Hepatic lobar atrophy: association with ipsilateral portal vein obstruction

OBJECTIVE: This study was performed to evaluate the association between hepatic lobar atrophy, bile duct obstruction, and portal vein obstruction. MATERIALS AND METHODS: Thirty cases of hepatic lobar atrophy identified on angiography with CT during arterial portography from August 1992 to March 1995 were retrospectively reviewed by two independent observers. Cases were evaluated for vascular patency and bile duct obstruction. Malignant diagnoses were present in 28 of 30 patients. RESULTS: Twenty-two patients (73%) had atrophy in the left lobe and eight patients (27%) had right lobar atrophy. Portal vein obstruction was unilateral and confined to the atrophic lobe in 26 patients (87%). In contrast, bile duct obstruction was bilateral in 23 patients (77%) and in only four patients (13%) was it isolated to the atrophic lobe. The correlation between atrophy and portal vein obstruction was significant, with 90% sensitivity, 97% specificity, and 96% positive predictive value (p < .00001). For the correlation between atrophy and biliary obstruction, the sensitivity of angiography with CT during arterial portography was 90%, specificity was 23%, and positive predictive value was 54% (p = .17). CONCLUSION: Hepatic lobar atrophy usually occurs in the setting of combined biliary and portal vein obstruction. A significant correlation exists between hepatic lobar atrophy and ipsilateral portal vein obstruction.     

Obstructive jaundice associated with extrahepatic portal vein obstruction: report of two cases

We herein report two cases of obstructive jaundice with markedly dilated collateral veins either in or around the bile duct in the setting of extrahepatic portal vein obstruction (EHPO). In the first case, a proximal splenorenal shunt provided relief of biliary stenosis as well as eradication of esophageal varices due to a decompression of portal hypertension. This evidence proved that the markedly extended collateral veins in the hepatoduodenal ligament caused biliary stenosis by compressing the bile duct. In the second case, obstructive jaundice was probably caused by cholangitis and was relieved with biliary drainage. Portal decompressive surgery was not indicated because of the slight degree of esophageal varices. The relationship between cholangitis and EHPO in these patients calls for further investigation. In cases with EHPO manifesting obstructive jaundice associated with risky esophageal varices, portal decompressive surgery is recommended as the procedure of choice.     

The lymph nodes of the porta hepatis

The area under the liver was dissected in 27 human autopsy specimens to search for lymph nodes in the fissures. Nodes were present in all instances. They were in the transverse fissure, posterior to the portal vein, posterior to pars transversus of the left portal vein and associated with the left hepatic artery. The size varied from 2 millimeters to 2 centimeters. Each node was histologically confirmed. Nodes were infrequent and small on the right. Nodes were not found between the portal vein, hepatic artery and bile ducts in the fissures. Nodes were found outside the fissures in the fascia between the bile duct and hepatic artery. Occlusion of the portal vein and hepatic artery could be expected before occlusion of the bile duct. Node enlargement in the transverse fissure is anticipated as a rare cause of jaundice.     

The orphan receptor CRF2-4 is an essential subunit of the interleukin 10 receptor

BACKGROUND/AIMS: Models of hepatopulmonary syndrome require both hepatic injury and portal hypertension to develop pulmonary microvascular and gas exchange abnormalities. Recently, increased endothelin-1 levels associated with vasodilatation, have been observed in cirrhosis. We investigated endothelin-1 production in common bile duct ligated animals with hepatopulmonary syndrome in comparison to partial portal vein ligated animals that do not develop hepatopulmonary syndrome. METHODS: Organ and plasma endothelin-1 were measured in sham, bile duct ligated and portal vein ligated rats, and Northern analysis and immunohistochemistry were performed in liver. Plasma endothelin-1 levels were correlated with pulmonary endothelial nitric oxide synthase levels and alveolar-arterial oxygen gradients. RESULTS: Hepatic and plasma endothelin-1 increased only after bile duct ligation, and were accompanied by increased hepatic endothelin-1 mRNA and increased endothelin-1 protein in biliary epithelium. Plasma endothelin-1 levels correlated directly with both pulmonary endothelial nitric oxide synthase levels and alveolar-arterial gradients. CONCLUSIONS: Enhanced hepatic production and increased plasma levels of endothelin-1 occur after bile duct ligation, but not after portal vein ligation, and correlate with associated molecular and gas exchange alterations in the lung. Endothelin-1 may contribute to the pathogenesis of hepatopulmonary syndrome.     

