Clinical Imaging 39 (2015) 363–366
Contents lists available at ScienceDirect
Clinical Imaging journal homepage: http://www.clinicalimaging.org
The breadth of imaging findings of groove pancreatitis John P. Hungerford, Meaghan Anne Neill Magarik, Andrew D. Hardie ⁎ Medical University of South Carolina, Department of Radiology and Radiological Science, 169 Ashley Avenue, Charleston, SC 29425
a r t i c l e
i n f o
Article history: Received 23 August 2014 Received in revised form 22 December 2014 Accepted 30 January 2015 Keywords: Pancreatitis Duodenal Calcification Bile duct Obstruction Mass effect
a b s t r a c t The pathogenesis of groove pancreatitis involves progressive cystic degeneration of hamartomatous pancreas rests which lie within the duodenal wall. Hamartomatous pancreatic rests can occur in other locations, but when located within the pancreaticoduodenal groove can lead to a particular clinical presentation following the development of fibrotic and inflammatory tissue. Although this is not a disease of the pancreas itself, the pancreatic duct and biliary system is frequently secondarily involved in this regional process. Identification of this entity and its varied appearances as a distinct pathology is essential given the unique management issues of groove pancreatitis. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Groove pancreatitis is an unusual cause of chronic abdominal pain which was first described in 1970 [1]. The imaging appearances and clinical features of this benign hamartomatous condition often overlap with pancreatic adenocarcinoma [2,4]. The prototypical patient is a 50-year-old male with a history of chronic relapsing abdominal pain and weight loss. Chronic alcoholism is the only well-established risk factor [3,4]. Duodenal luminal obstruction has been reported but appears to be a rare presenting symptom [4]. Serum laboratory values usually show only mildly elevated amylase and lipase which help to differentiate from typical acute interstitial or acute necrotic pancreatitis. Serum liver transaminases (aspartate transaminase and alanine transaminase) are also often mildly elevated. Tumor markers including CA19-9 are usually negative. Jaundice and hyperbilirubinemia are less common but can occur [3], mimicking ductal carcinoma. Fortunately, this is a treatable disease. The range of proposed therapies varies widely and includes the endoscopic stenting of the papilla, supportive therapy, Whipple procedure, and pancreas-sparing duodenectomy [3,5–9]. Since the first publication of groove pancreatitis in 1970, the radiological description has been fairly well typified [4,10–12]. However, beyond the typical findings, there has been little information published on the end-stage or atypical characteristics of groove pancreatitis. The spectrum of findings is wide, and the atypical characteristics can vary greatly from the typical form of the disease. Anecdotally, an understanding of the spectrum of the end-stage and atypical imaging features seems to be important as several of the cases diagnosed by ⁎ Corresponding author. Medical University of South Carolina, Department of Radiology and Radiological Science, 25 Courtenay Dr. MSC 226, Charleston SC 29401. Tel.: +1 843 876 7155; fax: +1 843 876 3157. E-mail address: [email protected] (A.D. Hardie). http://dx.doi.org/10.1016/j.clinimag.2015.01.018 0899-7071/© 2015 Elsevier Inc. All rights reserved.
