Gut, 1990, 31, 1144-1149

Pancreaticobiliary ductal union

S P Misra, M Dwivedi

AbstractThe main pancreatic duct and the common bileduct open into the second part of the duo-denum alone or after joining as a common

channel. A common channel of >15 mm (ananomalous pancreaticobiliary duct) is associ-ated with congenital cystic dilatation of thecommon bile duct and carcinoma of the gallbladder. Even a long common channel(38 mm) is associated with a higher frequencyof carcinoma of the gall bladder. Gail stonessmaller than the common channel and a longcommon channel predispose to gail stoneinduced acute pancreatitis. Separate openingsfor the two ductal systems predisposes todevelopment of gall stones and alcoholinduced chronic pancreatitis. The role ofductal union has also been investigated inprimary sclerosing cholangitis and biliaryatresia.

The anatomy of the distal ends of the commonbile duct and the main pancreatic duct hasreceived attention because of its importance inpancreaticobiliary diseases (Table I). The twoducts open in the duodenum either separately or

via a common channel. In the pre-endoscope era,a common channel was noted in 20-90% of thegeneral population at necropsy and in 7-50% bycholangiography.' In a later study a common

channel was found in 74% of specimens, 7% ofwhich had interposed septum and 19% separateopenings for the two ducts.2 Another necropsystudy noted separate ducts (separate openingsplus one opening without a common channel) in16-9% subjects while 83 1% had a commonchannel.3 Our own data, based on a retrospectiveanalysis of 259 selected endoscopic retrogradecholangiopancreaticograms (ERCPs), in whichthe pancreaticobiliary ductal union could beclearly seen, showed a common channel in 63%.4The length of the common channel in normal

people ranges from 1-12 mm, with a mean ofabout 4-5 mm45 (Table II). Jona et at7 noted thatthe length of the common channel was < 5 mm innormal people. A common channel of 4 mm ininfants and 6 mm in adults was consideredabnormal.8 In Di Magno's series 25% of patientshad a well defined ampulla, 31% had a common

Gastroenterology Unit,PostgraduateDepartment of Medicine,MLN Medical College,Allahabad-211001, IndiaS P MisraM DwivediCorrespondence to:Dr S P Misra.Accepted for publication30 October 1989

TABLE I Diseases associated with disorders ofthepancreaticobiliary ductal union

Anomalous pancreaticobiliary ductal union:Congenital cystic dilatationCarcinoma of the gall bladder

Long common channel:Carcinoma of the gall bladderGall stone induced acute pancreatitis

Separate openings ofthe common bile duct and the main pancreaticduct:

Gall stonesAlcohol induced chronic pancreatitis

TABLE ii Length ofthe common channel in normal subjects invarious series

Authors Mean (mm) Range (mm)

Misra et al4 4-7 1-018-4Kimura et al5 4.6 2-10Dowdy et al6 4-4 1-12

channel of <3 mm, and 18% had a commonchannel of >3 mm. The rhean length was notmentioned.2 In a necropsy study of 35 infants,Miyano et al' noted that the average length of thecommon channel was 1 3 mm.Kimura et al,' using cineradiography during

ERCP, have shown contractile motility of theductal wall extending well beyond the commonchannel, towards the liver. The mean (SD)length of the contractile segment was 20 5(4 6) mm (range 14-31 mm).

Anomalous pancreaticobiliary ductal union(APBD)In APBD the connection between the commonbile duct and the main pancreatic duct is locatedoutside the duodenal wall and is therefore notunder the influence of the sphincter of Boyden(Table III)." The frequency of APBD variesfrom 1 5-3 2%.4 0ll5 The highest incidenceof 3-2% was reported by Kimura et all andUnozawa et al." If it appears that the pancreaticduct is joining the common bile duct it is denotedas P-B type and if the common bile duct appearsto join the main pancreatic duct it is denoted asB-P type (Fig 1).Kimura et all have shown that the contractile

segment of the common channel, in APBD,ended well below the common channel. Themean (SD) length of the contractile segment was14-8 (4 6)mm (range 11-22 mm) in subjects withAPBD compared to 205 (4 6) mm (range14-31 mm) in those without APBD. The differ-ence between the two groups was significant(p<O OO1).

