Editorial Open Access
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World J Gastroenterol. Oct 21, 2011; 17(39): 4349-4364
Published online Oct 21, 2011. doi: 10.3748/wjg.v17.i39.4349
Cystic dystrophy of the duodenal wall is not always associated with chronic pancreatitis
Raffaele Pezzilli, Donatella Santini, Lucia Calculli, Riccardo Casadei, Antonio Maria Morselli-Labate, Andrea Imbrogno, Dario Fabbri, Giovanni Taffurelli, Claudio Ricci, Roberto Corinaldesi
Raffaele Pezzilli, Antonio Maria Morselli-Labate, Andrea Imbrogno, Dario Fabbri, Roberto Corinaldesi, Pancreas Unit, Department of Digestive Diseases and Internal Medicine, Sant’Orsola-Malpighi Hospital, 40138 Bologna, Italy
Donatella Santini, Department of Pathology, Sant’Orsola-Malpighi Hospital, University of Bologna, 40138 Bologna, Italy
Lucia Calculli, Department of Radiology, Sant’Orsola-Malpighi Hospital, University of Bologna, 40138 Bologna, Italy
Riccardo Casadei, Giovanni Taffurelli, Claudio Ricci, Department of Surgery, Sant’Orsola-Malpighi Hospital, University of Bologna, 40138 Bologna, Italy
Author contributions: Pezzilli R, Santini D, Calculli L, Casadei R, Taffurelli G and Ricci C followed the patients clinically; Imbrogno A, Fabbri D and Morselli-Labate AM collected the literature data; Morselli-Labate AM and Pezzilli R analyzed the data and interpreted the results; Pezzilli R and Corinaldesi R co-ordinated and collected all the patient information; Pezzilli R designed the study and wrote the manuscript.
Correspondence to: Dr. Raffaele Pezzilli, Pancreas Unit, Department of Digestive Diseases and Internal Medicine, Sant’Orsola-Malpighi Hospital, 40138 Bologna, Italy. raffaele.pezzilli@aosp.bo.it
Telephone: +39-051-6364148 Fax: +39-051-6364148
Received: February 18, 2011
Revised: March 31, 2011
Accepted: April 7, 2011
Published online: October 21, 2011

Abstract

Cystic dystrophy of the duodenal wall is a rare form of the disease which was described in 1970 by French authors who reported the presence of focal pancreatic disease localized in an area comprising the C-loop of the duodenum and the head of the pancreas. German authors have defined this area as a “groove”. We report our recent experience on cystic dystrophy of the paraduodenal space and systematically review the data in the literature regarding the alterations of this space. A MEDLINE search of papers published between 1966 and 2010 was carried out and 59 papers were considered for the present study; there were 19 cohort studies and 40 case reports. The majority of patients having groove pancreatitis were middle aged. Mean age was significantly higher in patients having groove carcinoma. The diagnosis of cystic dystrophy of the duodenal wall can now be assessed by multidetector computer tomography, magnetic resonance imaging and endoscopic ultrasonography. These latter two techniques may also add more information on the involvement of the remaining pancreatic gland not involved by the duodenal malformation and they may help in differentiating “groove pancreatitis” from “groove adenocarcinoma”. In conclusion, chronic pancreatitis involving the entire pancreatic gland was present in half of the patients with cystic dystrophy of the duodenal wall and, in the majority of them, the pancreatitis had calcifications.

Key Words: Pancreatitis, Cystic dystrophy of duodenal wall, Therapy, Outcome



INTRODUCTION

Cystic dystrophy of the duodenal wall is a rare form of the disease which was described for the first time in 1970 by Potet and Duclert[1]. Potet and Duclert and other French authors[2,3] described the presence of focal pancreatic disease localized in an area comprising the C-loop of the duodenum and the head of the pancreas (Figure 1A). In 1991, Becker and Mischke[4] defined this area as a “groove” and pointed out that it serves as a bed for the large vessels, lymph nodes, common bile duct (CBD) and main pancreatic duct. These authors also reported that pancreatitis can be found in this area and they suggested the term “groove pancreatitis” which was well received. They also classified groove pancreatitis as “pure groove pancreatitis” (Figure 1B), segmental pancreatitis of the head and chronic pancreatitis with groove involvement (Figure 1C). In addition, in recent years, Adsay and Zamboni[5] proposed the term “paraduodenal pancreatitis” in patients classified as having “cystic dystrophy of the heterotopic pancreas” or “paraduodenal wall cyst” or “groove pancreatitis”; they also recognized two types of pancreatitis: one characterized by cystic changes and the other characterized by solid lesions. These authors pointed out that the latter type of pancreatitis is difficult to distinguish from an adenocarcinoma originating in this area. Finally, the presence of cystic dystrophy of the duodeno-pancreatic space together with chronic pancreatitis of the remaining pancreas is not always true because there is also the possibility of disease limited to the CBD[6]. Thus, in this review, we report our recent experience on cystic dystrophy of the space from the C-loop of the duodenum and the pancreas by reporting three cases observed in the last year, and also systematically review and discuss the data in the literature on the alteration of the groove space.

Figure 1
Figure 1 Classification of the various types of groove pancreatitis. A: Typical finding of groove pancreatitis (purple area); B: Segmental head pancreatitis: the scar tissue (dark blue) expands towards the duodenum; C: Pancreatitis of the head: the scar tissue (dark blue) expands to the duodenal area, determining duodenal stenosis and displacement of the common bile duct.
OUR EXPERIENCE ON THREE RECENT OBSERVED CASES OF CYSTIC DYSTROPHY OF THE DUODENAL WALL

We report our experience on three recently observed cases of cystic dystrophy of duodenal wall. Patients were one female and two males aged 49-65 years having persistent abdominal pain and weight loss. One male patient was a drinker and the diagnosis in all 3 patients was confirmed at laparotomy. The pathological examination in two cases confirmed cystic dystrophy of duodenal wall associated with chronic pancreatitis in one case and autoimmune pancreatitis and pancreatic carcinoma in the remaining one.