The developing human biliary system at the porta hepatis level between 29 days and 8 weeks of gestation: a way to understanding biliary atresia. Part 1

The developing biliary system in normal human embryos from 29 days to 8 weeks post-fertilization was studied. The primitive extrahepatic bile duct that originates from the embryonic hepatic foregut diverticulum is in contact with the hepatic anlage from the start of organogenesis and remains so throughout the gestational ages examined. The primitive extrahepatic bile duct maintains continuity with the ductal plate from which intrahepatic bile ducts are eventually formed. Contrary to long-held concepts of biliary development, no 'solid stage' of entodermal occlusion of the common bile duct lumen was found at any stage of gestation in the material investigated. Therefore, biliary atresia is not caused by incomplete vacuolization of the 'solid stage'.     

Surgical treatment of extrahepatic bile duct carcinoma

OBJECTIVE: To evaluate the experience in the diagnosis and surgical treatment of the extrahepatic bile duct carcinomas. METHODS: 242 patients with extrahepatic bile duct carcinoma over the past 20 years was retrospectively studied. RESULTS: The origin points were carcinomas of the upper bile duct in 168, of the middle bile duct in 18, and of the lower bile duct in 56 patients. The preoperative diagnostic rates for the location and the nature of the lesion were respectively raised to 97.2% and 94.5% by combination of ultrasonography and CT. The curative resection rates for the tumors in the upper, middle, and lower bile duct over the recent five years reached to 50.0%, 50.0% and 71.4%. respectively. Follow-up of patients with curative resection showed a one year recurrent rate of 73.9% and a three year recurrent rate of 100.0% with a mean recurrent time of 9.6 months in patients with local metastasis, in contrast to 13.3%, 71.4% and 17.5 months in those without metastasis. Metastasis was mainly responsible for the recurrence. Liver or multiple organ failure, intra-abdominal infection and gastrointestinal hemorrhage were the common and serious complications. CONCLUSION: The case number of the bile duct carcinoma presented a remarkable increment tendency. Ultrasonography and CT were satisfactory enough for diagnosis. To reduce the recurrent rate, resection of the tumor together with the lymph, nervous, fatty and connective tissues in the hepatic hilus, even the right celiac ganglia, should be considered the necessary procedure. Monitoring and protecting the main organs to prevent the multiple organ failure, controlling the gastrointestinal hemorrhage and the intra-abdominal infection are important to decreasing the mortality.     

Spontaneous regression of renal cell carcinoma: a pitfall in diagnosis of renal lesions

Lobar atrophy is a rare morphologic change of the liver. We describe a 73-year-old woman with mild liver dysfunction and history of Sj?gren's syndrome who had right hepatic lobar atrophy. Serum biochemistry levels were as follows: albumin, 4.5 g/dl; total bilirubin, 1.0 mg/dl; alanine aminotransferase, 25 international units/l; aspartate aminotransferase, 27 international units/l; alkaline phosphatase, 333 international units/l; and gamma-glutamyl transpeptidase, 332 international units/l. Serological data were as follows: rheumatoid factor, 27.9; anti-nuclear antibody, 1:640; and antismooth muscle antibody, 1:80. Viral markers for hepatitis B were all negative. Anti-hepatitis C virus (anti-c-100) was negative. Portal hypertension developed thereafter, and the patient died of hepatic failure at age 76. Postmortem examination revealed autoimmune hepatitis with moderate fibrosis, portal vein thrombus, and complete obstruction of the right hepatic duct due to hepatolithiasis. Terminal hepatic failure resulted from combination of decreased hepatic volume due to the right lobar atrophy, exacerbation of autoimmune hepatitis in the remnant left hepatic lobe, decreased portal venous blood flow due to thrombosis, portal hypertension, and cholangitis with hepatolithiasis. This is the first reported case of hepatic lobar atrophy due to autoimmune hepatitis. From a clinical standpoint, patients with hepatic lobar atrophy, even if asymptomatic, should be followed up with careful attention to progression of liver diseases, portal hypertension, and biliary complications.     

