig. 15.4).
Other CT findings include increased fat density, fibrofat ty proliferation, and
mesenteric lymphadenopathy (Figs. 15.5, 15.6, and 15.7). Engorgement of
mesenteric vasculature and mesenteric edema are also seen (Fig. 15.8). Stenosis
and sacculation in the mesentery may also be seen on small intestinal radiography
(Fig. 15.9).
Radiographic images can demonstrate synchronicity between intestinal organs
and the mesentery, predicting disease activity and anatomical changes such as
fibrosis. For example, Sakurai et al. recently demonstrated that the findings of
mesenteric hypervascularity and enlarged mesenteric lymph nodes correlated with
endoscopically visualized mucosal ulceration. Gale et al. compared CT
15 Crohn’s Disease and the Mesentery 135
Fig. 15.4 Abdominal CT
(sagittal view) of a patient
with active Crohn’s disease.
Stretching of the mesenteric
vessels, also known as the
Comb sign is seen (arrows).
Diffuse ileal involvement and
wall thickening is present
(arrowhead)
Fig. 15.5 Abdominal CT in
a patient with Crohn’s disease
demonstrating fi bofatty
proliferation (asterisk)
enterography and MR enterography in 84 children and adolescents with active
Crohn’s disease. In the pediatric population, mesenteric inflammatory changes
including mesenteric hypervascularity, edema, fibrofatty proliferation and lymphadenopathy correlate closely with active mucosal Crohn’s disease.
136 E. D. Ehrenpreis
Fig. 15.6 Coronal MRI of
the abdomen in a patient with
Crohn’s disease
demonstrating fatty
proliferation and increased fat
density on a T2 imaging
(arrowheads)
Fig. 15.7 Abdominal CT
(coronal view) of a patient
with active Crohn’s disease in
the right lower quadrant of the
abdomen. Multiple small
lymph nodes (arrows) and
stretched, hyperemic
mesenteric vessels are
demonstrated
15 Crohn’s Disease and the Mesentery 137
Fig. 15.8 Axial view near
the level of the umbilicus
showing mesenteric edema
(large arrow) and engorged
mesenteric vasculature (white
arrow)
Fig. 15.9 Spot film of the
distal ileum on small
intestinal radiography. The is
a long segment stricture of the
distal ileum. A segment with
asymmetric sparing along the
non-mesenteric boarder
results in an area of relative
outpouching (black arrows).
This area of outpouching is
referred to as
pseudosacculation. Images are
courtesy of Dr. Abraham
Dachman
Mesenteric Disorders that Are Associated with Crohn’s Disease
Arterial and venous thrombi within the mesenteric vasculature and mesenteric
venous congestion are associated with Crohn’s disease. These may be complicated
by bowel ischemia and perforation. Small intestinal lymphoma is more common in
patients with Crohn’s disease and may present as a mesenteric mass with some
thickening of surrounding tissues.
138 E. D. Ehrenpreis
Inflammatory Disorders of the Mesentery and Inflammatory Bowel Disease
The most common primary inflammatory disorder of the mesentery is mesenteric
panniculitis (also known as sclerosing mesenteritis). (See Chap. 20 Mesenteric
Panniculitis). Mesenteric panniculitis shares common features with inflammatory
bowel disease, especially Crohn’s disease. Typically, patients with mesenteric
panniculitis have a waxing and waning clinical course, abdominal signs and
symptoms, fever and weight loss, and response to anti-inflammatory agents. Some
cases of mesenteric panniculitis have ileocolic involvement. Both conditions
demonstrate elevated CRP and erythrocyte sedimentation rates (ESR). As in
Crohn’s disease, inflammatory masses in mesenteric panniculitis can produce
obstructive signs and symptoms from extrinsic compression of the small intestine.
Longstanding inflammation in the mesentery may produce mesenteric fibrosis
and scarring, similar to fibrotic bowel seen in Crohn’s disease. A family history of
inflammatory bowel disease is seen in some patients with mesenteric panniculitis.
In addition, mesenteric panniculitis-like findings on abdominal imaging studies
caused by local mesenteric inflammation have been described in patients with
Crohn’s disease. Finally, both Crohn’s disease and mesenteric panniculitis are
treated with immunomodulating agents.