Case 1

A 65-year-old female was admitted to our department in April 2009 for persistent abdominal discomfort and progressive weight loss (about 5 kg in two months). Before this admission, she had had a one-year history of recurrent epigastric pain; an ultrasonographic (US) examination showed gallstones and the patient had been cholecystectomized in another hospital. After surgery, she continued to have recurrent and frequent episodes of epigastric pain; US showed a dilation of the CBD and, two months after surgery, she underwent an endoscopic sphincterotomy. One month after this procedure, epigastric pain reappeared and, due to the presence of scleral jaundice (total bilirubin 3.2 mg/dL), the patient underwent another endoscopic retrograde cholangiopancreatography (ERCP). The papilla of Vater was substenotic and another sphincterotomy was carried out without any clinical improvement. On admission to our department, physical examination was unremarkable as was a routine blood examination; her body temperature was 37.2  °C, her arterial pressure was 110/60 mmHg and her cardiac rate was 73 bpm. Contrast-enhanced multidetector computer tomography (MDCT) was carried out. This examination showed the presence of multiple hypodense lesions in the liver (Figure 2); a US fine needle biopsy of one of these lesions was carried out and the pathological specimen was compatible with an abscess; the liver tissue was also cultured and the patient was treated with a specific antibiotic. At computer tomography (CT) examination, there was the presence of biliary sludge and a dilation of the left intrahepatic biliary tree. There was also the presence of duodenal bulging (Figure 3A) while the pancreatic gland was normal (Figure 3B). An endoscopic US (EUS) was finally carried out. It confirmed the presence of duodenal bulging (Figure 4A) and showed CBD sludge; in addition, cysts in the duodenal wall were seen (Figure 4B) and a diagnosis of cystic dystrophy of duodenal wall was made. The patient refused surgery, and conservative treatment with ursodeoxycholic acid was carried out. Twenty months after discharge, the patient was free of abdominal discomfort and regained her lost weight.

Figure 2
Figure 2 Case No. 1 computer tomography liver evaluation. Liver multiple hypodense lesions compatible with abscesses.
Figure 3
Figure 3 Case No. 1 computer tomography duodenal and pancreatic gland evaluation. A: Presence of duodenal bulging; B: Normal appearance of the pancreatic gland.
Figure 4
Figure 4 Case No. 1 computer tomography duodenal and pancreatic gland evaluation. A: Presence of duodenal bulging; B: Presence of cysts in the duodenal wall.
Case 2

A 49-year-old male patient with a history of chronic alcoholic consumption (about 40 g of pure alcohol intake per day) was admitted to our Department in May 2010 with persistent epigastric pain of seven months duration associated with nausea and biliary vomiting; there was also weight loss of 13 kg. The following biochemical tests were carried out: Hb 11.9 g/dL, MCV 85.8; amylase 156 U/L (upper reference value 100), CA 19-9: 52 U/mL (upper reference value 37). The patient underwent an upper gastrointestinal endoscopy which was normal. Ultrasonographic examination did not show alterations of the abdominal parenchyma. MDCT showed an enlarged pancreatic head and the presence of multiple cysts between the enlarged pancreatic head and the duodenum (Figure 5A); the remaining pancreas was normal as was demonstrated by magnetic resonance imaging (MRI) (Figure 5B). The patient was operated on and a pancreatic head resection was performed. The pathology of the resected specimen showed cystic dystrophy of the duodenal wall with hypertrophy of the Brunner glands and the presence of an ectopic pancreas (Figure 6A), showing chronic pancreatitis (Figure 6B). Seven months after surgery, the patient was symptom free and in good general health.

Figure 5
Figure 5 Case No. 2 computer tomography duodenal and pancreatic gland evaluation. A: Enlarged pancreatic head and the presence of multiple cysts between the enlarged pancreatic head and the duodenum (multidetector computer tomography); B: The remaining pancreas was normal as demonstrated by the magnetic resonance imaging.
Figure 6
Figure 6 Case No. 2 pancreatic and duodenal surgical specimens. A: Resected specimen showing cystic dystrophy of the duodenal wall with hypertrophy of the Brunner glands and the presence of an ectopic pancreas (arrows); B: Chronic pancreatitis in the remaining pancreas together with cystic dystrophy of the duodenal wall.
Case 3

A 56-year-old male affected by Crohn’s disease was seen in August 2010 with persistent epigastric pain of one month duration associated with jaundice, weight loss, nausea and intermittent vomiting. The patient was not an alcohol drinker. The following biochemical tests were carried out: total bilirubin, 25.4 mg/dL, AST, 63 U/L (upper normal limit 38), ALT, 66 U/L (upper normal limit 40), alkaline phosphatases, 1105 U/L (normal value 98-280), amylase, 108 U/L (upper normal limit 100), lipase, 293 U/L (upper normal limit 60), CA, 19-9 2345 U/mL (upper reference value 37). The patient underwent US which showed a dilated CBD and a mass of 2.5 cm in the head of the pancreas. The MDCT showed the pancreatic head focally enlarged with a 2.5 cm heterogeneous area extending to and involving the wall of the posterior bulbar duodenum. The main pancreatic duct was uniformly dilated in caliber and appearance with no changes in the pancreatic body or tail. The patient underwent a pancreaticoduodenectomy and surgical pathology showed the presence of cystic dystrophy of the duodenal wall (Figure 7A) with aspects of chronic pancreatitis in the heterotopic pancreas (Figure 7A), aspects of autoimmune pancreatitis (Figure 7B) and, finally, groove adenocarcinoma extending to the pancreatic head (Figure 7C). At present, the patient is still alive and is in adjuvant chemotherapy with gemcitabine.

Figure 7
Figure 7 Case No. 3 pancreatic and duodenal pathological specimens. A: Cystic dystrophy of the duodenal wall with aspects of chronic pancreatitis in the heterotopic pancreas; B: Aspects of autoimmune pancreatitis (arrow); C: Groove adenocarcinoma extending to the pancreatic head (arrow).
CLINICAL CONSIDERATIONS AND AIMS

The present report involving three cases of cystic dystrophy of the duodenal wall represents one of the few case series published concerning this rare entity. All of our patients presented with symptoms consistent with chronic pancreatitis; however, pancreatic diseases were found in two and these two patients improved dramatically after surgical head pancreatic resection while one is symptom free after medical treatment. It is important to diagnose the pathological involvement of the proximal duodenum in order to detect the presence of malignancy and to evaluate the prognosis of these subjects. In order to better establish the features of this rare entity we also undertook a systematic review of the literature.

LITERATURE SEARCH AND DATA EXTRACTION

A search was carried out on December 18, 2010 using the MEDLINE/PubMed database (United States National Library of Medicine National Institutes of Health) in order to select the data existing in the literature under the headings of pancreatitis and groove pancreatitis. The terms used were “groove pancreatitis” or “duodenal cystic dystrophy” (explanatory variables) and “pancreatic diseases” (outcome variable). The search was limited to human studies written in English. We identified additional studies by means of a hand search of the bibliographies from the primary studies, review articles and key journals. A total of 70 citations were found in MEDLINE/PubMed[4-73]. Four investigators (Pezzilli R, Morselli-Labate AM, Fabbri D, and Imbrogno A) independently screened all articles for those meeting the broad inclusion criteria. Of the 70 papers, 4 were excluded because they contained data regarding diseases other than those searched for[8,15,48,71]. Of the remaining 66 papers, 10 were excluded because they were review articles not containing data useful for the analyses[4,5,24,41,42,45,56,58,60,68] and one because it was a comment on an article[19] without new data/cases; therefore, 55 papers with available data remained. Of these 55 papers, 4 were also excluded for the following reasons: 1 because it was a duplicated publication[55] and 3 because it was not possible to extract useful data[49,57,73]. Eight papers were added to these 51 papers because they were extracted from the references[74-81]. Thus, 59 papers were considered for the present study; there were 19 cohort studies[6,7,10-13,16,18,23,30,36,37,39,40,46,47,52,63,81] and 40 case reports[9,14,17,20-22,25-29,31-35,38,43,44,50,51,53,54,59,61,62,64-67,69,70,72,74-80].