Complications of laparoscopy: a prospective multicentre observational study

Extrahepatic obstruction of the portal vein is a well known cause of portal hypertension in childhood, that causes severe morbidity. We evaluated 34 children (24 boys, 10 girls, age 4.5 months to 12 years, mean 5.5 +/- 3.8 years) with this diagnosis, to define the clinical picture, laboratory changes, diagnostic tools and therapeutic modalities. Gastrointestinal bleeding was the commonest mode of presentation (64.7%), with the second being splenomegaly. The cause of the obstruction could be determined in 38.2% (13/34) of the subjects. At the beginning of the study the main diagnostic procedure was splenoportography although in more recent years pulsed duplex Doppler ultrasonography has been used. The follow up period was median of 5 years (range 1-11 years). The mean number of bleeding episodes was 4.7 +/- 5.9 (range 1-26), while nine patients never bled. There was no mortality. Ten patients underwent surgery, while sclerotherapy was performed on 10. Twenty-one patients received beta-blocker drugs. No difference was found among these therapeutic modalities. It is well established that the major risk for children with extrahepatic portal vein obstruction is gastrointestinal bleeding which is tolerated quite well. Surgery should be indicated only in children where bleeding cannot be controlled by medical means including sclerotherapy.     

Septic cholangitis occurring 11 years after inadvertent ligation of the right hepatic duct during cholecystectomy: a case report

We report a case of acute cholangitis caused by the inadvertent ligation of the right hepatic duct during a cholecystectomy performed 11 years before. When the condition of the right hepatic duct or accessory bile duct ligation persists for more than several years, resulting in atrophy of the relevant part of the liver, bile duct ligation will rarely cause severe clinical problems. However, acute cholangitis may occur, as in our patient, so long-term follow-up of the patient is warranted.     

Anomalous junction of the pancreaticobiliary duct accompanied by gallbladder cancer and obstructive jaundice in a patient with high serum and bile cytokine levels

BACKGROUND: Decompression of extrahepatic portal hypertension by directly bypassing the thrombosed portal vein has never been reported in cases of children with idiopathic (or neonatal) portal vein obstruction and cavernoma. METHODS: Seven children (15 years or younger) with portal vein obstruction requiring surgical decompression (urgently in two cases), and in whom preoperative Doppler had shown that the intrahepatic portal branches were hypoplastic but free of thrombus, were included in a pilot study. The cavernoma was bypassed by interposing a venous jugular autograft between the superior mesenteric vein and the distal portion of the left portal vein. Patients received follow-up using routine clinical parameters, upper gastrointestinal endoscopy, and Doppler ultrasound. RESULTS: The mesenterico-portal bypass restored a direct (physiological) hepatopetal portal flow. The operation resulted in effective portal decompression as demonstrated by decrease of the pressure gradient, rapid regression of clinical signs of portal hypertension, and definitive control of bleeding. CONCLUSIONS:This study shows that direct bypassing of portal cavernoma is possible and results in effective portal decompression. Restoration of the hepatic portal flow is a major advantage compared with conventional surgical shunting procedures. This new technique is potentially applicable to two thirds of children with portal vein thrombosis and should be considered when shunting procedures are indicated.     

CT and MRI in detection of intrahepatic portosystemic shunts in patients with liver cirrhosis

OBJECTIVE: Our goal was to determine the prevalence and anatomic location of intrahepatic portosystemic shunts (IPSs) in patients with hepatic cirrhosis as shown by CT and MRI. MATERIALS AND METHODS: We retrospectively reviewed CT and MR scans of 33 cirrhotic patients who had IPSs. In addition, two series of 100 consecutive CT or MR were reviewed to determine the prevalence of IPSs and the percentage of intrahepatic and extrahepatic paraumbilical veins. RESULTS: Intrahepatic portosystemic shunts were divided into three groups according to the intrahepatic course: paraumbilical shunt between the left portal vein and the paraumbilical vein anterior to the liver (n = 29); inferior vena caval shunt between the posterior branch of the right portal vein and the inferior vena cava (n = 2); and miscellaneous (n = 2). Shunts of the paraumbilical type ran through the medial (n = 23), lateral (n = 3), or both medial and lateral (n = 3) segments of the left lobe of the liver. Twenty-five patients had one shunt, and four had more than one. Six cases were also associated with extrahepatic paraumbilical veins. CONCLUSION: Intrahepatic portosystemic shunts, especially the paraumbilical type, were not infrequently visualized in patients with hepatic cirrhosis.     