Suggested Reading
1. Lakhan SE, Kirchgessner A. Neuroinflammation in inflammatory bowel disease. J Neuroinflammation. 2010;7:37.
2. Burke JP, Velupillai Y, O'connell PR, Coffey JC. National trends in intestinal resection for
Crohn's disease in the post-biologic era. Int J Color Dis 2013;28:1401–1406.
3. Coffey JC, O’Leary DP, Kiernan MG, Faul P. The mesentery in Crohn’s disease: friend or
foe? Curr Opin Gastroenterol. 2016;32:267–73.
4. Peyrin-Biroulet L, Chamaillard M, Gonzalez F, et al. Mesenteric fat in Crohn’s disease: a
pathogenetic hallmark or an innocent bystander? Gut. 2007;56:577–83.
5. Paeschke A, Erben U, Kredel LI, Kühl AA, Siegmund B. Role of visceral fat in colonic
inflammation: from Crohn’s disease to diverticulitis. Curr Opin Gastroenterol. 2017;33
(1):53–8.
6. Peyrin-Biroulet L, Gonzalez F, Dubuquoy L, Rousseaux C, Dubuquoy C, Decourcelle C,
Saudemont A, Tachon M, Béclin E, Odou MF, Neut C, Colombel JF, Desreumaux P. Mesenteric fat as a source of C reactive protein and as a target for bacterial translocation in Crohn’s
disease. Gut. 2012;61(1):78–85.
7. Batra A, et al. Mesenteric fat—control site for bacterial translocation in colitis? Mucosal
Immunol. 2012;5(5):580–91.
8. Li Y, Zhu W, Zuo L, Shen B. The role of the mesentery in Crohn’s disease: the contributions
of nerves, vessels, lymphatics, and fat to the pathogenesis and disease course. Inflamm Bowel
Dis. 2016;22:1483–95.
9. Randolph GJ, Bala S, Rahier JF, Johnson MW, Wang PL, Nalbantoglu I, Dubuquoy L,
Chau A, Pariente B, Kartheuser A, Zinselmeyer BH, Colombel JF. Lymphoid Aggregates
Remodel Lymphatic Collecting Vessels that Serve Mesenteric Lymph Nodes in Crohn
Disease. Am J Pathol. 2016;186(12):3066–73.
15 Crohn’s Disease and the Mesentery 139
10. von der Weid PY, Rehal S, Ferraz JG. Role of the lymphatic system in the pathogenesis of
Crohn’s disease. Curr Opin Gastroenterol. 2011;27(4):335–41.
11. Park MJ, Lim JS. Computed Tomography Enterography for Evaluation of Inflammatory
Bowel Disease. Clin Endosc. 2013;46(4):327–66.
12. Sakurai T, Katsuno T, Saito K, Yoshihama S, Nakagawa T, Koseki H, Taida T, Ishigami H,
Okimoto KI, Maruoka D, Matsumura T, Arai M, Yokosuka O. Mesenteric findings of CT
enterography are well correlated with the endoscopic severity of Crohn’s disease. Eur J
Radiol. 2017;89:242–8.
13. Gale HI, Sharatz SM, Taphey M, Bradley WF, Nimkin K, Gee MS. Comparison of CT
enterography and MR enterography imaging features of active Crohn disease in children and
adolescents. Pediatr Radiol. 2017;47(10):1321–8.
14. Zezos P, Kouklakis G, Saibil F. Inflammatory bowel disease and thromboembolism. World J
Gastroenterol. 2014;20(38):13863–78.
15. https://rarediseases.org/rare-diseases/mesenteric-panniculitis/. Accessed 3 Jan 18
16. Ehrenpreis ED, Roginsky G, Gore RM. Clinical significance of mesenteric panniculitis-like
abnormalities on abdominal computerized tomography in patients with malignant neoplasms.
World J Gastroenterol. 2016;22(48):10601–8.
17. Miranda-Bautista J, Fernández-SimónA,Pérez-Sánchez I, Menchén L. Weber-Christian
disease with ileocolonic involvement successfully treated with infliximab. World J Gastroenterol. 2015;21(17):5417–20.