For each study, the following information was recorded: gender, mean age for the cohort studies or age of the subjects studied in the case reports, interval time from the appearance of the symptoms to diagnosis, alcoholism, the presence of clinical variables (such as abdominal pain, weight loss and jaundice, hyperamylasemia, CBD stenosis, duodenal stenosis), the need for surgery and the type of surgery, the possible presence of chronic pancreatitis in the pancreas together with cystic dystrophy as well as the presence of pseudocysts, the possible presence of pancreatic neoplasms, the time of follow-up and death.

Data are presented as absolute numbers and relative frequencies, mean ± SD, medians, ranges, and interquartile ranges (IQR); follow-up data are also presented as crude survival.

EVALUATION OF THE SELECTED STUDIES

Due to the low frequency of diseases, such as groove pancreatitis and groove carcinomas, there is a limited number of cohort studies (No. 19) and a large number of case reports (No. 40). All the cohort studies were retrospective and patients were enrolled from 1959[11] to 2008[6]. Thus, the changes in diagnostic techniques with the appearance of MRI and EUS in clinical practice render the studies not comparable as to what is the best technique for diagnosing groove diseases. Furthermore, the mean follow-ups vary greatly and the longest follow-up is about 8 years which is that reported by Casetti et al[63]. As shown in Tables 1, 2, 3, 4, 5, 6, 7 and 8, we found no substantial differences between the data reported in the cohort studies and those we calculated when grouping the series of case reports by gender, age at diagnosis, alcoholism, presence of pain, weight loss, jaundice, hyperamylasemia, CBD stenosis, duodenal stenosis and the need for surgery. The presence of chronic pancreatitis and deaths were more frequently reported in the cohort studies than in the case reports while associated adenocarcinoma and pseudocysts were more frequently reported in the case reports than in the cohort studies.