MECHANISM OF APBDIt may be that APBD is a result of unevenproliferation of bile duct epithelium during fetallife. II The union ofthe common bile duct and themain pancreatic duct is located lateral to theduodenum up to the eighth week ofgestation andthen it shifts medially to lie finally within the

TABLE in Definition ofanomalous pancreaticobiliary ductalunion used by various workers

Common channel > 15 mm4 5'0'4Common channel >20 mm or ducts joining perpendicular to each

other, or both"Common channel > 15 mm plus amylase activity in bile> 10 000 IU"l

Common channel >6 mm outside duodenum'6

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Pancreaticobiliary ductal union

Figure 1: Two types ofunion. In theBP type thecommon bile duct appears tojoin the main pancreaticduct, while in the PB typethe main pancreatic ductappears to join the commonbile duct.

PB

duodenal wall. Failure of this movemresult in APBD.'8

APBD and congenital cystic dilatatioicommon bile ductIn 1906 Arnolds noted an associationAPBD and congenital dilatation of thebile duct. 19 Since then many workreported this association.57 10 14-17 20-27 Tence of this association in variousshown in Table IV.Ono et al'6 found APBD in 15 (68

patients with congenital cystic dilatatiSameshima et a126 found APBD inpatients with congenital cystic dilataticother studies APBD was noted in 3100%7 of patients with congenital cystion.

TYPE OF UNIONKimura'° and Komi et a124 noted that Bunion is usually associated with congendilatation, while another study frcnoted the P-B union in nine of 15 (606/In a recent series 28 (56%) of 50 cases wP-B type and 22 (44%) of the B-P typand Akita noted the B-P type in 66°atype in 34% of patients.25

MECHANISM OF CONGENITAL CYSTIC DILiThe exact cause of congenital cystic dinot known. Babbitt et a120 proposed thaof the abnormally long common chaidevelopment of the sphincter of Odcwhich results in a reversed pressurebetween the common bile duct andpancreatic duct. This leads to regurgthe pancreatic juice into the commonand repeated attacks of cholangitis. TIin thickening of the common bile dstenosis, and finally dilatation. Komthat bile from patients with dilatation,

TABLE IV Incidence ofcongenital cystic dilataticcommon bile duct in patients with anomalouspancreaticobiliary ductal union

Author

Kimura et allKato et alYamauchi et al 4

Sameshima et a12P

amylase,22 but he failed to produce localiseddilatation by regurgitating pancreatic juiceexperimentally into the common bile duct.24Cylindrical dilatation of varying degrees hasbeen produced by injecting pancreatic juicethrough the bile duct in mongrel dogs.27Oguchi et al27 found epithelial hyperplasia

with round cell infiltration and thickening of thewall with fibrosis in all of their patients withcystic dilatation (n=40). They divided theirpatients into two groups. One group presented

BPwith abdominal pain; 86-4% showed pre-dominant epithelial hyperplasia and round cellinfiltration (glandular type). The amylaseactivity in bile was increased. The other group

ent could presented with obstructive jaundice; 73-7% ofthese patients showed predominant thickeningof the wall with fibrosis (fibrotic type). Amylaseactivity, in bile of these patients, was signifi-

a of the cantly less than in the other group. 14 of 31patients with cystic dilatation had glandular type

between while the other 17 had fibrotic type but all ninecommon patients with cylindrical cystic dilatation had

cers have glandular type. In their animal model, where a'he incid- pancreatico-cholecystostomy was done, theystudies is observed only cylindrical dilatation. They

concluded that cylindrical congenital cystic3%) of 22 dilatation may be accounted for by an APBDion, while union, with resultant reflux of pancreatic juice47-5% of into the common bile duct. But for cysticmn. In two dilatation both an APBD union and an obstruc-33%24 and tive element in the lower part of the cyst play atic dilata- part.

APBD and carcinoma of the gall bladderSeveral Japanese workers have reported an

-P type of association between APBD and carcinoma of thelital cystic gall bladder."'3-15 28-35 Kato et al'5 reported that)m Japan four of nine (44-4%) patients with APBD hadio) cases.'6 carcinoma of the gall bladder. Only four of 291vere of the (1-3%) patients without APBD had carcinoma ofoe.5 Arima the gall bladder.and P-B Kimura et all noted APBD in 16-7% of

patients with carcinoma of the gall bladdercompared to only 2-8% of patients with otherhepatobiliary and pancreatic diseases. They also

ATATION found that of the 65 cases ofAPBD, carcinoma of.latation is the gall bladder was present in 24-6% comparedat because to 1-9% in those without APBD. Of these 65nnel mal- patients with APBD, 50 had congenital cysticii occurs, dilatation of the common bile duct. Of thegradient remaining 15 (who did not have congenital cysticthe main dilatation), 11 (73 3%) had gall bladder cancerPitation of compared to only five (10%) of the 50 patients.bile duct Ours is the only group, outside Japan, to find anhis results association between APBD and carcinoma of theluct wall, gall bladder.4ii showed The prevalence of carcinoma of the gallcontained bladder in APBD varies from 57% to 77% in