computed tomography (CT) and magnetic resonance imaging (MRI) from our quaternary referral center have been complicated by such features [5]. It is essential for the radiologist to have an understanding of the varied radiographic appearances of this disease in order to differentiate it from other pathologies which often have some overlapping imaging characteristics including, but not limited to, pancreatic adenocarcinoma. This is especially important considering that the prognoses and therapies for those mimicking conditions may vary significantly from groove pancreatitis. 2. Gross pathology and histology Groove pancreatitis is described histopathologically as chronic inflammation and scarring in the anatomical space between the medial wall of the duodenum and the head of the pancreas, which is termed the “groove” [4,13]. Hamartomatous rests of pancreas within the medial duodenal wall undergo cystic degeneration from chronic episodes of stress, which are presumed to be related to alcohol-induced ischemia [14]. Microscopic pathologic findings include, fibrosis, cysts, Brunner gland hyperplasia, and smooth muscle hyperplasia [5,8,14–16]. Gross ductal abnormalities are not uncommon with groove pancreatitis [17]. Pancreatic duct and common bile duct stenoses occur due to strictures, proteinacous plugs, and abnormally viscous ductal fluid. The most frequent duct involved is the accessory duct of Santorini at the minor papilla [4,13,15]. Occasionally, there are findings of chronic calcific pancreatitis [4,15,19]. The features of chronic calcific pancreatitis correspond to the severity of ductal abnormalities, with chronic stenosis leading to upstream stasis and eventual intraductal stone formation [10]. There are two established typical gross morphologic forms of this disease: the pure form and the segmental form [11,13,15]. In the “pure” form, the abnormalities are confined to the pancreaticoduodenal
364
J.P. Hungerford et al. / Clinical Imaging 39 (2015) 363–366
Fig. 1. Coronal contrast-enhanced CT demonstrates typical groove pancreatitis (GP) with a sheet-like mass in the groove and adjacent duodenal thickening. This is an example of the “pure form” with the abnormalities largely confined to the pancreaticoduodenal groove.
groove, and the head of the pancreas proper is spared. In the “segmental” form, the inflammation and scarring extend to directly involve the head of the pancreas proper which frequently leads to intrapancreatic abnormalities including cysts and fibrotic masses [18]. 3. Radiological findings The imaging findings of typical groove pancreatitis have been relatively well established. The typical morphology includes a “sheet-like mass” of nonenhancing fibrotic tissue within the groove, medial duodenal wall thickening and cystic degeneration, and possibly mild common biliary ductal dilation (Figs. 1 and 2) [4]. There are several other less typical morphologies of groove pancreatitis which are not altogether uncommon. These atypical forms have a wide range of imaging features which can vary greatly from the typified form. The morphologic spectrum of the fibrotic mass can vary greatly from the typical “sheet like” form (Fig. 3). The mass can be large, solid, cystic,
Fig. 3. Coronal HASTE T2W images demonstrate the wide spectrum of morphologies of the groove mass ranging from (a) a small cystic lesion to (b) a large cystic and solid mass.
Fig. 2. Axial contrast-enhanced CT (CECT) demonstrates another typical case of GP. This is an example of the “segmental form” with the round fibrotic mass centered in the pancreaticoduodenal groove but involving the head of the pancreas.
multicystic, heterogeneous, or complex [4]. Often, with these atypical morphologies of the fibrotic mass, the major diagnostic dilemma is differentiating a benign hamartomatous fibrotic mass from a carcinomatous scirrhous mass. When assessing the mass, it is the absence of certain features which is important in order to discriminate from carcinoma including vascular encasement, distant metastases, lymphadenopathy, and direct invasion of neighboring organs (other than for the duodenum or the pancreas). Cystic degeneration within the medial duodenal wall is a somewhat specific imaging characteristic for groove pancreatitis. Typical findings are small discrete cysts and associated focal medial duodenal wall thickening. The cysts are within the thickened wall are more often seen with MRI. Atypical cystic degeneration can vary greatly in appearance and can include multiple, large, complex multicystic masses (Fig. 4). Ductal abnormalities are common imaging findings with groove pancreatitis. The typical findings are gradually tapered narrowings and mild
J.P. Hungerford et al. / Clinical Imaging 39 (2015) 363–366
365
Fig. 5. Coronal HASTE T2WI images demonstrate the spectrum of ductal abnormalities. (a) Mild common bile duct dilation is typical. (b) Extrinsic compression on the pancreatic head from larger groove masses can lead to more significant ductal dilation.
