Volume 1, Issue 3 | April 2014
Case Report | Pancreas/Biliary

Groove Pancreatitis: Four Cases from a Single Center and Brief Review of the Literature

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Tyler P. Black, MD1, Cynthia D. Guy, MD2, Rebekah R. White, MD3, Jorge Obando, MD4, and Rebecca A. Burbridge, MD4

1Department of Internal Medicine, Duke University Medical Center, Durham, NC
2Department of Pathology, Duke University Medical Center, Durham, NC
3Department of Surgery, Duke University Medical Center, Durham, NC
4Department of Gastroenterology, Duke University Medical Center, Durham, NC

ACG Case Rep J 2014;1(3):154–157. http://dx.doi.org/10.14309/crj.2014.35. Published: April 4, 2014.


Groove pancreatitis is a rare form of chronic pancreatitis that affects the groove anatomical area between the head of the pancreas, duodenum, and common bile duct. We provide a summary of the clinical findings of 4 groove pancreatitis cases diagnosed at a tertiary academic medical center over a 5-year period. A detailed review of the current literature surrounding this clinical entity is also provided. Although rare, groove pancreatitis should be considered in the differential diagnosis of patients presenting with pancreatic head mass lesions, as appropriate diagnosis can help avoid unnecessary surgical procedures.


Groove pancreatitis is a rare condition characterized by fibrotic inflammation affecting the anatomical area between the head of the pancreas, duodenum, and common bile duct.1 This condition can often be difficult to differentiate from adenocarcinoma of the pancreatic head, but certain clinical, radiological, and histological features can be useful in making a diagnosis. The prevalence of groove pancreatitis has been difficult to establish, but has been reported as high as 24.5% in pancreaticoduodenectomy specimens from patients with chronic pancreatitis.2 It often presents in middle-aged males (aged 40–50 years) with a history of alcohol consumption, recurrent or chronic pancreatitis, and pancreatic head mass lesions on imaging.3 Its presentation is similar to adenocarcinoma of the pancreatic head or, more rarely, autoimmune pancreatitis, but can often be cured by conservative management.4,5 We present a series of 4 cases of groove pancreatitis diagnosed at a tertiary medical center over a 5-year period, with a detailed review of the current medical literature.

Case Report

Four cases of suspected groove pancreatitis were identified over a 5-year period. Two cases had histological confirmation of groove pancreatitis. The other 2 cases were considered to be likely diagnoses based on the clinical presentation and imaging findings. Table 1 shows a summary of the findings for each case.



The average age was 56.5 years. Two patients were African-American and 2 were female. All patients presented with abdominal pain and were given a diagnosis of pancreatitis based on an elevation of lipase and/or amylase. Two patients had both computed tomography (CT) and magnetic resonance imaging (MRI), while the other 2 patients had either CT or MRI. A representative CT image from patient 3 is shown in Figure 1.


Figure 1. Abdominal CT from patient 3 showing a 6-mm hypoenhancing pancreatic head mass.

Patients 1 and 4 were given a diagnosis of groove pancreatitis based on their imaging findings, whereas patients 2 and 3 were diagnosed by a combination of imaging and histological findings. Histology was obtained for patient 1, but was non-diagnostic. The pancreatic head mass seen on the imaging from patient 1 resolved on a follow-up MRI 2 months later. Histology was not obtained for patient 4. Patients 1 and 3 presented with recurrent episodes of pancreatitis, which is often seen before a diagnosis of groove pancreatitis is established. All 4 patients were active or former smokers. One patient had a significant alcohol use history.