The Role of the Mesentery in Pancreatic Diseases
Charles Broy, Chloe Lee, and Eli D. Ehrenpreis
Embryology of the Pancreas and Pancreatic Mesentery
Between the gestational ages of 30–47 days, the endodermal lining of the foregut
forms two outgrowths caudal to the developing liver. These are the ventral pancreatic bud and the dorsal pancreatic bud. Within each pancreatic bud, the endoderm develops into branched tubules that are attached to secretory acini, thus
forming the exocrine portion of the pancreas. The endocrine pancreas, including of
the islets of Langerhans, arise from stem cells at the duct branch points. These
develop into discrete islands of vascularized endocrine tissue within the parenchyma of the exocrine glandular tissue. During the seventh week of gestation, the
ventral and dorsal buds merge together to form a single organ. Within the newly
formed pancreas, the uncinate process of the head of the pancreas is derived from
the ventral pancreatic bud and the remaining portion of the head, body and tail of
the pancreas is derived from the dorsal pancreatic bud. It is during the process of
fusion of the ventral and dorsal pancreatic buds that heterotopic pancreas tissue
(pancreatic tissue in extra-pancreatic sites) is believed to occur. Exocrine function
of the pancreas begins after birth, while endocrine function, specifically the release
of hormones, can be measured after the 10th to 15th week of gestation.
16
C. Broy
Department of Gastroenterology, Edward Hines Jr VA, Hines, IL 60141, USA
e-mail: Charles.Broy@va.gov
C. Lee
Department of Internal Medicine, Advocate Lutheran General Hospital, Park Ridge, IL
60068, USA
E. D. Ehrenpreis (&)
Department of Medicine, Advocate Lutheran General Hospital, 1775 Dempster St, 6 South,
Park Ridge, IL 60068, USA
e-mail: e2bioconsultants@gmail.com
© Springer Nature Switzerland AG 2021
E. D. Ehrenpreis et al. (eds.), The Mesenteric Organ in Health and Disease,
https://doi.org/10.1007/978-3-030-71963-0_16
141
142 C. Broy et al.
The embryology of the mesentery is closely intertwined with its attendant
organs. The dorsal mesentery of the upper abdomen develops synchronically with
the rapid and asymmetric development of the stomach. As the stomach and duodenum expand laterally, the lesser sac develops. The pancreas grows into this area
and is the part of the fusion of the mesogastrium with the dorsal peritoneum. The
dorsal mesentery later develops into the gastrosplenic and splenorenal ligaments.
Aside from its function as a conduit for blood vessels, nerves and lymphatics, the
mesentery has been shown to influence the normal function of adjacent organs and
can also be involved with the development of diseases within these organs. It is
probable that the mesentery has a role in normal pancreatic function as well as
pancreatic disease.
Pancreatic Diseases
The pancreas is a retroperitoneal organ with anatomic contiguity with other peritoneal organs in the abdomen including the mesentery. It is known that pancreatic
cancer as well as pancreatitis can spread via the portion of the mesentery known as
the transverse mesocolon. The root of the mesentery extends from the horizontal
portion of the duodenum to the iliac fossa, creating an avenue the spread of pancreatic cancer in the subperitoneum. In addition, fat necrosis and inflammation may
traverse from the mesentery from its mesocolic to small bowel mesenteric sites due
to their direct connection.
Acute Pancreatitis
While the initiation of acute pancreas involves the release of pancreatic digestive
enzymes, complications of pancreatic inflammation may occur from primary
responses within the mesentery. Multiple animal studies suggest that mesenteric
lymph has toxic factors that may be the prime driver of multiple organ dysfunction.
One study of hemorrhagic shock in male rats compared trauma from laparotomy to
no trauma with or without mesenteric lymph duct ligation. CD11b and CD18
expression was increased in rats with trauma but prevented by ligation of the
mesenteric lymph duct. Since these integrins increase myeloid phagocytic cells,
these data provide evidence that neutrophil activation and sequestration are carried
by the mesenteric lymph. MicroRNAs (miRNAs) regulate gene expression associated with acute pancreatitis and are being studied as a clinical biomarker for the
disease. Blenkiron, et al performed a study in rats having three groups of control,
mild and moderate taurocholate-induced acute pancreatitis. Seven different miRNAs, comprising miR-375, -217, -148a, -216a, -122, -214, and -138, were
increased in the mesenteric lymph of rats with acute pancreatitis. The degree of
increase of these miRNAs also correlated with the severity of disease.
16 The Role of the Mesentery in Pancreatic Diseases 143
Translocated bacteria may also function as a cofactor in these processes.