Fig. 4. (a) Coronal CECT, (b) coronal HASTE T2WI, and (c) another coronal HASTE T2WI demonstrate the spectrum of features of duodenal cystic degeneration. Typical degeneration with focal wall thickening and small discrete intramural cysts (a). Atypical cases demonstrate larger cysts (b) and even a multicystic complex conglomerate (c).
upstream ductal dilation [5,10]. The spectrum of ductal abnormalities varies greatly from the typified mild narrowing and dilation (Fig. 5), and the ductal dilation can be quite severe and extensive. The intrahepatic bile ducts, extrahepatic bile ducts, and pancreatic ducts can all be greatly dilated. Ductal irregularities have been described as particularly common with the “segmental form” of this disease, as the pancreatic head is directly involved by the fibrosis [13]. However, ductal dilatation can be seen with the “pure form” of this disease, subsequent to extrinsic pancreatic head compression from the groove mass. With more severe extrinsic
compression, there are worse narrowing and stenosis often leading to upstream glandular atrophy and dramatic ductal dilation. Chronic calcific pancreatitis is another atypical feature of groove pancreatitis. This also occurs from longstanding chronic intrinsic (segmental form) or extrinsic (pure form) compression of the ducts which leads to pancreatic ductal dilation, glandular atrophy, and intraductal stones (Fig. 6). Upstream glandular atrophy is also a feature of ductal adenocarcinoma and is therefore not a helpful feature for making that distinction. 4. Conclusion The breadth of imaging findings in groove pancreatitis is wide. The typical imaging appearance is somewhat specific and fairly well established. The typical form demonstrates a sheet-like mass in the pancreaticoduodenal groove with mild duodenal wall thickening,
366
J.P. Hungerford et al. / Clinical Imaging 39 (2015) 363–366
Fig. 6. Coronal CECT demonstrates chronic calcific pancreatitis superimposed upon groove pancreatitis with a large cystic mass centered in the groove.
duodenal cystic change, and mild common bile duct dilation. However, atypical forms are not uncommon and can include large irregular complex “groove” masses, extensive cystic duodenal wall degeneration, dramatic ductal dilation, upstream ductal atrophy, and superimposed chronic calcific pancreatitis. These atypical morphologies vary drastically from the typified form and can potentially make the distinction from ductal adenocarcinoma even more difficult.
References [1] Potet F, Duclert N. Cystic dystrophy on aberrant pancreas of the duodenal wall. Arch Fr Mal App Dig 1970;59(4):223–38.
[2] Malde DJ, Oliveira-Cunha M, Smith A. Pancreatic carcinoma masquerading as groove pancreatitis: case report and review of literature. J Pancreas (Online) 2011;12(6): 598–602. [3] Levenick JM, Gordon SR, Sutton JE, Suriawinata A, Gardner TB. A comprehensive, case-based review of groove pancreatitis. Pancreas 2009;38(6):e169–75. [4] Raman SP, Salaria SN, Hruban RH, Fishman EK. Groove pancreatitis: spectrum of imaging findings and radiology–pathology correlation. AJR Am J Roentgenol 2013; 201(1):W29–39. [5] Levenick JM, Sutton JE, Smith KD, Gordon SR, Suriawinata A, Gardner TB. Pancreaticoduodenectomy for the treatment of groove pancreatitis. Dig Dis Sci 2012;57(7):1954–8. [6] Casetti L, Bassi C, Salvia R, Butturini G, Graziani R, Falconi M, et al. "Paraduodenal" pancreatitis: results of surgery on 58 consecutives patients from a single institution. World J Surg 2009;33(12):2664–9. [7] Isayama H, Kawabe