Japanese series.59 12 132 -30 Two of four (50%)patients in our series had carcinoma of the gall

on ofthe bladder4 (Fig 2b and c).Patients with APBD develop carcinoma of the

gall bladder earlier than those without APBD.Incidence(%) The median age was lower by about a decade in

those with APBD.'4 In another report from33 Japan the mean (SD) age of patients with75 8 carcinoma of the gall bladder associated with82A8

APBD was 49-8 (9-8) years compared to 61-7

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Misra, Dwivedi

Figure 2: (a) Separate openings ofthe common bile duct and the main pancreatic duct in a patient with choledocholithiasis.(b) Anomalous pancreaticobiliary ductal union in a patient with carcinoma ofthe gall bladder. The common hepatic duct shows narrowing (arrow) withdilatation ofproximal ducts (arrow head).(c) Endoscopic retrograde cholangiopancreatogram ofa patient with carcinoma ofthe gall bladder and a long common channel. The common bile duct isnarrowed (arrow) with dilation ofthe intrahepatic biliary radicles (arrow head).

(10-3) years for those without APBD (p<0o5).5

TYPE OF UNION IN CARCINOMA OF THEGALL BLADDER ASSOCIATED WITH APBDIn a review of all 47 reported cases of carcinomaof the gall bladder associated with APBD,Yamauchi et al'4 observed that in 39 of 42(92 9%) cases the union was of the P-B type. Inthe remaining five patients the type of union wasnot mentioned. In another study 13 of 42 (31%)patients with a P-B union had carcinoma of thegall bladder compared to only three of 23 (13%)with a B-P union.5

MECHANISM OF GALL BLADDER CARCINOMA INAPBDA review of all 47 reported cases of carcinoma ofthe gall bladder associated with APBD up to1985 showed that gall stones were present in only17-5% of patients'4 compared to 74% found byPiehler and Crichlow in patients with gallbladder cancer36 and 57% in a Japanese study.37Kimura et all found gall stones in only 12-5%of patients with APBD associated carcinoma ofthe gall bladder compared to 66-9% in those withcarcinoma of the gall bladder without APBD.Gall stones are probably not an important aetio-logical factor in patients with carcinoma of thegall bladder with APBD.

It has been postulated that in APBD pan-creatic juice refluxes freely into the biliary tree,leading to chronic inflammation and meta-plasia.5 '4 When pancreatic juice is mixed withbile, lysolecithin and phospholipase A2 are pro-duced, which may also be irritants.'4 The gallbladder acts as a reservoir in patients with APBDwithout congenital cystic dilatation and thuscarcinoma of the gall bladder occurs morefrequently in such patients. In patients with

congenital cystic dilatation irritation occurs inthe cyst rather than in the gall bladder, and it iswell known that there is a high incidence ofcarcinomatous change.38"3 The amylase contentin bile was high in 10 of 11 such patients.'4 Thehighest activity recorded was 567000 IU byKinoshita et al.'3 Sphincteric action stoppedshort of pancreaticobiliary ductal union inpatients with APBD and thus the normal controlmechanism preventing regurgitation of pan-creatic juice into the biliary tree is absent in thesepatients.5 In an experimental study on mongreldogs, development of mucosal and intestinalmetaplasia was observed in the gall bladder afterthe creation of a cholecystopancreatic communi-cation.35 Thus APBD is a predisposing factor forcarcinoma of the gall bladder and may be apremalignant condition, especially in patientswithout congenital cystic dilatation of thecommon bile duct. One worker even goes as faras to recommend prophylactic cholecystectomyin these patients. 14

Long common channelWe have defined a long common channel as acommon channel of 8mm.4In our study 12 (5%)of 259 ERCPs examined showed a long commonchannel. Eight (67%) of these patients hadcarcinoma of the gall bladder (Fig 2c), onepatient had gall stones, and three were in thecontrol group. The prevalence of a long commonchannel in the control group was three (3%) of102 and one (1%) of 95 patients with gall stonedisease compared to eight (38%) of 21 withcarcinoma ofthe gall bladder. Ifonly those with acommon channel were considered, three (5%) of64 control subjects, one (3 5%) of 28 patientswith gall stone disease, and eight (57%) of 14patients with carcinoma had a long commonchannel. The mechanism ofcarcinoma of the gall

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Pancreaticobiliary ductal union

bladder may be the same as that for APBDassociated carcinoma.

