Groove pancreatitis (GP) is an uncommon form of chronic pancreatitis (CP) involving the space between duodenum, pancreatic head and common bile duct (CBD) known as pancreatic-duodenal groove.
Most patients with GP are male, aged 40–50 years, with a history of severe chronic alcoholism and, in a lower percentage, also associated with smoking.
Abdominal pain, postprandial vomiting and weight loss, primarily due to duodenal obstruction, are the most common manifestations of GP, with concomitant twofold or threefold increase of serum amylase concentration, or heavy levels of serum lipase.
About 80% of the patients with the clinical symptoms of acute pancreatitis present such high concentrations of the serum of pancreatic amylase and serum lipase levels. Tumor markers (CA 19-9 and CEA) are usually normal.
It has also been reported that diarrhea or diabetes mellitus are commonly associated with GP. The clinical symptoms of the syndrome spread over the time span ranging from a few weeks to a year, then the GP becomes chronic. In a high number of patients with alcohol abuse, obstructive jaundice has been observed especially in the course of chronic disease if late stenosis of the CBD has occurred.
Etiology and pathogenesis
The etiology of GP is likely heterogeneous implying a series of factors possibly playing a role in its development. There is general agreement about the effects for people who abuse of ethyl alcohol on disease development and all its clinical manifestations.
Chronic alcohol intake causes a decrease in bicarbonate secretion which increases viscosity and consequent stagnation of pancreatic secretion in pancreatic ducts; it follows an increase in pressure inside the Santorini duct with the release of the secretion in the groove that promotes the formation of pseudocysts.
One of the mechanisms hypothesized for the development of CP associated with the alcohol abuse provides that alcohol predispose acinar cells to autodigestive injury and necro-inflammation by increasing the synthesis of digestive and lysosomal enzymes leading to autodigestive cellular damage, acinar injury and pancreatic necro-inflammation.
It is now accepted that the disease progresses irreversibly from the initial stages of necro-inflammation towards chronic stage of acute pancreatic through repeated attack episodes.
The latter produce additional and permanent structural damage to the gland, in the segmental form, resulting in the changes of CP characterized histologically by acinar atrophy and fibrosis (the necrosis-fibrosis sequence), which impair both endocrine and exocrine pancreatic functions.
The classic MDCT imaging features consist of loss of fat planes between head of pancreas and the duodenum with an ill-defined crescentic frank soft tissue mass seen with the pure form of GP.
On MRI imaging, GP is characterized by sheet-like mass between the pancreatic head and the duodenum. The mass is hypointense to pancreatic parenchyma on T1-weighted images, and according to the time of disease onset can be hypo-, iso- or slightly hyperintense on T2-weighted images.
On delayed gadolinium-enhanced images, the diagnostic accuracy of MRI is comparable to that of CT in the characterization of fibrotic mass.
Cystic degeneration within the duodenal wall is a specific sign of GP. The typical findings are cysts, variable in size and complexity in the thickened duodenal wall.
MRCP has become an important diagnostic tool in a variety of pancreaticobiliary disorders and in particular in imaging workup of patients with GP.
Using MRCP, it is possible to detect the reduction of the caliber with regular smooth profile of the distal CBD.
MRCP may show dilatation of the MPD in the form of segmental GP, while it may appear normal in the pure form.
MRCP may show the dilation of the ampulla of Vater and the MPD, both of which are common gross features of segmental GP, detect relationships among cysts, CBD and MP, and also reveal the increase of the distance between duodenal lumen and distal duct.
EUS represents one of the most sensitive methods for detecting pancreaticobiliary lesions. The potentialities of the EUS are multiple, as it can also detect thickening and stenosis of the second duodenal part with intramural cysts, smooth stenosis of the CBD.
- Pancreatic adenocarcinoma
- Duodenal adenocarcinoma
- Periampullary cancers
- Pancreatic groove neuroendocrine tumor
- Cystic dystrophy of the duodenum
- Conventional edematous pancreatitis with involvement of the groove
- Acute pancreatitis
The management is usually conservative, with medical and endoscopic therapy in the initial stages. Conservative management options are a healthy balanced diet, pain management, pancreatic rest, and abstinence from alcohol and smoking.
Usually, these measures provide short-term relief, and occasionally they do provide long-term benefits.
Endoscopic therapies are beneficial but could involve a therapeutic failure in about 10 to 20% of patients.
The usual definitive therapy is surgery (Whipple pancreaticoduodenectomy) in most cases that are refractory to conservative therapy or in which the diagnosis is inconclusive.
Addeo G, Beccani D, Cozzi D, Ferrari R, Lanzetta MM, Paolantonio P, Pradella S, Miele V. Groove pancreatitis: a challenging imaging diagnosis. Gland Surg. 2019 Sep;8(Suppl 3):S178-S187. doi: 10.21037/gs.2019.04.06. PMID: 31559185; PMCID: PMC6755950.
Brar HS, Shah NJ, Bukeirat F. Groove Pancreatitis. [Updated 2023 Feb 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK589647/#