T, Komatsu Y, Sasahira N, Toda N, Tada M, et al. Successful treatment for groove pancreatitis by endoscopic drainage via the minor papilla. Gastrointest Endosc 2005;61(1):175–8. [8] Pezzilli R, Santini D, Calculli L, Casadei R, Morselli-Labate AM, Imbrogno A, et al. Cystic dystrophy of the duodenal wall is not always associated with chronic pancreatitis. World J Gastroenterol 2011;17(39):4349–64. [9] Egorov VI, Butkevich AC, Sazhin AV, Yashina NI, Bogdanov SN. Pancreas-preserving duodenal resections with bile and pancreatic duct replantation for duodenal dystrophy. Two case reports. JOP 2010;11(5):446–52. [10] Blasbalg R, Baroni RH, Costa DN, Machado MC. MRI features of groove pancreatitis. AJR Am J Roentgenol 2007;189(1):73–80. [11] Castell-Monsalve FJ, Sousa-Martin JM, Carranza-Carranza A. Groove pancreatitis: MRI and pathologic findings. Abdom Imaging 2008;33(3):342–8. [12] Irie H, Honda H, Kuroiwa T, Hanada K, Yoshimitsu K, Tajima T, et al. MRI of groove pancreatitis. J Comput Assist Tomogr 1998;22(4):651–5. [13] Becker V, Mischke U. Groove pancreatitis. Int J Pancreatol 1991;10(3–4):173–82. [14] Adsay NV, Zamboni G. Paraduodenal pancreatitis: a clinico-pathologically distinct entity unifying "cystic dystrophy of heterotopic pancreas", "para-duodenal wall cyst", and "groove pancreatitis". Semin Diagn Pathol 2004;21(4):247–54. [15] Kim JD, Han YS, Choi DL. Characteristic clinical and pathologic features for preoperative diagnosed groove pancreatitis. J Korean Surg Soc 2011;80(5):342–7. [16] Shanbhogue AK, Fasih N, Surabhi VR, Doherty GP, Shanbhogue DK, Sethi SK. A clinical and radiologic review of uncommon types and causes of pancreatitis. Radiographics 2009;29(4):1003–26. [17] Triantopoulou C, Dervenis C, Giannakou N, Papailiou J, Prassopoulos P. Groove pancreatitis: a diagnostic challenge. Eur Radiol 2009;19(7):1736–43. [18] Stolte M, Weiss W, Volkholz H, Rosch W. A special form of segmental pancreatitis: "groove pancreatitis". Hepato-Gastroenterology 1982;29(5):198–208. [19] Ishigami K, Tajima T, Nishie A, Kakihara D, Fujita N, Asayama Y, et al. Differential diagnosis of groove pancreatic carcinomas vs. groove pancreatitis: usefulness of the portal venous phase. Eur J Radiol 2010;74(3):e95-100.
Contents lists available at ScienceDirect
Clinical Imaging journal homepage: http://www.clinicalimaging.org
The breadth of imaging findings of groove pancreatitis John P. Hungerford, Meaghan Anne Neill Magarik, Andrew D. Hardie ⁎ Medical University of South Carolina, Department of Radiology and Radiological Science, 169 Ashley Avenue, Charleston, SC 29425
a r t i c l e
i n f o
Article history: Received 23 August 2014 Received in revised form 22 December 2014 Accepted 30 January 2015 Keywords: Pancreatitis Duodenal Calcification Bile duct Obstruction Mass effect
a b s t r a c t The pathogenesis of groove pancreatitis involves progressive cystic degeneration of hamartomatous pancreas rests which lie within the duodenal wall. Hamartomatous pancreatic rests can occur in other locations, but when located within the pancreaticoduodenal groove can lead to a particular clinical presentation following the development of fibrotic and inflammatory tissue. Although this is not a disease of the pancreas itself, the pancreatic duct and biliary system is frequently secondarily involved in this regional process. Identification of this entity and its varied appearances as a distinct pathology is essential given the unique management issues of groove pancreatitis. © 2015 Elsevier Inc. All rights reserved.