Pancreaticobiliary ductal union in gall stonediseaseIn a retrospective analysis a total of 95 patientswith gall stone disease of whom 59 patients hadstones seen at ERCP, either in the common bileduct or the gall bladder, and 36 patients who hadundergone cholecystectomy in the past for gallstone disease were evaluated by ERCP for post-cholecystectomy symptoms.4 Sixty seven of 95(70%) had separate openings of the common bileduct and the main pancreatic duct (Fig 2a).When compared to the control group (separateopening for the two ducts in 37%) this differencewas highly significant (p<0001), but the mean(SD) length of the common channel in gall stonedisease (4 6 (2 6) mm) was similar to that in thecontrol group (4 7 (2 5) mm).

MECHANISMTwo hypotheses might explain the higherincidence of gall stone disease in those who haveseparate openings for the two ducts. Firstly, thesphincteric mechanism at the distal end of thecommon bile duct may behave differently inthese patients, leading to prolonged stasis of bilein the common bile duct and gall bladder, thuscausing stone formation. Sphincterotomyinhibits gall stone formation in prairie dogs,"and this effect is reversed by giving atropine.45The alternative hypothesis is that a commonchannel may prevent gall stone formationbecause of reflux of pancreatic juice in thecommon bile duct where the glyco and proteo-lytic properties of the pancreatic juice dissolvethe mucin nidus of gall stones, which is found atthe core of most cholesterol gallstones." An invitro study has shown that trypsin enhances thedissolution of gall stones.49 Furthermore, studiesfrom Japan have shown a much lower incidenceof gall stones in patients with carcinoma of thegall bladder and APBD compared to thosewithout APBD.5 '4 Amylase levels in the bile ofpatients with carcinoma of the gall bladder withAPBD were also high in 1O of 1 1 patients. 14

Pancreaticobiliary ductal union in acute gallstone pancreatitisOpie5' noted impacted gall stones at the ampullaof Vater in a patient with pancreatitis, and it wassuggested that reflux of bile into the pancreaticduct causes pancreatitis in patients with choleli-thiasis.5' This led to the common channeltheory.52 Since then many workers have shownthat common bile duct stones are involved in thepathogenesis of gall stone pancreatitis 312 and arefound in 20-30% of patients with gall stone pan-creatitis at necropsy.53555960 When surgery wasperformed early, stones were found causingampullary obstruction in 63-72% of patients.5561Stones can be recovered from the stools of mostpatients with gall stone pancreatitis.5 57 63A common pancreaticobiliary channel occurs

in 67-80% of patients with gall stone pan-creatitis.'758"6 Jones et all noted a common

pancreaticobiliary channel in 67% of 37 patientswith gall stone pancreatitis compared to 32% of109 patients with other biliary tract diseases.Most of the stones found in patients with gall

stone pancreatitis are small.8 Even microliths(stones <3 mm) have been implicated in thepathogenesis.69

Jones et a166 correlated the size of the gall stoneto the length of the common channel. The lengthof the common channel was greater than thediameter of the smallest stone in nine of 27 (33%)patients with gall stone pancreatitis compared to13 of 109 (12%) with other biliary tract disease.Thus, a common channel occurs more fre-quently in patients with gall stone pancreatitis,and the size ofthe stone and the common channelhave important implications in the pathogenesisof gall stone induced acute pancreatitis.

Pancreaticobiliary angle (angle of reflux)Even the width of the pancreatic duct and theangle at which the common bile duct and themain pancreatic duct meet are important inthe pathogenesis of gall stone pancreatitis. In astudy of 53 patients who had had attacks of acutegall stone pancreatitis and 561 patients withoutsuch a history (controls), it was noted thatpancreatic duct reflux occurred in 33 (62 5%)patients with a previous history of acute gallstone pancreatitis compared to only 82 (14-6%)of the controls. Among all patients with pan-creatic reflux, those with a past history of acutegall stone pancreatitis had wider cystic, commonbile, and pancreatic ducts and the angle of refluxwas greater (mean (SD) 40 (12)°) compared tothose with no history of acute gall stone pan-creatitis (angle of reflux 21 (15)0). The length ofthe common channel was greater in patients witha history of gall stone pancreatitis compared tocontrols (8 mm v 4 mm). Furthermore, 72% ofpatients had a common channel of 5 mm or morecompared to only 20% in the control group.Apart from the frequency of pancreatic ductreflux, similar results were found in anotherstudy.7"