Table 1 Epidemiological and clinical characteristics of patients in the 18 retrospective studies involving patients with a benign cystic duodenal wall.
Author[Ref.] yrTime interval ofn (%)Age (yr)Alcohol drinkers
patient enrollmentTotalMalesFemalesMean (range)n (%)
Stolte et al[7] 1982NR3030 (100)-41.3 (NR)22 (73.3)
Yamaguchi et al[10] 19921983-198988 (100)-58.0 (33-70)4 (50.0)
Fléjou et al[11] 19931959-19911010 (100)-41.0 (31-56)2 (20.0)
Itoh et al[12] 1994NR43 (75.0)1 (25.0)43.0 (37-53)NR
Fékété et al[13] 19961989-199366 (100)-40.0 (35-46)4 (66.7)
Procacci et al[16] 19971992-19961010 (100)-41.0 (32-59)9 (90.0)
Irie et al[18] 19981995-199655 (100)-41.0 (33-46)2 (40.0)
Vullierme et al[23] 20001988-19982018 (90.0)2 (10.0)44.0 (36-56)NR
Aoun et al[81] 2005NR42 (50.0)2 (50.0)69.0 (66-71)NR
Pessaux et al[36] 20061990-20041211 (91.7)1 (8.3)42.4 (34-54)9 (75.0)
Jouannaud et al[37] 20061990-20022320 (87.0)3 (13.0)45.0 (30-66)23 (100)
Tison et al[39] 20071983-200198 (88.9)1 (11.1)48.0 (37-63)8 (88.9)
Rebours et al[40] 20071995-200410596 (91.4)9 (8.6)46.0 (24-75)86 (81.9)
Rahman et al[46] 20072000-20051110 (90.9)1 (9.1)48.0 (35-61)10 (90.9)
Castell-Monsalve et al[47] 2008NR54 (80.0)1 (20.0)47.0 (40-53)4 (80.0)
Jovanovic et al[52] 20081996-20061310 (76.9)3 (23.1)41.5 (17-60)6 (6.2)
Casetti et al[63] 20091990-20065854 (93.1)4 (6.9)44.7 (IQR 36.8-51.8)57 (98.3)
Ishigami et al[6] 20102001-20081514 (93.3)1 (6.7)48.0 (31-64)NR
Overall-348319 (91.70)29 (8.30)-246/305 (80.70)
Table 2 Epidemiological and clinical characteristics of patients in the 18 retrospective studies involving patients with a benign cystic duodenal wall (continues from Table 1) n (%).
Author[Ref.] yrTime interval from the symptoms to the diagnosisAbdominal painWeight lossJaundiceHyperamylasemia
Mean (range)No. of casesType
Stolte et al[7] 1982NRNRNR30 (100)NRNR
Yamaguchi et al[10] 1992NR3 (37.5)NR02 (25.0)NR
Fléjou et al[11] 1993NR7 (70.0)Persistent9 (90.0)4 (40.0)NR
Itoh et al[12] 1994NR3 (75.0)NRNRNR3 (75.0)
Fékété et al[13] 1996NR6 (100)Recurrent6 (100)06 (100)
Procacci et al[16] 19974.5 yr (1-9)10 (100)Recurrent4 (40.0)1 (10.0)NR
Irie et al[18] 1998NR4 (80.0)NR00NR
Vullierme et al[23] 200041.5 d (1-140)NRNRNRNRNR
Aoun et al[81] 2005NR3 (75.0)NR01 (25.0)NR
Pessaux et al[36] 2006NR9 (75.0)Persistent in 4 (44.4)12 (100)2 (16.7)NR
Jouannaud et al[37] 2006NR22 (95.7)NR16 (69.6)0NR
Tison et al[39] 2007NR9 (100)NR9 (100)2 (22.2)NR
Rebours et al[40] 20071 yr (0-24)91 (86.7)Continuous in 35 (38.4); occasional in 56 (61.5)73 (69.6)13 (12.4)NR
Rahman et al[46] 2007NR11 (100)Recurrent in 8 (72.7)10 (90.9)02 (18.2)
Castell-Monsalve et al[47] 2008NR5 (100)PersistentNRNR5 (100)
Jovanovic et al[52] 20087.5 mo (0.5-36)12 (92.3)NR4 (30.8)4 (30.8)NR
Casetti et al[63] 2009NR46 (79.3)PersistentNR3 (5.2)NR
Ishigami et al[6] 2010NRNRNRNRNRNR
Overall-241/283-173/24632/27416/26
(85.20)(70.30)(11.70)(61.50)
Table 3 Epidemiological and clinical characteristics of patients in the 18 retrospective studies involving patients with a benign cystic duodenal wall (continues from Table 2) n (%).
Author[Ref.] yrImagingDuodenal findingsCBD stenosisDuodenal stenosis
Stolte et al[7] 1982NRBrunner hyperplasia in 2515 (50.0)NR
Yamaguchi et al[10] 1992US, CT, ERCP, PTCEdema and nodular appearance; Brunner hyperplasia4 (50.0)5 (62.5)
Fléjou et al[11] 1993ERCP, EUSEdema and congestion of the mucosa07 (70.0)
Itoh et al[12] 1994CTNRNRNR
Fékété et al[13] 1996CT, ERCP, EUSEdema and congestion of the mucosa05 (83.3)
Procacci et al[16] 1997CT, ERCP, EUSInflammation in 82 (20.0)2 (20.0)
Irie et al[18] 1998MRIBrunner hyperplasia in 32 (40.0)3 (60.0)
Vullierme et al[23] 2000CTNR3 (15.0)20 (100)
Aoun et al[81] 2005US, CT, ERCP, EUSNR4 (100)NR
Pessaux et al[36] 2006US, EUS, CT, ERCP, MRINRNRNR
Jouannaud et al[37] 2006EUS, CTInflammation in 3NR8 (34.8)
Tison et al[39] 2007US, CT, MRI, angiographyNon specific inflammation in 95 (55.6)9 (100)
Rebours et al[40] 2007CT, EUSBrunner hyperplasia in 6126 (24.8)50 (47.6)
Rahman et al[46] 2007CT, MRI, EUSBrunner hyperplasia05 (45.5)
Castell-Monsalve et al[47] 2008MRI, EUSDuodenal stenosis in 33 (60.0)3 (60.0)
Jovanovic et al[52] 2008US, CT, MRI, EUSNR6 (46.2)NR
Casetti et al[63] 2009US, CT, MRI, EUSNR3 (5.2)NR
Ishigami et al[6] 2010CT, MRINR9 (60.0)NR
Overall--82/309117/212
(26.50)(55.20)
Table 4 Epidemiological and clinical characteristics of patients in the 18 retrospective studies involving patients with a benign cystic duodenal wall (continues from Table 3) n (%).
Author[Ref.] yrSurgeryAssociated chronic pancreatitisAssociated neoplasmsPseudocystFollow-up
No. of casesTypeMean (range)DeathLost
Stolte et al[7] 198230 (100)PD4 (13.3) (all with calcification)No5 (16.7)NRNRNR
Yamaguchi et al[10] 19928 (100)PDNRNoNo2 yr1 (12.5)NR
Fléjou et al[11] 199310 (100)WP in 8;0NoNo1-5 yr1 (10.0)4 (40.0)
derivative in 2
Itoh et al[12] 19943 (75.0)PDNRNoNoNoNRNR
Fékété et al[13] 19966 (100)PD in 5;NRNoNo32 mo (18-64)NoNR
antrectomy in 1
Procacci et al[16] 199710 (100)PD7 (70.0) (calcifications in 5)No5 (head) (50.0)NRNRNR
Irie et al[18] 19983 (60.0)PD2 (40.0) (all with calcifications)NoNoNRNRNR
Vullierme et al[23] 200020 (100)PD9 (45.0)(calcifications in 5)NoNoNRNRNR
Aoun et al[81] 20054 (100)PDNRNRNRNRNRNR
Pessaux et al[36] 200612 (100)PD8 (66.7) (calcification in 2)NoNo64 mo (6-158)1 (8.3)1 (8.3)
Jouannaud et al[37] 200614 (60.9)PD in 11;17 (73.9) (calcification in 10)NoNo47 mo1 (4.3)NR
derivative in 3
Tison et al[39] 20079 (100)PD5 (55.6)NoNo72 mo4 (44.4)NR
Rebours et al[40] 200729 (27.6)PD in 17; digestive and biliary by pass in 1297 (92.4) (calcification in 96)NoNo15 mo (0-243)NRNR
Rahman et al[46] 200711 (100)PD0NoNoNRNRNR
Castell-Monsalve et al[47] 20084 (80.0)WP in 3;3 (60.0)NoNoNR (13-36 mo)NoNR
1 laparotomy
Jovanovic et al[52] 200813 (100)PD6 (46.2)NoNoNRNRNR
Casetti et al[63] 200958 (100)PDNRNeuroendocrine in 1No93.6 moNRNR