1. Introduction Groove pancreatitis is an unusual cause of chronic abdominal pain which was first described in 1970 [1]. The imaging appearances and clinical features of this benign hamartomatous condition often overlap with pancreatic adenocarcinoma [2,4]. The prototypical patient is a 50-year-old male with a history of chronic relapsing abdominal pain and weight loss. Chronic alcoholism is the only well-established risk factor [3,4]. Duodenal luminal obstruction has been reported but appears to be a rare presenting symptom [4]. Serum laboratory values usually show only mildly elevated amylase and lipase which help to differentiate from typical acute interstitial or acute necrotic pancreatitis. Serum liver transaminases (aspartate transaminase and alanine transaminase) are also often mildly elevated. Tumor markers including CA19-9 are usually negative. Jaundice and hyperbilirubinemia are less common but can occur [3], mimicking ductal carcinoma. Fortunately, this is a treatable disease. The range of proposed therapies varies widely and includes the endoscopic stenting of the papilla, supportive therapy, Whipple procedure, and pancreas-sparing duodenectomy [3,5–9]. Since the first publication of groove pancreatitis in 1970, the radiological description has been fairly well typified [4,10–12]. However, beyond the typical findings, there has been little information published on the end-stage or atypical characteristics of groove pancreatitis. The spectrum of findings is wide, and the atypical characteristics can vary greatly from the typical form of the disease. Anecdotally, an understanding of the spectrum of the end-stage and atypical imaging features seems to be important as several of the cases diagnosed by ⁎ Corresponding author. Medical University of South Carolina, Department of Radiology and Radiological Science, 25 Courtenay Dr. MSC 226, Charleston SC 29401. Tel.: +1 843 876 7155; fax: +1 843 876 3157. E-mail address: [email protected] (A.D. Hardie). http://dx.doi.org/10.1016/j.clinimag.2015.01.018 0899-7071/© 2015 Elsevier Inc. All rights reserved.
computed tomography (CT) and magnetic resonance imaging (MRI) from our quaternary referral center have been complicated by such features [5]. It is essential for the radiologist to have an understanding of the varied radiographic appearances of this disease in order to differentiate it from other pathologies which often have some overlapping imaging characteristics including, but not limited to, pancreatic adenocarcinoma. This is especially important considering that the prognoses and therapies for those mimicking conditions may vary significantly from groove pancreatitis. 2. Gross pathology and histology Groove pancreatitis is described histopathologically as chronic inflammation and scarring in the anatomical space between the medial wall of the duodenum and the head of the pancreas, which is termed the “groove” [4,13]. Hamartomatous rests of pancreas within the medial duodenal wall undergo cystic degeneration from chronic episodes of stress, which are presumed to be related to alcohol-induced ischemia [14]. Microscopic pathologic findings include, fibrosis, cysts, Brunner gland hyperplasia, and smooth muscle hyperplasia [5,8,14–16]. Gross ductal abnormalities are not uncommon with groove pancreatitis [17]. Pancreatic duct and common bile duct stenoses occur due to strictures, proteinacous plugs, and abnormally viscous ductal fluid. The most frequent duct involved is the accessory duct of Santorini at the minor papilla [4,13,15]. Occasionally, there are findings of chronic calcific pancreatitis [4,15,19]. The features of chronic calcific pancreatitis correspond to the severity of ductal abnormalities, with chronic stenosis leading to upstream stasis and eventual intraductal stone formation [10]. There are two established typical gross morphologic forms of this disease: the pure form and the segmental form [11,13,15]. In the “pure” form, the abnormalities are confined to the pancreaticoduodenal
364
J.P. Hungerford et al. / Clinical Imaging 39 (2015) 363–366
Fig. 1. Coronal contrast-enhanced CT demonstrates typical groove pancreatitis (GP) with a sheet-like mass in the groove and adjacent duodenal thickening. This is an example of the “pure form” with the abnormalities largely confined to the pancreaticoduodenal groove.
groove, and the head of the pancreas proper is spared. In the “segmental” form, the inflammation and scarring extend to directly involve the head of the pancreas proper which frequently leads to intrapancreatic abnormalities including cysts and fibrotic masses [18]. 3. Radiological findings The imaging findings of typical groove pancreatitis have been relatively well established. The typical morphology includes a “sheet-like mass” of nonenhancing fibrotic tissue within the groove, medial duodenal wall thickening and cystic degeneration, and possibly mild common biliary ductal dilation (Figs. 1 and 2) [4]. There are several other less typical morphologies of groove pancreatitis which are not altogether uncommon. These atypical forms have a wide range of imaging features which can vary greatly from the typified form. The morphologic spectrum of the fibrotic mass can vary greatly from the typical “sheet like” form (Fig. 3). The mass can be large, solid, cystic,
Fig. 3. Coronal HASTE T2W images demonstrate the wide spectrum of morphologies of the groove mass ranging from (a) a small cystic lesion to (b) a large cystic and solid mass.