Pancreaticobiliary ductal union in chronicpancreatitisYatto and Siegel72 reported separate openings ofthe common bile duct and the main pancreaticduct in 24 (86%) of 28 patients with alcoholicpancreatitis compared to only six (20%) of 30alcoholics without chronic pancreatitis. Thedifference was significant (p<O0OO1). We evalu-ated ERCP films of 49 patients with chronicpancreatitis: 18 (37%) had alcoholic pancreatitisand 31 (63%) had non-alcoholic pancreatitis.Thirteen (72%) of the 18 patients with alcoholicpancreatitis had separate openings for the twoducts, and 14 (45%) of 31 patients with non-alcoholic pancreatitis had separate openings.The difference between the two groups justfailed to reach statistical significance. Whencompared to our earlier study in a controlpopulation4 separate openings in alcoholic pan-creatitis patients were much more common (72%v 37%). If the entire series of 49 patients isconsidered, separate openings were noted in 27

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1148 Misra, Dwivedi

(55%), which, when compared to the controlgroup, was significantly higher. The length ofthe common channel was, however, similar (4 5(1-2) v 4-7 (2-5) mm) (unpublished observa-tions).

Mechanism of chronic pancreatitisDi Magno et al2 observed that separate openingsfor the common bile duct and the main pan-creatic duct were associated with hyperplasia ofthe pancreatic ductular epithelium. This mightlead to obstructed flow of pancreatic secretions.An association between pancreatic ductularepithelial changes, obstruction of pancreaticsecretion, and chronic pancreatitis has beenobserved.73 Chronic alcohol intake results inhyperplasia of the pancreatic ductular epithe-lium and increased secretion of pancreaticjuice.74 It may be that separate openings for thetwo ducts lead to hyperplasia of the pancreaticductular epithelium which is enhanced bychronic alcohol intake, resulting in obstructionof the flow of pancreatic juice and later precipita-tion of protein plugs and chronic pancreatitis.Protein plugs form in the initial stages in mostpatients with chronic pancreatitis."

APBD and abnormal pancreatogramsKato et all' in a study of nine cases of APBDnoted abnormality of the pancreatogram in eight(77 8%). An abnormal pancreatogram was foundin only 24 (36-9%) of 65 patients with some typeof biliary disease without APBD. There is nomention of an abnormal pancreatogram in mostseries of APBD. In our study4 we found noabnormality of the pancreatogram in our fourpatients with APBD.4

Pancreaticobiliary ductal union in primarysclerosing cholangitisMuller et a176 studied the role of pancreatico-biliary ductal union in primary sclerosingcholangitis. In 20 of the 46 patients, in whom thepancreaticobiliary ductal union could be clearlyseen, anomalous union was noted in only two(10%) cases. Fourteen (70%) patients had acommon channel of 1 or 2 mm, three patientshad a common channel of 3 to 10 mm, and onepatient had separate openings for the two ducts.Pancreatic duct abnormalities were found inhalf of these patients. It was concluded that thevariations in the pancreaticobiliary ductal unionwere rare in patients with primary sclerosingcholangitis.

Pancreaticobiliary ductal union in otherdiseasesAbnormally long pancreaticobiliary ductal unionwas found in two (12%) of 17 children withinfantile hepatitis, three (5%) of 57 with biliaryatresia, and one patient with chronic pancreati-tis.25

In another study of 28 cases with biliaryatresia, the junction of the common bile duct andthe main pancreatic duct was situated below thepropria muscularis of the duodenum in 17

(60 7%). The common channel was longer(>6 mm) in these patients than in the controlsubjects. The angle at which the two ducts joinedwas less acute than in the control subjects. Thecommon channel in patients with choledochalcyst was longer than in patients with biliaryatresia. An APBD was noted in all patients withcholedochal cyst compared to 60% of patientswith biliary atresia.9Two cases of anomalous drainage of the

common bile duct into the fourth portion of theduodenum have been described.8 Both were inyoung children who had recurrent attacks ofabdominal pain and vomiting and, on investiga-tion, hyperbilirubinaemia and hyperamylasemia.The common channels measured 1 0 and 2-7 cm.

1 Hansson K. Experimental and clinical studies in aetiologic roleof bile reflux in acute pancreatitis. Acta ChirScand 1967; 375(suppl): 1-102.

2 Di Magno EP, Shorter RG, Taylor WG, Go LW. Relationshipbetween pancreaticobiliary ductal anatomy and pancreaticductal and parenchymal histology. Cancer 1982; 49: 361-8.

3 Suda K, Miyano T, Konuma I, Matsumoto M. An abnormalpancreatico-choledocho ductal junction in cases of biliarytract carcinoma. Cancer 1983; 52: 2086-8.

4 Misra SP, Gulati P, Thorat VK, Vij JC, Anand BS. Pan-creatico biliary ductal union in biliary diseases. An endo-scopic retrograde cholangiopancreaticographic study.Gastroenterology 1989; %: 907-12.