(IQR 59.7-129.7)
Ishigami et al[6] 20106 (40.0)PD in 3, derivative surgery in 3NRNRNRNRNRNR
Overall250/348-158/2531/32910/329-8/735/22
(71.8)(62.5)(0.3%)(3.0)(11.0)(22.7)
Table 5 Epidemiological and clinical characteristics of patients in the 38 case report papers involving 46 subjects with a benign cystic duodenal wall (a paper may report more than one patient), the three cases reported in the present paper are also shown.
Author[Ref.] yrGenderAge (yr)Alcohol drinker
Bill et al[74] 1982Male64Yes
Holstege et al[75] 1985Male44Yes
Tio et al[9] 1991Male48NR
Tio et al[9] 1991Male53NR
Flaherty et al[75] 1992Female20 moNo
Izbicki et al[77] 1994Male25NR
Fujita et al[14] 1997Male42Yes
Shudo et al[17] 1998Male66Yes
Wu et al[78] 1998Male39NR
Babál et al[79] 1998Female70NR
Rubay et al[21] 1999Male46Yes
Balachandar et al[22] 1999Male18NR
Mohl et al[25] 2001Male44Yes
Mohl et al[25] 2001Male42Yes
Munthali Lovemore et al[26] 2001Male24No
Indinnimeo et al [27] 2001Male46Yes
Shudo et al[28] 2002Male53Yes
Glaser et al[29] 2002Male51Yes
Hwang et al[31] 2003Male46Yes
Jovanovic et al[32] 2004Male38No
McFaul et al[80] 2004Male29Yes
McFaul et al[80] 2004Male62Yes
Isayama et al[33] 2005Male56Yes
Chatelain et al[34] 2005Male47Yes
Chatelain et al[34] 2005Female44Yes
Balzan et al[35] 2005Male47NR
Sanada et al[43] 2007Male81No
Balakrishnan et al[44] 2007Male40Yes
de Tejada et al[50] 2008Male47Yes
Stefanescu et al[51] 2008Male15No
Varma et al[53] 2008Female23NR
Galloro et al[54] 2008Male44Yes
Thomas et al[59] 2009Male43NR
Levenick et al[61] 2009Female35Yes
Levenick et al[61] 2009Male47Yes
Levenick et al[61] 2009Female36Yes
Levenick et al[61] 2009Female54NR
Yoshida et al[62] 2009Male63Yes
Meesiri[64] 2009Male44Yes
Funamizu et al[65] 2009Female54NR
Viñolo Ubiña et al[66] 2010Male40Yes
Tezuka et al[67] 2010Male55Yes
Lee et al[69] 2010Male75NR
Egorov et al[70] 2010Male32Yes
Egorov et al[70] 2010Male43NR
German et al[72] 2010Male34Yes
Pezzilli2011 Present paperFemale65No
Pezzilli 2011 Present paperMale49Yes
Pezzilli 2011 Present paperMale56No
OverallMales: 40 (81.6%)45.3 ± 15.229/36
Females: 9 (18.4%)(80.50%)
Table 6 Epidemiological and clinical characteristics of patients in the 38 case report papers involving 46 subjects with a benign cystic duodenal wall (a paper may report more than one patient), the three cases reported in the present paper are also shown (continues from Table 5).
Author[Ref.] yrTime interval from the onset of symptoms to diagnosisAbdominal painWeight lossJaundiceHyperamylasemia
Bill et al[74] 1982NRYes (Persistent)YesNoNo
Holstege et al[75] 19856 moYes (Persistent)YesNoYes
Tio et al[9] 1991NRYes (NR)NoNoNR
Tio et al[9] 1991NRYes (NR)NoYesNR
Flaherty et al[75] 1992NRYes (NR)NoNoNR
Izbicki et al[77] 1994NRYes (Recurrent)NoNoNo
Fujita et al[14] 1997NRYes (Recurrent)YesNoNo
Shudo et al[17] 1998NRYes (Persistent)NoNoYes
Wu et al[78] 199810 yrYes (Recurrent)YesNoNR
Babál et al[79] 1998NRNoNoNoNR
Rubay et al[21] 19997 yrYes (Recurrent)YesNoYes
Balachandar et al[22] 1999NRNoNoYesNo
Mohl et al[25] 20011 yrYes (Recurrent)YesNoNR
Mohl et al[25] 20011 yrYes (Persistent)YesNoNR
Munthali Lovemore et al[26] 2001NRYes (Persistent)NRYesYes
Indinnimeo et al[27] 200110 yrYes (Recurrent)NoNoYes
Shudo et al[28] 2002NRYes (Persistent)NoNoYes
Glaser et al[29] 2002NRYes (Persistent)YesNoNo
Hwang et al[31] 2003NRYes (Persistent)YesNoYes
Jovanovic et al[32] 2004NRYes (Persistent)YesNoYes
McFaul et al[80] 200413 moYes (Recurrent)YesNoNR
McFaul et al[80] 20042 yrYes (Recurrent)YesYesNR
Isayama et al[33] 20052 yrYes (Persistent)YesNoNo
Chatelain et al[34] 20051 yrYes (Recurrent)YesNoNo
Chatelain et al[34] 2005NRYes (Persistent)YesNoNo
Balzan et al[35] 20052 yrYes (Persistent)NoNoYes
Sanada et al[43] 2007NRYes (Persistent)NoNoYes
Balakrishnan et al[44] 2007NRYes (Persistent)YesNoYes
de Tejada et al[50] 20082 moYes (Persistent)YesNoNR
Stefanescu et al[51] 20085 moYes (Persistent)YesNoNR
Varma et al[53] 20083 moYes (Persistent)YesNoNR
Galloro et al[54] 2008NRYes (Recurrent)YesNoYes
Thomas et al[59] 2009NRYes (NR)YesNoNR
Levenick et al[61] 2009NRYes (Recurrent)NRNoNR
Levenick et al[61] 2009NRYes (Recurrent)YesNoNR
Levenick et al[61] 2009NRYes (Recurrent)YesNoNR
Levenick et al[61] 2009NRNoYesNoNR
Yoshida et al[62] 2009NRYes (Persistent)NoNoYes
Meesiri[64] 2009NRYes (Recurrent)NoNoYes
Funamizu et al[65] 2009NRYes (Persistent)NoYesYes
Viñolo Ubiña et al[66] 20103 moYes (Persistent)NoNoYes
Tezuka et al[67] 2010NRYes (NR)NoNoYes
Lee et al[69] 2010NRYes (Recurrent)NoNoYes
Egorov et al[70] 20102 moYes (Persistent)YesNoYes
Egorov et al[70] 20101 yrYes (Persistent)YesYesNo
German et al[72] 2010NRYes (Recurrent)YesNoYes
Pezzilli 2011 Present paper1 yrYes (Recurrent)YesYesNo
Pezzilli 2011 Present paper7 moYes (Persistent)YesNoYes
Pezzilli 2011 Present paper1 moYes (Persistent)YesYesYes
Overall2.1 ± 3.1 yr46/4930/478/4922/33
(93.90%)(63.80%)(16.30%)(66.70%)
Table 7 Epidemiological and clinical characteristics of patients in the 38 case report papers involving 46 subjects with a benign cystic duodenal wall (a paper may report more than one patient), the three cases reported in the present paper are also shown (continues from Table 6).
Author[Ref.] yrImagingDuodenal findingsCBD stenosisDuodenal stenosis
Bill et al[74] 1982US, ERCP, angiographyNRYesNo
Holstege et al[75] 1985US, CT, ERCPSevere erosive gastritis + bulging of the duodenumNoYes
Tio et al[9] 1991ERCP, EUS, USPolypoid lesionYesYes
Tio et al[9] 1991ERCP, EUS, USNRNoYes
Flaherty et al[75] 1992USNoNoNo
Izbicki et al[77] 1994US, angiography, ERCPNRYesYes
Fujita et al[14] 1997US, CT, ERCPInflammationNoYes
Shudo et al[17] 1998CT, US, ERCP, EUS, celiac angiographyEdema duodenal wall, Brunner hyperplasiaNoYes
Wu et al[78] 1998CTNRNoNo
Babál et al[79] 1998NRNRNoNo
Rubay et al[21] 1999CT, ERCP, MRI, EUSNo alterationsNRYes
Balachandar et al[22] 1999CT, ERCPNo duodenal alterationYesNo