Fig. 2. Axial contrast-enhanced CT (CECT) demonstrates another typical case of GP. This is an example of the “segmental form” with the round fibrotic mass centered in the pancreaticoduodenal groove but involving the head of the pancreas.
multicystic, heterogeneous, or complex [4]. Often, with these atypical morphologies of the fibrotic mass, the major diagnostic dilemma is differentiating a benign hamartomatous fibrotic mass from a carcinomatous scirrhous mass. When assessing the mass, it is the absence of certain features which is important in order to discriminate from carcinoma including vascular encasement, distant metastases, lymphadenopathy, and direct invasion of neighboring organs (other than for the duodenum or the pancreas). Cystic degeneration within the medial duodenal wall is a somewhat specific imaging characteristic for groove pancreatitis. Typical findings are small discrete cysts and associated focal medial duodenal wall thickening. The cysts are within the thickened wall are more often seen with MRI. Atypical cystic degeneration can vary greatly in appearance and can include multiple, large, complex multicystic masses (Fig. 4). Ductal abnormalities are common imaging findings with groove pancreatitis. The typical findings are gradually tapered narrowings and mild
J.P. Hungerford et al. / Clinical Imaging 39 (2015) 363–366
365
Fig. 5. Coronal HASTE T2WI images demonstrate the spectrum of ductal abnormalities. (a) Mild common bile duct dilation is typical. (b) Extrinsic compression on the pancreatic head from larger groove masses can lead to more significant ductal dilation.
Fig. 4. (a) Coronal CECT, (b) coronal HASTE T2WI, and (c) another coronal HASTE T2WI demonstrate the spectrum of features of duodenal cystic degeneration. Typical degeneration with focal wall thickening and small discrete intramural cysts (a). Atypical cases demonstrate larger cysts (b) and even a multicystic complex conglomerate (c).
upstream ductal dilation [5,10]. The spectrum of ductal abnormalities varies greatly from the typified mild narrowing and dilation (Fig. 5), and the ductal dilation can be quite severe and extensive. The intrahepatic bile ducts, extrahepatic bile ducts, and pancreatic ducts can all be greatly dilated. Ductal irregularities have been described as particularly common with the “segmental form” of this disease, as the pancreatic head is directly involved by the fibrosis [13]. However, ductal dilatation can be seen with the “pure form” of this disease, subsequent to extrinsic pancreatic head compression from the groove mass. With more severe extrinsic
compression, there are worse narrowing and stenosis often leading to upstream glandular atrophy and dramatic ductal dilation. Chronic calcific pancreatitis is another atypical feature of groove pancreatitis. This also occurs from longstanding chronic intrinsic (segmental form) or extrinsic (pure form) compression of the ducts which leads to pancreatic ductal dilation, glandular atrophy, and intraductal stones (Fig. 6). Upstream glandular atrophy is also a feature of ductal adenocarcinoma and is therefore not a helpful feature for making that distinction. 4. Conclusion The breadth of imaging findings in groove pancreatitis is wide. The typical imaging appearance is somewhat specific and fairly well established. The typical form demonstrates a sheet-like mass in the pancreaticoduodenal groove with mild duodenal wall thickening,
366
J.P. Hungerford et al. / Clinical Imaging 39 (2015) 363–366
Fig. 6. Coronal CECT demonstrates chronic calcific pancreatitis superimposed upon groove pancreatitis with a large cystic mass centered in the groove.
duodenal cystic change, and mild common bile duct dilation. However, atypical forms are not uncommon and can include large irregular complex “groove” masses, extensive cystic duodenal wall degeneration, dramatic ductal dilation, upstream ductal atrophy, and superimposed chronic calcific pancreatitis. These atypical morphologies vary drastically from the typified form and can potentially make the distinction from ductal adenocarcinoma even more difficult.
References [1] Potet F, Duclert N. Cystic dystrophy on aberrant pancreas of the duodenal wall. Arch Fr Mal App Dig 1970;59(4):223–38.