5 Kimura K, Ohto M, Saisho H, et al. Association of gallbladder carcinoma and anomalous pancreaticobiliary ductunion. Gastroenterology 1985; 89: 1258-65.

6 Dowdy GS, Waldron GW, Brown WG. Surgical anatomy ofthe pancreaticobiliary ductal system. Arch Surg 1962; 84:229-46.

7 Jona JZ, Babbitt DP, Starshak RJ, La Porta AJ, Glicklich M,Cohen RD. Anatomic observations and etiologic andsurgical considerations in choledochal cyst. J Paediatr Surg1979; 14: 315-20.

8 Doty J, Hassal E, Fonkalsrud EW. Anomalous drainage of thecommon bile duct into the fourth portion of the duodenum.Arch Surg 1985; 120: 1077-9.

9 Miyano T, Suruga K, Suda K. Abnormal choledocho-pancreatico ductal junction related to the etiology of infantileobstructive jaundice. J Paediatr Surg 1979; 14: 16-26.

10 Kimura K. Studies in 28 cases of congenital cystic dilatation ofthe common bile duct in adults. Roentgenological featuresand a union between the choledochus and the main pan-creatic duct. JpnJ7 Gastroenterol 1976; 73: 61-74 (in Japanesewith English abstract).

11 Unozawa T, Kimura K, Ohto M, et al. Clinical study onrelationship between anomalous pancreaticobiliary ductalunion and carcinoma of the gall bladder. JpnJI Gastroenterol1985; 82: 473-82 (in Japanese with English abstract).

12 Kato T, Koyama K. Anomalous choledocho-pancreaticjunction and its pathology. J Clin Surg 1986; 28: 34-43 (inJapanese).

13 Kinoshita H, Nagata E, Hirohashi K, Sakai K, Yasutsugu Y.Carcinoma of the gall bladder with an anomalous connectionbetween the choledochus and the pancreatic duct. Cancer1984; 54: 762-9.

14 Yamauchi S, Koga A, Matsumoto S, Tanaka M, Nakayama F.Anomalous junction of pancreaticobiliary duct withoutcongenital choledochal cyst. A possible risk factor for gallbladder carcinoma. AmJ Gastroenterol 1987; 82: 20-4.

15 Kato 0, Hattori K, Suzuki T, Tachino F, Yuasa T. Clinicalsignificance of anomalous pancreaticobiliary union.GastrointestEndosc 1983; 29: 94-8.

16 Ono J, Sakoda K, Akita H. Surgical aspect of cystic dilatationof the bile duct. Ann Surg 1982; 195: 203-8.

17 Yotsuyanagi S. Contributions to aetiology and pathology ofidiopathic cystic dilatation of the common bile duct withreport of three cases. New aetiological theory. Gann 1935;30: 601-53.

18 Wong KC, Lister J. Human fetal development of hepatopan-creatic duct junction - a possible explanation of congenitaldilatation of the biliary tract. J Pediatr Surg 1981; 16:139-45.

19 Arnolds. Eine manneskopfgrossen Retentionszyste desCholedochus. Dtsch Med Wochenschr 1906; 32: 1804.

20 Babbitt DP, Starshak RJ, Clemett AR. Choledochal cyst: aconcept of etiology. AmJ Roentgenol 1973; 119: 57-62.

21 Oi , Doki F, Takemoto T. Analysis of anomalous connectionbetween the pancreatic and biliary ducts. J'pnJf Gastroenterol1974; 71: 191.

22 Komi N. Anomalous arrangement of pancreaticobiliary ducts.Shuzustsu 1975; 29: 73-83 (in Japanese).

23 Kimura K, Ohto M, Ono T, et al. Congenital cystic dilatationof the common bile duct - relationship to anomalouspancreaticobiliary ductal union. AmJy Roentgenol 1977; 928:571-7.

24 Komi N, Kashiwagi Y, Ikeda N. The etiology of congenitaldilatation of the biliary duct. Jfpn J Paediatr Surg 1977; 9:1101-9 (in Japanese).

group.bmj.com on February 12, 2018 - Published by http://gut.bmj.com/Downloaded from

Pancreaticobiliary ductal union 1149

25 Arima E, Akita H. Congenital biliary tract dilatation andanomalous junction of the pancreaticobiliary system.J PaediatrSurg 1979; 14: 9-15.

26 Sameshima Y, Uchimura M, Muto Y, Maeda J, TsuchiyamaH. Coexistent carcinoma in congenital dilatation of the bileduct and anomalous arrangement of the pancreaticobileduct. Cancer 1987; 60: 1883-90.