Mohl et al[25] 2001CTStenosisNoYes
Mohl et al[25] 2001US, CT, ERCPNormal duodenal mucosaNoNo
Munthali Lovemore et al[26] 2001US, CT, ERCPNRYesNo
Indinnimeo et al[27] 2001CT, MRI, EUSNo alterationsNoNo
Shudo et al[28] 2002CT, US, ERCP, EUS, celiac angiographyIrregular polypoid bulging; inflammation of the mucosaNRYes
Glaser et al[29] 2002USSevere deformation + inflammatory changesNoYes
Hwang et al[31] 2003US, CT, MRIDuodenal inflammation, duodenal stenosisNRYes
Jovanovic et al[32] 2004US, CT, EUS, MRIStenosisNoYes
McFaul et al[80] 2004US, CT, MRIBrunner hyperplasiaYesYes
McFaul et al[80] 2004US, PET-CTBrunner hyperplasiaNoNo
Isayama et al[33] 2005CT, EUS, MRCP, ERCPNRNoYes
Chatelain et al[34] 2005EUS, CTDuodenal stenosis, inflammationNoYes
Chatelain et al[34] 2005EUS, CTDuodenal stenosisNoYes
Balzan et al[35] 2005US, MRI, CTNRNRNR
Sanada et al[43] 2007CT, ERCPEdema duodenal wall, Brunner hyperplasiaYesNo
Balakrishnan et al[44] 2007CT, ERCP, EUSEdematous, shiny, reddish raise mucosa with polypoid appearance; Brunner hyperplasiaNoNo
de Tejada et al[50] 2008MRI, EUSBulging, Brunner hyperplasiaNoNo
Stefanescu et al[51] 2008CT, EUSNRNoYes
Varma et al[53] 2008US, CTBrunner hyperplasiaNoNo
Galloro et al[54] 2008US, CT, EUSDuodenal stenosisNoYes
Thomas et al[59] 2009US, CT, EUS, octreotide scanBrunner hyperplasiaNoYes
Levenick et al[61] 2009EUS, MRCPDuodenal stenosisNoYes
Levenick et al[61] 2009CT, EUSDuodenal inflammation, duodenal stenosisNRYes
Levenick et al[61] 2009CT, EUSEdema with acute and chronic inflammationNoYes
Levenick et al[61] 2009CT, EUS, ERCPNRYesNo
Yoshida et al[62] 2009CT, MRCPNormal mucosaNoYes
Meesiri[64] 2009US, CT, MRIEdema and hemorrhagic mucosa with inflammationNRNo
Funamizu et al[65] 2009ERCP, CT, angiographyNRYesNo
Viñolo Ubiñaet al[66] 2010CTStenosisNRYes
Tezuka et al[67] 2010CT, ERCPEdema duodenal wallNoYes
Lee et al[69] 2010CT, MRCPActive ulcerYesNo
Egorov et al[70] 2010US, CT, EUSDeformation, infiltration and ulcer; InflammationNoYes
Egorov et al[70] 2010US, CT, MRI, EUSNRYesYes
German et al[72] 2010US, CT, MRIEdema duodenal wall; Brunner hyperplasiaYesYes
Pezzilli 2011 Present paperUS, CT, EUS, ERCPNoYesNo
Pezzilli 2011 Present paperUS, CT, MRIHypertrophy of the Brunner glandsNoNo
Pezzilli 2011 Present paperUS, CTNoYesNo
Overall--14/4228/48
(33.30%)(58.30%)
Table 8 Epidemiological and clinical characteristics of patients in the 38 case report papers involving 46 subjects with a benign cystic duodenal wall (a paper may report more than one patient), The three cases reported in the present paper are also shown (continues from Table 7).
Author[Ref.] yrSurgeryType of surgeryEndoscopic treatmentAssociated chronic pancreatitisAssociated neoplasmsPseudocystFollow-upDeath
Bill et al[74] 1982YesPDNoNRNoNoNoNR
Holstege et al[75] 1985YesWPNoNoNoNoNoNR
Tio et al[9] 1991NoNoNoNoNo7 yrNo
Tio et al[9] 1991YesDerivative surgeryNoNoNoNo6 moNR
Flaherty et al[75] 1992YesPDNoNoNoNo9 moNo
Izbicki et al[77] 1994YesPDNoNoNoNo6 yrNo
Fujita et al[14] 1997YesPDNoNoNoNo3 yrNo
Shudo et al[17] 1998YesPDNoNoNoNoNRNR
Wu et al[78] 1998YesWPNoNoNoNo9 moNo
Babál et al[79] 1998NoNoNoNoNoNRDuring hospitalization
Rubay et al[21] 1999YesPDNoNoNoNo2 moNo
Balachandar et al[22] 1999YesDerivativeNoYesNoNoNRNR
Mohl et al[25] 2001YesPDNoNoNoNoNoNR
Mohl et al[25] 2001YesPDNoNoNoNo4 wk after surgeryNo
Munthali Lovemore et al[26] 2001YesDerivative CBDNoNoNoNoNoNR
Indinnimeo et al[27] 2001YesPDNoNoNoNo2 yrNo
Shudo et al[28] 2002YesPDNoNoNoNoNRNR
Glaser et al[29] 2002NoNoNoNoNoNoNR
Hwang et al[31] 2003NoNoNoNoNoNRNR
Jovanovic et al[32] 2004YesPDNoNoNoNoNoNR
McFaul et al[80] 2004YesPDNoYesNoNo2 yrNo
McFaul et al[80] 2004YesWPNoYesNoNoNRNo
Isayama et al[33] 2005NoYesNoNoNo12 moNo
Chatelain et al[34] 2005YesPDNoNoNoNo6 moNo
Chatelain et al[34] 2005YesPDNoNoNoNo12 moNo
Balzan et al[35] 2005YesPDNoYesNoYes (head)NoNR
Sanada et al[43] 2007YesPDNoNoNoYes (head)NoNR
Balakrishnan et al[44] 2007YesLaparotomyNoYesNoNoNRNR
de Tejada et al[50] 2008YesWPNoNoNoNo3 moNo
Stefanescu et al[51] 2008YesDerivativeNoNoNoNo8 moNo
Varma et al[53] 2008YesWPNoNoNoNo9 moNo
Galloro et al[54] 2008YesWPNoYesCystadenomaYes14 moNo
(with calcifications)
Thomas et al[59] 2009YesPDNoNoNoNoNRNR
Levenick et al[61] 2009YesPDNoNoNoNo3 yrNo
Levenick et al[61] 2009YesPDNoYesNoNoNRNR
Levenick et al[61] 2009YesPDNoNoNoNoNRNR
Levenick et al[61] 2009YesPDNoNoNoNoNRNR
Yoshida et al[62] 2009YesPDNoNoNoNoYes (time NR)No
Meesiri[64] 2009NoNoNoNoNoYes (time NR)No
Funamizu et al[65] 2009YesPDNoNoYesNo15 moNo
Viñolo Ubiña et al[66] 2010YesPDNoNoNoNoNRNo
Tezuka et al[67] 2010YesPDNoNoNoNoNRNo
Lee et al[69] 2010NoNoNoNoNoNRNR
Egorov et al[70] 2010YesPancreas-preserving duodenal resectionNoNoNoNo6 moNo
Egorov et al[70] 2010YesPancreas-preserving duodenal resectionNoNoNoNo5 moNo
German et al[72] 2010YesPDNoNoNoNo2 moNR
Pezzilli 2011 Present paperNoYesNoNoNo20 moNo
Pezzilli 2011 Present paperYesPDNoNoNoNo7 moNo
Pezzilli 2011 Present paperYesPDNoAutoimmune pancreatitisYesNo4 moNo
Overall41/49-2/498/483/493/4917.9 ± 20.6 mo1/28
(83.70%)(4.10%)(16.70%)(6.10%)(6.10%)(3.60%)
Figure 8
Figure 8 New surgical option for patients having cystic dystrophy of duodenal wall. A: Scheme of the pancreas-preserving resection of the second portion of the duodenum. The second part of the duodenum, including the main papilla, is removed and the segment of the proximal jejunum supplied by the artery and vein is cut out and prepared for transposition between the 1st and 3rd portions of the duodenum; B: The shifted segment is interposed between the 1st and the 3rd parts of the duodenum. Jejuno-jejuno- and duodeno-jejuno-anastomoses are performed. The bile and the pancreatic ducts were implanted in the neodudenum 4 cm below the proximal duodeno-jejuno-anastomosis (from Egorov et al[70] with the kind permission of the authors).
EPIDEMIOLOGY