Bile duct cysts in adults

INTRODUCTION: Bile duct cysts are rare, congenital dilations of the intrahepatic and/or extrahepatic biliary tract. Most of them present during childhood. The classical triad right upper quadrant pain, jaundice and abdominal mass is present only in a few instances. We report here the bile duct cysts which were diagnosed at our institution from 1989 to 1996. METHODS: 3245 consecutive endoscopic retrograde cholangiopancreatograms (ERCP) were evaluated retrospectively. Diagnosis was made when localized cystic dilations of the intrahepatic and/or extrahepatic biliary tract were present. Diffuse dilations of the intrahepatic and extrahepatic biliary tract were excluded. RESULTS: Bile duct cysts were found in 20 patients (17 females, 3 males) among 3245 ERCPs. Their mean age was 56 +/- 20 (median 64, range 10 to 83) years. The cyst types (according to the Alonso-Lej classification with the Todani modification) were type I in 11 (55%), type II, III and IV in two instances each (10%), and type V (or Caroli's disease) in 3 patients (15%). Leading symptoms were cholestasis in 14 patients, 10 of whom had abdominal pain, jaundice in 4 patients, and single cases of pancreatitis, cholangitis, and abdominal mass. In 2 patients the diagnosis was made incidentally. 10 patients had bile duct stones. We performed endoscopic sphincterotomy in 15 patients with concretions or persistent symptoms, 3 patients had cyst resection. One of these, with a type I cyst, already had a disseminated cholangiocarcinoma. 10 of 17 patients without cyst resection are currently symptom-free after complete removal of all gallstones. One male patient with cholecystolithiasis, who is not operable due to advanced liver disease, has recurrent cholangitis, 4 patients have died from causes unrelated to the bile duct cysts, and 2 patients are lost to follow up. CONCLUSION: Bile duct cysts in adults are rare. There is a preponderance in the female gender, and the most common type is the extrahepatic (choledochal) cyst. The leading symptoms are cholestasis and right upper quadrant pain. There is an increased risk of cholangiocarcinoma. In young patients the cysts should be entirely removed to prevent malignancy. Older persons are usually symptomless after complete removal of gallstones.     

Acute acalculous cholecystitis associated with common hepatic duct obstruction: a variant of Mirizzi's syndrome

A variation of Mirizzi's syndrome is described in which common hepatic duct obstruction occurs due to extrinsic compression by an acutely inflamed acalculous gallbladder abutting the common hepatic duct. This case suggests that extrinsic compression and inflammation in the absence of stones can result in complete obstruction of extrahepatic biliary flow.     

Hepatic adenine nucleotides and microsomal cholesterol 7 alpha-hydroxylase activity in the obstructed and freely draining lobes of the liver after selective bile duct obstruction

BACKGROUND: The effect of selective bile duct obstruction (SBDO) on hepatic reserve function of the bile duct obstructed (BDO) and nonobstructed freely draining (FD) lobes of the liver is obscure. METHODS: The bile duct branches draining from the left lateral and median lobes of the liver were ligated for 4 and 10 days in rats, and hepatic reserve functions in BDO and FD lobes were assessed by microsomal cholesterol 7 alpha-hydroxylase activities and by hepatic adenine nucleotides and energy charge levels. The values were compared with those in the sham-operated control liver. Cholesterol 7 alpha-hydroxylase activities were determined by gas-liquid chromatography--mass spectrometry, and hepatic adenosine triphosphate (ATP), adenosine diphosphate (ADP), and adenosine monophosphate (AMP) levels with high-pressure liquid chromatography. RESULTS: The histological examination of the BDO lobes showed proliferation and formation of new bile ductules and fibrous connective tissues linking portal areas. Microsomal cholesterol 7 alpha-hydroxylase activities, hepatic energy charge and each adenine nucleotide level did not differ between FD and BDO lobes, and the values were similar to those in the sham-operated liver. CONCLUSIONS: Selective bile duct obstruction shows no adverse effects on microsomal and mitochondrial functions in both the BDO and FD lobes of the liver.     