Vascular complications of pancreatitis including hemorrhage can affect local
organs including the mesentery. Computerized tomography (CT) of the abdomen in
patients with acute pancreatitis often demonstrate concomitant inflammatory
changes occurring in the mesentery (Fig. 16.1).
In one study of MRI findings in the transverse mesocolon, 40 patients without
pancreatic disorders were compared with 210 patients with acute pancreatitis. One
hundred and thirty patients (61.9%) with acute pancreatitis demonstrated involvement of the transverse mesocolon portion of the mesentery. The grading of transverse mesocolon effect was strongly correlated with the MRI severity index and the
APACHE-II score (r = 0.759 and 0.384 respectively).
Mesenteric Panniculitis Involving the Pancreas and Pancreatic Panniculitis
Mesenteric panniculitis is a rare condition in which a mass-like lesion of the
mesentery or less organized “misty mesentery” occurs. Mesenteric panniculitis is
characterized by chronic inflammation and fat necrosis. It commonly involves the
Fig. 16.1 Necrotizing pancreatitis with mesenteric involvement. Decreased enhancement seen on
contrast-enhanced CT images in the head and neck of the pancreas indicate areas of necrosis (white
arrows). Mesenteric fat stranding and free fluid in the upper abdomen are common sequelae (black
arrows). Image is courtesy of Dr. Abraham Dachman and Dr. Justin Ramirez
144 C. Broy et al.
portion of the mesentery that is proximal to the small intestine. One retrospective
review of patients with mesenteric panniculitis that was performed at the Mayo
Clinic suggested an association between elevated IgG4 (with possible autoimmune
pancreatitis) and mesenteric panniculitis, but this finding has not been repeated in
other studies. Mesenteric panniculitis has also been described in the peripancreatic
region. (Also see Chap. 20. Mesenteric Panniculitis and Chap. 17 The Mesentery
and IgG4-Related Diseases).
Panniculitis can be a manifestation of a number of local and systemic diseases,
with erythema nodosum being the most common form of panniculitis. Panniculitis
has been divided into different etiologic subtypes that guide management: inflammatory, infectious, enzymatic destruction, traumati c, malignant and deposition
(Table 16.1). Systemic forms of panniculitis may at times also involve the
mesentery.
Symptoms of panniculitis depend on the area impacted, but the most common
presentations of these conditions are the development of painful, tender nodules in
the lower extremities. Pancreatic panniculitis (also known as enzymatic panniculitis) is an extremely rare disea se and is most commonly associated with acute or
chronic pancreatitis. Pancreatic panniculitis may occur in 2–3% of patients with a
variety of pancreatic disorders. At present, little is known about the pathophysiology of pancreatic panniculitis. One study that included 15 patients with necrotizing pancreatitis showed increased lipase in fat that was adjacent to the pancreas.
Furthermore, free fatty acid levels in visceral fat impact the severity of acute
pancreatitis. A direct effect of circulating pancreatic enzymes may be an important
factor in the development of pancreatic panniculitis. However, other factors are
needed for pancreatic panniculitis to occur, since acute pancreatitis in general is
characterized by elevated levels of lipase and amylase, and most patients do not
develop pancreatic panniculitis. Additionally, some causes of pancreatic panniculitis are not associated with elevated lipase such as pancreatic cancer. Other
potential factors leading to the development of pancreatic panniculitis include
trypsin activation and deposition of immune complexes.
Histopathology may reveal subcutaneous lobular fat necrosis with anuclear
adipocytes called ghost cells without vasculitis. Fat saponification and dystrophic
calcification may be present. Although these histologic findings can be pathognomonic of pancreatic panniculitis, often histology evaluation results in an equivocal diagnosis.
Metastatic fat necrosis is a known entity that can involve the heart, joints, lung,
bone marrow and the mesentery. One case series describes six patients with
mesenteric panniculitis and pancreatic disease. The clinical and radiographic findings in these patients mimicked primary pancreatic cancer. In this series, all patients
reported abdominal pain and three reported weight loss. The pancreatic
histopathology was typical for panniculitis with fat necrosis, lymphocytes, plasma
cells and rare eosinophils. Four of 5 of these patients had at least a partial response
to therapy which consisted of corticosteroids, tamoxifen, azathioprine, resection or
a combination of these.