We have no epidemiological data regarding the prevalence and incidence of cystic dystrophy of the duodenal wall in the general population. The data regarding this anomaly mainly describes patients with associated chronic pancreatitis. A recent Italian survey which reviewed the data on chronic pancreatitis in Italy in mixed medical/surgical cases from 2000 to 2005[57] reported that the frequency of groove pancreatitis was 6.2% (55 out of 893 patients) with a higher frequency in males (7.6%, 50/660) than in females (2.1%, 5/233). In a surgical setting, groove pancreatitis ranges from 2.7% to 24.5%[4,7,10,63]; in these cases, the frequency in males is also higher than that in females. We have no epidemiological data regarding groove carcinomas or biliary involvement without pancreatitis or pancreatic adenocarcinoma. In all these studies, the patients having groove pancreatitis were middle aged (about 45 years of age), having a wide range from 20 mo[76] to 75 years of age[40]. Only two of the patients described were children (a 20-mo-old girl and a 15-year-old boy)[51,76]. Mean age was significantly higher in patients having groove carcinoma than in those having groove pancreatitis, namely 70 years of age (range 57 to 80 years)[51].

CLINICAL AND BIOCHEMICAL FEATURES

As shown in Tables 1-8, the main symptoms of cystic dystrophy of the duodenal wall were epigastric pain, weight loss and jaundice. These symptoms were similar in those patients having associated chronic groove pancreatitis and in those patients having groove carcinoma. All these symptoms can be present, further complicating the differential diagnosis with ampullary and periampullary cancers. Pain may be persistent or recurrent, and nausea and vomiting are usually present as accompanying symptoms. The majority of these patients are heavy alcohol drinkers (275/341, 80.6%), and this may explain the fact that most of the patients with groove pancreatitis are males. In addition, in the 18 patients with groove adenocarcinoma, the majority of cases were males (11/18, 61.1%) (Tables 9, 10, 11 and 12).

Table 9 Epidemiological and clinical characteristics of patients in the two retrospective studies and two case report papers involving two subjects with groove adenocarcinoma.
Author[Ref.] yrType of studyTime interval of patient enrollmentNo. of patientsAge (yr)Alcohol drinkers
TotalMalesFemalesMean (range)
Suehara et al[20] 1998Case report199511-61Yes
Gabata et al[30] 2003Retrospective1998-200194 (44.4%)5 (55.6%)72 (56-87)NR
Tan et al[38] 2006Case reportNR1-169NR
Ishigami et al[6] 2010Retrospective2001-200876 (85.7%)1 (14.3%)70 (57-80)NR
Table 10 Epidemiological and clinical characteristics of patients in the two retrospective studies and two case report papers involving two subjects with groove adenocarcinoma (continues from Table 9).
Author[Ref.] yrAbdominal painWeight lossJaundiceHyperamylasemia
Suehara et al[20] 1998Yes (Persistent)NoYesYes
Gabata et al[30] 2003NRNRNRNR
Tan et al[38] 2006Yes (Persistent)YesYesYes
Ishigami et al[6] 2010NRNRNRNR
Table 11 Epidemiological and clinical characteristics of patients in the two retrospective studies and two case report papers involving two subjects with groove adenocarcinoma (continues from Table 10).
Author[Ref.] yrImagingDuodenal findingsCBD stenosisDuodenal stenosis
Suehara et al[20] 1998US, EUS, CT, MRI, angiographyNRYesNo
Gabata et al[30] 2003CT, RMI, ERCP, angiographyEdema with erosions9 (100%)9 (100%)
Tan et al[38] 2006US, MRI, ERCPNRYesNo
Ishigami et al[6] 2010CT, MRINR7 (100%)NR
Table 12 Epidemiological and clinical characteristics of patients in the two retrospective studies and two case report papers involving two subjects with groove adenocarcinoma (continues from Table 11).
Author[Ref.] yrSurgeryAssociated chronic pancreatitisPseudocystFollow-up
No. of casesType
Suehara et al[20] 1998YesPDNoNoNR
Gabata et al[30] 20039 (100%)PD in 7; derivative in 2NoNoNR
Tan et al[38] 2006YesBy-pass surgeryNoNoNR
Ishigami et al[6] 20106 (85.7%)PD in 5; derivative in 1NoNRNR

Regarding the laboratory examinations, serum amylase activity was usually abnormally high in these patients (38/59, 64.4%) (Tables 1-8), but the magnitude of this elevation varied greatly. An increase in bilirubin may have also been present, along with an increase in alkaline phosphatases in patients with jaundice. Finally, it has also been reported in the literature that tumor markers, such as serum CA 19-9, are usually within the normal limits[10,58].

ASSOCIATED DISEASES

The majority of patients with cystic dystrophy of the duodenal wall have been reported to have chronic groove pancreatitis or groove carcinoma. However, the lesions in the remaining pancreatic gland not affected by groove pancreatitis have not been fully evaluated. As shown in Tables 1-12, in patients with groove pancreatitis as well as in those with groove carcinoma, the pancreatic gland above the groove lesion is generally not affected by chronic pancreatitis. Chronic pancreatitis of the entire pancreas was reported in 166 of the 302 (55.1%) patients and there were pancreatic calcifications in 125 of these 166 patients (75.3%) (Tables 1-8). The presence of pancreatic pseudocysts was usually rare (13 out of 378, 3.4%) (Tables 1-8), and, in most cases, they were localized in the head of the pancreas (7/13, 53.8%). In addition, some authors have reported that groove pancreatitis is associated with the occasional findings of neuroendocrine tumors[63] or pancreatic cystadenoma[54].

IMAGING ASSESSMENT

As shown in Tables 3, 7, 8 and 11, the imaging diagnosis of dystrophy of the duodenal wall is rarely assessed using a single radiological modality. Even if US is the first line imaging modality in these patients, it is rarely diagnostic. ERCP, which was frequently used in the past, is feasible and in typical cases it demonstrates smooth tubular stenosis at the distal part of the CBD without abnormality of the main pancreatic duct or, occasionally, with only slight irregularities[44,65]. ERCP may also demonstrate irregularity, tapering obstruction or dilatation of the Santorini duct and its branches, sometimes with intraductal stones or protein plugs[44]. At present, ERCP is used mainly for endoscopic therapy[33]; in fact, successful treatment for groove pancreatitis by endoscopic drainage via the minor papilla was carried out in only one patient[33].