Intrahepatic peripheral cholangiocarcinoma: mode of spread and choice of surgical treatment

BACKGROUND: Classification of macroscopic appearance and standard operative procedures for intrahepatic cholangiocarcinoma (ICC) are still controversial. METHODS: The mode of spread of 12 resected ICCs was examined by light microscopy, and the appropriate operative procedures for the various tumours were considered. RESULTS: Macroscopically, nine tumours were classified as mass-forming type and three as periductal infiltrating type. All patients were treated by major hepatectomy; resection of the extrahepatic bile duct was included in two cases of the periductal infiltrating type. Microscopically, invasion into the portal vein, intrahepatic metastasis and perineural or lymphatic vessel invasion occurred in none, one and all of three tumours of the periductal infiltrating type and in eight, six and six of nine tumours of the mass-forming type. CONCLUSION: ICC of the periductal infiltrating type has a tendency to spread along Glisson's sheath via lymphatic vessels. By contrast, ICC of the mass-forming type tends to invade the liver via the portal vein system; such tumours begin to invade Glisson's sheath through the lymphatic vessels when the tumour has increased in size. Therefore, major hepatectomy with combined resection of the extrahepatic bile duct should be performed for all ICCs of the periductal infiltrating type and for those of the mass-forming type with invasion of Glisson's sheath.     

Hepatic and portal surface veins: a new anatomic variant revealed during abdominal CT

OBJECTIVE: The objective of this paper is to describe a new finding on CT of hepatic and portal vein segments located in a subcapsular location on the surface of the liver. SUBJECTS AND METHODS: From a series of more than 11,000 contrast-enhanced abdominal CT scans performed from 1993 to 1997, 14 patients were identified as having hepatic or portal vein segments or both in a subcapsular location on the surface of the liver. RESULTS: We found seven portal vein surface segments in seven patients and 14 hepatic vein surface segments in 12 patients. Of the 14 patients, five had both portal and hepatic vein surface segments. Therefore, in a cohort that exceeded 11,000 patients, the incidence of this finding was 0.1%. Four patients had cirrhosis, two had small hypervascular liver lesions, and eight had healthy livers. The surface veins were not associated with any other recognized vascular anomalies or with anastomoses to extrahepatic systemic veins. CONCLUSION: Hepatic and portal veins can course to a subcapsular location on the surface of the liver. This anatomy is believed to be a normal variant and can be found in patients with healthy livers and normal hepatic vein hemodynamics and in patients with portal hypertension.     

Reducing the addictiveness of cigarettes. Council on Scientific Affairs, American Medical Association

Biliary atresia is a disorder of infants in which there is obliteration or discontinuity of the extrahepatic biliary system, resulting in obstruction of bile flow. Untreated, the resulting cholestasis leads to progressive conjugated hyperbilirubinemia, cirrhosis, and hepatic failure. Biliary atresia has an incidence of approximately one in 10,000 live births worldwide. Evidence to date supports a number of pathogenic mechanisms for the development of biliary atresia. An infectious cause, such as by a virus, would seem most pausible in many cases. The clinical observation that biliary atresia is rarely encountered in premature infants would support an agent acting late in gestation. However, no infectious or toxic agent has been conclusively implicated in biliary atresia. Genetic mechanisms likely play important roles, even regarding susceptibility to other specific causes, but no gene whose altered function would result in obstruction or atresia of the biliary tree has been identified. The variety of clinical presentations support the notion that the proposed mechanisms are not mutually exclusive but may play roles individually or in combination in certain patients. Biliary atresia, when untreated, is fatal within 2 years, with a median survival of 8 months. The natural history of biliary atresia has been favorably altered by the Kasai portoenterostomy. Approximately 25 to 35% of patients who undergo a Kasai portoenterostomy will survive more than 10 years without liver transplantation. One third of the patients drain bile but develop complications of cirrhosis and require liver transplantation before age 10. For the remaining one third of patients, bile flow is inadequate following portoenterostomy and the children develop progressive fibrosis and cirrhosis. The portoenterostomy should be done before there is irreversible sclerosis of the intrahepatic bile ducts. Consequently, a prompt evaluation is indicated for any infant older than 14 days with jaundice to determine if conjugated hyperbilirubinemia is present. If infectious, metabolic, endocrine disorders are unlikely and if the child has findings consistent with biliary atresia, then exploratory laparotomy and intraoperative cholangiogram should be done expeditiously by a surgeon who has experience doing the Kasai portoenteostomy. Biliary atresia represents the most common indication for pediatric liver transplantation, representing more than 50% of cases in most series. Transplantation is indicated when symptoms of end stage liver disease occur, including recurrent cholangitis, progressive jaundice, portal hypertension complications, ascites, decreased synthetic function, and growth/nutritional failure.     