27 Oguchi Y, Okada A, Nakamura T, et al. Histopathologicstudies of congenital dilatation of the bile duct as related toan anomalous junction of the pancreaticobiliary ductalsystem. Clinical and experimental studies. Surgery 1988;103: 168-73.

28 Sameshima Y, Uchimura M, Muto Y, et al. A case ofanomalous arrangement of pancreatico-biliary duct withpapillary adenocarcinoma and papillary adenoma of the gallbladder. JpnJ Gastroenterol 1978; 756: 909-15.

29 Konishi T, Nagakawa T, Jinno M, et al. Four cases ofanomalous arrangement of pancreaticobiliary duct associ-ated with gall bladder cancer. Biliary Tract and Pancreas1981; 2: 435-41 (in Japanese).

30 Hanyu F, Ohashi M, Ohi T. Clinical aspects of biliary ductcarcinoma associated with anomalous arrangement betweenthe choledochus and the pancreatic duct. Biliary Tract andPancreas 1981; 2: 1637-50 (in Japanese).

31 Kinoshita H, Osada E, Chimata Y, et al. Carcinoma of thegall bladder with anomalous arrangement between thecholedochus and the pancreatic duct. Report of 7 cases andreview of literature. Biliary Tract and Pancreas 1981; 2:1701-9 (in Japanese).

32 Uchimura M, Muto Y, Waki S, et al. Association of carcinomawith congenital dilatation of the bile duct. Biliary Tract andPancreas 1982; 3: 333-42 (in Japanese).

33 Sugihara J, Sekita M, Saito Y, et al. Anomalous arrangementof pancreaticobiliary duct and cancer. Biliary Tract andPancreas 1982; 3: 487-95 (in Japanese).

34 Mihara 0, Murahisa T, Tsugama M, et al. A case of earlycarcinoma of the gall bladder with anomalous arrangementbetween the choledochus and the pancreatic duct withoutcholedochal cyst dilatation. Biliary Tract and Pancreas 1984;5: 617-21 (in Japanese).

35 Nagata E, Sakai K, Kinoshita H, et al. The relation betweencarcinoma of the gall bladder and anomalous connectionbetween the choledochus and the pancreatic duct. Ann Surg1985; 202: 182-90.

36 Piehler JM, Crichlow RW. Primary carcinoma of the gallbladder. Surg Gynecol Obstet 1978; 147: 929-42.

37 Yokayama I, Tashiro S, Kanno T, et al. Current problems onsurgical treatment of primary carcinoma of the gall bladderin Japan. Nippon Shokakigeka Gakkai Zasshi 1980; 13:1362-8.

38 Alonso-Lej F, Rever WB, Pessagno DJ. Congenitalcholedochal cyst, with a report of two and an analysis of 94cases. IntAbstrSurg 1959; 108: 1-30.

39 Tsuchiya R, Harada N, Ito T, et al. Malignant tumors incholedochal cysts. Ann Surg 1977; 186: 22-8.

40 Bloustein PA. Association of carcinoma with congenital cysticconditions of the liver and bile ducts. Am J Gastroenterol1977; 67: 40-6.

41 Todani T, Kobuchi KM, Watanabe Y, etal. Carcinoma arisingin the wall of congenital bile duct cyst. Cancer 1979; 44:1134-41.

42 Chaudhary PK, Chaudhari B, Schuler JJ, Nyhus L.Carcinoma associated with congenital cystic dilatation of bileducts. Arch Surg 1982; 117: 1349-51.

43 Voyles CR, Smadja C, Shands WC, et al. Carcinoma incholedochal cysts. Arch Surg 1983; 118: 968-8.

44 Hulton SW, Sievert CE Jr, Vennes JA, Dunane WC. Theeffect of sphincterectomy on gallstone formation in prairiedog. Gastroenterology 1981; 81: 663-71.

45 Hulton SW, Sievert CE Jr, Vennes JA, Duane WD. Inhibitionofgallstone formation by sphincterectomy in the prairie dog.Reversal by atropine. Gastroenterologv 1982; 82: 1308-13.

46 Womack N, Zeppa R, Irvin G. The anatomy ofgallstones. AnnSurg 1963; 157: 670-86.

47 Maki T, Matsushiro T, Susuki N, Nakamura N. Role ofsulphated glycoprotein in gall stone formation. Surg GynecolObstet 1974;132: 846-54.

48 Lee SP, La Mont JT, Carey MC. Role of gall bladder mucushypersecretion in the evolution of cholesterol gall stones.J Clin Invest 1981; 67: 1712-23.