For many years, CT has been an excellent imaging modality for diagnosing chronic pancreatitis or adenocarcinoma associated with cystic dystrophy of the duodenal wall[6,16]. In the pure form of groove pancreatitis, it may be visualized as a poorly enhancing hypodense lesion between the pancreatic head and the duodenum, near the minor papilla, reflecting the pathological characteristics of the mass. The delayed enhancement is mainly due to delayed blood circulation caused by fibrous tissue proliferation and artery constriction[12]. In addition, CT may reveal the presence of duodenal stenosis with wall thickening and cystic lesions in the duodenal wall or in the groove area. The cysts may be tiny even if multilocular cystic lesions may be observed. The main pancreatic duct may be mildly dilated above the lesion while, in the pure form, paraduodenal pancreatitis can be expected. In groove pancreatitis and in groove carcinoma, the CBD may be stenosed in its distal part and a dilation of the extra- and intra-hepatic biliary system can be observed[6,16].

The same CT findings can also be observed when utilizing MRI which may reveal a mass between the head of the pancreas and the duodenum associated with duodenal wall thickening. The mass visualized in the groove and/or in the adjacent head of the gland is hypointense to the pancreatic parenchyma. Delayed enhancement may also be seen in the thickened duodenal wall. These imaging features reflect the fibrous involvement of the lesions of groove pancreatitis. Cysts, which may be present in the groove area and the duodenal wall, have high signal intensity. An important diagnostic aspect of MRI, which cannot be evaluated by CT, is the fact that MRI can be followed by magnetic resonance cholangiopancreatography (MRCP); this additional evaluation provides images similar to those of ERCP without the morbidity of this latter technique. In addition, MRCP may visualize those lesions which are not seen in ERCP in the case of serrated duodenal stenosis[18]. The diagnostic value of MRI is superior to CT in evaluating biliary ducts in paraduodenal pancreatitis as well as in groove carcinomas. The stricture, or narrowing of the CBD, may be better approached by using MRCP rather than CT and/or ERCP. The dilation of the space comprising the main pancreatic duct, the CBD and the duodenum is another sign which can be observed in patients with groove pancreatitis or groove carcinoma when using MRCP[47].

In the last few years, EUS has emerged as a useful technique for diagnosing pancreatic diseases because of the accurate evaluation of the biliopancreatic structures through the gastro-duodenal lumen without interference of the abdominal wall or other organs[82]. EUS can easily demonstrate the hypoechoic area between the duodenal wall and the pancreatic parenchyma, narrowing of the duodenal lumen and stenosis of the CBD and/or pancreatic duct in both groove pancreatitis and groove carcinomas[50]. Furthermore, the diagnosis can be confirmed by EUS-guided fine-needle aspiration of the mass visualized.

PATHOLOGY

Macroscopically, groove pancreatitis is associated with an absent or narrow Santorini duct or the presence of pancreas divisum[17], and the difficult outflow of pancreatic fluid may be hypothesized for lesions of the groove similar to those of chronic pancreatitis[17]. The duodenal wall contains dilated ducts, in the majority of cases with thickened secretions, pseudocystic changes as well as adjacent stromal reactions, foreign-body type giant cell reaction engulfing mucoprotein material and myofibroblastic proliferation. Brunner gland hyperplasia is usually present as is dense myoid stromal proliferation, with intervening rounded lobules of pancreatic acinar tissue. Fibrosis into the adjacent pancreas and soft tissue occurs, especially in the groove area which involves the CBD[5].

In groove carcinoma, the macroscopic pathology is similar to that of groove pancreatitis while the pancreatic tissue has the same histology as that of pancreatic adenocarcinoma[6,20,30,38].

TREATMENT

Conservative treatment is the main option in the acute phase of the disease, including analgesia and parenteral nutrition. In some patients, enteral nutrition is not always possible due to the presence of duodenal stenosis[17]. The main therapeutic option for these patients is a surgical approach in benign as well as in malignant diseases of the groove, as shown in Tables 1-12. The most frequent surgical approach is a pylorus-preserving pancreaticoduodenectomy or a Whipple procedure; in a limited number of patients, a gastrointestinal by-pass, with or without biliary by-pass, has been carried out. More recently, a new approach has been reported by Egorov et al[70]; these authors have described a new surgical approach carried out on two patients who were successfully treated by two modifications of a pancreas-preserving duodenal resection with reimplantation of the bile and pancreatic ducts into the neoduodenum (Figure 8). The authors have claimed that these two cases are a good example of a pancreas-preserving approach to duodenal dystrophy treatment and that the technique may be an alternative to the Whipple procedure in cases of mild changes of the orthotopic gland.

Only in a few cases was a medical approach carried out (see Case 1 of our three patients), mainly because the patients refused surgery, and also in one patient in whom successful treatment for groove pancreatitis was carried out by endoscopic drainage via the minor papilla[33].

THE FATE OF PATIENTS

The first important question arising from the studies analyzed is the extreme length of time necessary from the onset of the symptoms to reach a diagnosis in patients with groove pancreatitis: it varies from a few days to ten years (Tables 1-8). In one of the larger studies in this field, such as that of Rebours et al[40], the mean time from the appearance of the symptoms and the diagnosis is 1 year with a range of 0 to 24 mo. This long time period is similar to that previously reported in chronic pancreatitis[83]. In patients with groove adenocarcinoma, we have no information on time to diagnosis. The perioperative mortality rate seems to be negligible, the only death being reported by Babál et al[79]. In the only study reporting this information (Tables 1-8), the mortality rate was 8.9% (9/101) in the follow-up period in patients with benign disease. However, this information should be taken with caution because, as previously stated, the follow-up period is not quite as long in the majority of studies.

CONCLUSION

The diagnosis of cystic dystrophy of the duodenal wall can be easily assessed by MDCT, MRI and EUS. These latter two techniques may also add more information on the involvement of the part of the pancreatic gland not involved in the duodenal malformation.

Chronic pancreatitis involving the entire pancreatic gland is present in half the patients with cystic dystrophy of the duodenal wall, and the pancreatitis has calcifications in the majority of them. We have no information about exocrine function in these patients and this topic requires additional study. In subjects without pancreatitis, the patients with cystic dystrophy of the duodenal wall are usually in satisfactory general condition after surgical treatment and they regain weight after surgery.

The fact that only two children have been reported to have cystic dystrophy of the duodenal wall confirms the hypothesis that pancreatic and biliary diseases develop over a long period of time.

ACKNOWLEDGMENTS

The authors wish to thank Mr. Paolo Bassi of the Surgical Department, Dr. Maurizio Zani and Dr. Maurizio Iorio of the University of Bologna Clinical Library at Sant’Orsola-Malpighi Hospital for their technical assistance.

Footnotes

Peer reviewer: José Julián calvo Andrés, Department of Physiolgy and Pharmacology, University of Salamanca, Edificio Departamentl, Plaza de los Doctores de la Reina, Campus Miguel de Unamuno. 37007 Salamanca, Spain

S- Editor Tian L L- Editor O’Neill M E- Editor Zhang DN

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