Groove pancreatitis was first described by Becker in 1973 in the German literature as “segmentare pancreatitis.”6 In 1982, Stolte et al defined groove pancreatitis as a special form of segmental pancreatitis characterized by fibrous scars of the anatomic space between the dorsocranial part of the head of the pancreas, the duodenum, and the common bile duct.7 In the early 1990s, Becker and Mischke further classified groove pancreatitis into pure and segmental forms. The pure form involves the groove area only, with preservation of the pancreatic parenchyma and main pancreatic duct. The segmental form involves both the groove and the head of the pancreas with stenosis of the pancreatic duct causing upstream dilatation.8

The prevalence of groove pancreatitis varies widely. In 3 surgical series, groove pancreatitis was diagnosed in 2.7%, 19.5%, and 24.5% of pancreaticoduodenectomy specimens taken from patients with chronic pancreatitis.7–9 Groove pancreatitis often presents in alcoholic men aged 40–50 years.7,8 Presenting symptoms consist of abdominal pain, nausea, vomiting, and weight loss.7,8 Laboratory evaluation often reveals an elevation in pancreatic enzymes and rarely an elevation in hepatic enzymes.10 Carcinoembryonic antigen and carbohydrate antigen 19-9 can also be elevated.9

A diagnosis of groove pancreatitis is often difficult to establish. The most important distinction to make is between groove pancreatitis and adenocarcinoma of the head of the pancreas. Ultrasound will typically show a hypoechoic mass, and CT will often reveal a hypodense, poorly enhancing mass between the head of the pancreas and a thickened duodenal wall.11 The most characteristic MRI finding is a sheet-like mass between the head of the pancreas and the duodenum associated with duodenal wall cystic changes and thickening.5 Endoscopic retrograde cholangiopancreatography (ERCP) and endoscopic ultrasonography (EUS) are often useful in the differentiation of groove pancreatitis from pancreatic adenocarcinoma, and should be used early in evaluation even when cross-sectional imaging is not suggestive of a mass.12 Table 2 lists characteristic imaging features differentiating groove pancreatitis from pancreatic adenocarcinoma.



The pathogenesis of groove pancreatitis remains unclear, and several mechanisms have been proposed. The most accepted mechanism is a disturbance of pancreatic outflow in the duct of Santorini through the minor papilla.13,14 Chronic alcohol consumption is felt to contribute by increasing the viscosity of the pancreatic juice, leading to Brunner gland hyperplasia and causing occlusion or dysfunction of the minor papilla.13,14 Another proposed mechanism is pancreatic heterotopia in the minor papilla causing dysfunction and occlusion of the papilla.13 Other factors, such as fibrous scarring secondary to peptic ulcers, gastric and duodenal resections, or true duodenal wall cysts may also be related.5

The treatment of choice is conservative in the acute phase of groove pancreatitis and includes bowel rest, analgesia, and intravenous fluids.10 Patients may have a protracted course requiring supplemental nutrition with tube feeding or total parenteral nutrition. One report demonstrated successful treatment of groove pancreatitis by endoscopic drainage of the accessory pancreatic duct via the minor papilla in patients where obstruction of the minor papilla appears to play a role in the pathogenesis.15 Groove pancreatitis can be resistant to medical treatment and require surgical intervention. The surgical treatment of choice is a Whipple procedure (pancreaticoduodenectomy) or a pylorus-preserving pancreaticoduodenectomy.2

In our series of 4 patients, a combination of clinical and radiological features was used to make the diagnosis of groove pancreatitis. Although other case reports show common alcohol use and a male predominance, 2 of our patients were female and only 1 patient had a history of significant alcohol use. Although rare, this condition should be considered in the differential diagnosis of pancreatic head masses with signs of duodenal wall infiltration. Alternatively, a careful and thorough evaluation to rule out adenocarcinoma should be performed before a definitive diagnosis of groove pancreatitis is established.


Author contributions: All authors contributed equally to the preparation of this manuscript. RA Burbridge is the author guarantor.

Financial disclosure: None to report.

Informed consent was obtained for this case report.

Correspondence: Tyler P. Black, Duke University Medical Center, 2301 Erwin Road, Durham, NC, 27710 (tylerpblack@gmail.com).

Received: December 20, 2013; Accepted: March 4, 2014


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