In situ nucleic acid hybridization of cytokines in primary biliary cirrhosis: predominance of the Th1 subset

Primary biliary cirrhosis (PBC) is an autoimmune liver disease characterized by destruction of the intrahepatic bile ducts. It is generally believed that cellular immune mechanisms, particularly involving T cells, result in this bile duct damage. The relative strength of Th1 and Th2 responses has recently been proposed to be an important factor in the pathophysiology of various autoimmune diseases. In this study, we have attempted to identify the Th subset balance in PBC, by detection of cytokines specific to the two T-cell subsets, i.e., interferon gamma (IFN-gamma) for Th1 cells and interleukin-4 (IL-4) for Th2 cells. We analyzed IFN-gamma and IL-4 messenger RNA (mRNA) positive cells in liver sections from 18 patients with PBC and 35 disease controls including chronic active hepatitis C, extrahepatic biliary obstruction (EBO), and normal liver, using nonisotopic in situ hybridization and immunohistochemistry. Mononuclear cells expressing IFN-gamma and IL-4 mRNA were aggregated in inflamed portal tracts in PBC livers, but were rarely present in extrahepatic biliary obstruction, alcoholic fibrosis, or normal liver sections. The IFN-gamma and IL-4 mRNA positive cells in PBC livers were detected in significantly higher numbers than in control livers (P < .01). Moreover, IFN-gamma mRNA expression was more commonly detected than IL-4 expression in PBC livers, and the levels of IFN-gamma mRNA expression were highly correlated with the degree of portal inflammatory activity. IFN-gamma mRNA-positive cells were detected primarily around damaged bile ducts that were surrounded by lymphoid aggregates. The data indicate that Th1 cells are the more prominent T-cell subset in the lymphoid infiltrates in PBC.     

Extrahepatic peribiliary glands express alpha-amylase isozymes, trypsin and pancreatic lipase: an immunohistochemical analysis

We examined expression of alpha-amylase isozymes (pancreatic and salivary), trypsin and pancreatic lipase on the epithelium of extrahepatic peribiliary glands immunohistochemically using 53 autopsied normal extrahepatic bile ducts. Three parts of the extrahepatic bile duct (common bile duct, intrapancreatic bile duct and bile duct at the ampulla of Vater) were examined in each case. Histologically, the extrahepatic bile duct harbored branched tubular glands (extrahepatic peribiliary glands). Extrahepatic peribiliary glands were few in the common bile duct and intrapancreatic bile duct and numerous in the bile duct at the ampulla of Vater. Immunohistochemically, pancreatic alpha-amylase was expressed in the epithelium of extrahepatic peribiliary glands in 42 cases (79%). Salivary alpha-amylase was expressed in the epithelium of the glands in 38 cases (72%). Trypsin was expressed in the epithelium of the glands in 32 cases (60%). Pancreatic lipase was expressed in the epithelium of the glands in 45 cases (85%). The immunoreactivity of these enzymes was granular and located in the supranuclear cytoplasm (corresponding to the Golgi apparatus) of the epithelium of the glands. We confirmed the specificity of the immunoreactivity of these enzymes with various methods. These results suggest that extrahepatic peribiliary glands produce alpha-amylase isozymes, trypsin and pancreatic lipase and secrete these enzymes into lumens of the extrahepatic bile duct. The secreted enzymes may play an important role in the physiology of the extrahepatic bile duct and bile.     

Persistent obstructive jaundice, cholangitis, and biliary cirrhosis due to common bile duct stenosis in chronic pancreatitis

Long strictures of the intrapancreatic portion of the common bile duct were found in 6 patients with chronic pancreatitis. These strictures were responsible for painless obstructive jaundice, recurrent cholangitis, secondary biliary cirrhosis, and chronic abdominal pain difficult to distinguish from that caused by pancreatitis. Endoscopic retrograde cholangiopancreatography and intraoperative cholangiography were invaluable in making the diagnosis and in planning surgical correction. Decompression of the biliary tree by anastomosis of the gallbladder or common duct to the small intestine completely relieved symptoms and allowed liver function to improve significantly. Common duct stricture as a complication of chronic pancreatitis should be considered in the differential diagnosis of extrahepatic biliary obstruction and whenever surgical treatment of chronic pancreatitis is contemplated.