[2] Malde DJ, Oliveira-Cunha M, Smith A. Pancreatic carcinoma masquerading as groove pancreatitis: case report and review of literature. J Pancreas (Online) 2011;12(6): 598–602. [3] Levenick JM, Gordon SR, Sutton JE, Suriawinata A, Gardner TB. A comprehensive, case-based review of groove pancreatitis. Pancreas 2009;38(6):e169–75. [4] Raman SP, Salaria SN, Hruban RH, Fishman EK. Groove pancreatitis: spectrum of imaging findings and radiology–pathology correlation. AJR Am J Roentgenol 2013; 201(1):W29–39. [5] Levenick JM, Sutton JE, Smith KD, Gordon SR, Suriawinata A, Gardner TB. Pancreaticoduodenectomy for the treatment of groove pancreatitis. Dig Dis Sci 2012;57(7):1954–8. [6] Casetti L, Bassi C, Salvia R, Butturini G, Graziani R, Falconi M, et al. "Paraduodenal" pancreatitis: results of surgery on 58 consecutives patients from a single institution. World J Surg 2009;33(12):2664–9. [7] Isayama H, Kawabe T, Komatsu Y, Sasahira N, Toda N, Tada M, et al. Successful treatment for groove pancreatitis by endoscopic drainage via the minor papilla. Gastrointest Endosc 2005;61(1):175–8. [8] Pezzilli R, Santini D, Calculli L, Casadei R, Morselli-Labate AM, Imbrogno A, et al. Cystic dystrophy of the duodenal wall is not always associated with chronic pancreatitis. World J Gastroenterol 2011;17(39):4349–64. [9] Egorov VI, Butkevich AC, Sazhin AV, Yashina NI, Bogdanov SN. Pancreas-preserving duodenal resections with bile and pancreatic duct replantation for duodenal dystrophy. Two case reports. JOP 2010;11(5):446–52. [10] Blasbalg R, Baroni RH, Costa DN, Machado MC. MRI features of groove pancreatitis. AJR Am J Roentgenol 2007;189(1):73–80. [11] Castell-Monsalve FJ, Sousa-Martin JM, Carranza-Carranza A. Groove pancreatitis: MRI and pathologic findings. Abdom Imaging 2008;33(3):342–8. [12] Irie H, Honda H, Kuroiwa T, Hanada K, Yoshimitsu K, Tajima T, et al. MRI of groove pancreatitis. J Comput Assist Tomogr 1998;22(4):651–5. [13] Becker V, Mischke U. Groove pancreatitis. Int J Pancreatol 1991;10(3–4):173–82. [14] Adsay NV, Zamboni G. Paraduodenal pancreatitis: a clinico-pathologically distinct entity unifying "cystic dystrophy of heterotopic pancreas", "para-duodenal wall cyst", and "groove pancreatitis". Semin Diagn Pathol 2004;21(4):247–54. [15] Kim JD, Han YS, Choi DL. Characteristic clinical and pathologic features for preoperative diagnosed groove pancreatitis. J Korean Surg Soc 2011;80(5):342–7. [16] Shanbhogue AK, Fasih N, Surabhi VR, Doherty GP, Shanbhogue DK, Sethi SK. A clinical and radiologic review of uncommon types and causes of pancreatitis. Radiographics 2009;29(4):1003–26. [17] Triantopoulou C, Dervenis C, Giannakou N, Papailiou J, Prassopoulos P. Groove pancreatitis: a diagnostic challenge. Eur Radiol 2009;19(7):1736–43. [18] Stolte M, Weiss W, Volkholz H, Rosch W. A special form of segmental pancreatitis: "groove pancreatitis". Hepato-Gastroenterology 1982;29(5):198–208. [19] Ishigami K, Tajima T, Nishie A, Kakihara D, Fujita N, Asayama Y, et al. Differential diagnosis of groove pancreatic carcinomas vs. groove pancreatitis: usefulness of the portal venous phase. Eur J Radiol 2010;74(3):e95-100.