49 Leuschner J, Baumgattel H. Gallstone dissolution in thebiliary tract. In vitro investigations in inhibiting factors andspecial dissolution agents. Am J Gastroenterol 1982; 77:222-6.

50 Opie EL. The relation of cholelithiasis to disease of thepancreas and to fat necrosis. Bull,Johns Hopkins Hosp 1901;12: 119-21.

51 Halstead WS. Retrojection of bile into the pancreas, a cause ofacute haemorrhagic pancreatitis. Bull Johns Hopkins Hosp1901; 12: 179-81.

52 Opie EL. The etiology of acute haemorrhagic pancreatitis.BullJohns Hopkins Hosp 1901; 12: 182.

53 Calen F, Frey C. Re-evaluation of the treatment of pancreatitisassociated with biliary tract disease. Ann Surg 1964; 160:723-6.

54 Dixon JA, Hillam JD. Surgical treatment of biliary tractdisease associated with acute pancreatitis. Am J Surg 1970;120: 371-5.

55 Acosta JM, Ledesma CL. Gallstone nigration as a cause ofacute pancreatitis. N EnglJ Med 1974; 290: 484-7.

56 Imrie W, Whyte AS. A prospective study of acute pancreatitis.BrJ Surg 1975; 62: 490-4.

57 Kelly TR. Gallstone pancreatitis. Pathophysiology. Surgery1976; 80:488-92.

58 Freunh H, Pfeffermann R, Dinst AL, Rabinovici N. Explora-tion of biliary system in acute and recurrent pancreatitis.Arch Surg 1976; 111: 1106-7.

59 Ong BB, Lam KH, Lam SK, et al. Acute pancreatitis in Hong-Kong. BrJ Surg 1979; 66: 398-403.

60 Ranson JHC. The timing of surgery in acute pancreatitis. AnnSurg 1979; 189: 654-63.

61 Kelly TR. Gallstone pancreatitis. The timing of surgery.Surgery 1980; 88: 345-50.

62 Kelly TR. Gallstone pancreatitis. The second time around.Surgery 1982; 92: 571-5.

63 Acosta JM, Rossi R, Ledesma CL. The usefulness of stoolscreening for diagnosing cholelithiasis in acute pancreatitis.A description of the technique. Am J Dig Dis 1977; 22:168-72.

64 Bergvist A, Selainger SI. Pancreatic reflux in operativecholangiography in relation to pre and post operativepancreatic affection. Acta ChirScand 1957; 114: 191-6.

65 Thyrston OG. Pathogenesis of gallstone pancreatitis. Am JSurg 1975; 129: 301-3.

66 Jones BA, Salsberg BB, Bohnen JMA, Mehta MH. Commonpancreaticobiliary channels and their relationship to gallstone size in gallstone pancreatitis. Ann Surg 1987; 205:123-5.

67 McMohan MJ, Playforth MJL. The relationship between gallstone and cystic duct anatomy in acute pancreatitis. Br JSurg 1978; 65: 361.

68 Frey CF. Gallstone pancreatitis. SurgClin North Am 1981; 61:923-38.

69 Houssin D, Casaing D, Lemioine J, Bismuth H. Microlithiasisof the gall bladder. SurgGynecol Obstet 1983; 157: 20-4.

70 Armstrong CP, Taylor TV. Pancreatic duct reflux and acutegallstone pancreatitis. Ann Surg 1986; 204: 59-64.

71 Yveyneaux JP. [Letter]. Ann Surg 1987; 205: 594-6.72 Yatto RP, Siegel JH. The role of pancreaticobiliary duct

anatomy in the etiology of alcoholic pancreatitis. J ClinGastroenterol 1984; 6: 419-23.

73 VolkholfG, Stolle M, Beeker V. Epithelial dysplasia in chronicpancreatitis. VirchowsArch(PatholAnat) 1982; 392: 331-49.

74 Dreiling DA, Greenstein AJ, Bortalo 0. The hypersecretorystates of the pancreas. Implications in the pathophysiologyof peptic ulcer diathesis. Am J Gastroenterol 1973; 59:505-11.

75 Sarles H. Etiopathogenesis and definition of chronic pan-creatitis. Dig Dis Sci 1986; 31 (suppl): 91S-107S.

76 Muller EL, Miyamoto T, Pitt HA, Longmire WP. Anatomy ofthe choledochopancreatic duct junction in primary scleros-ing cholangitis. Surgery 1985; 97: 21-6.

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Pancreaticobiliary ductal union.

S P Misra and M Dwivedi

doi: 10.1136/gut.31.10.11441990 31: 1144-1149 Gut

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