Cases reported "Cholestasis"

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1/85. Villous adenoma of the bile ducts: a case report and a review of the reported cases in korea.

    Villous adenomas are benign epithelial lesions with malignant potential which can occur at any site in the gastrointestinal tract. They are usually encountered in the rectum and colon, less frequently in the small bowel and very rarely in the biliary trees. Nine cases of bile duct villous adenomas have been reported in the literature. However, 4 cases of bile duct villous adenomas have been reported in the Korean literature. Recently, we experienced a case of villous adenoma in the common hepatic duct in a 77-year-old man presenting with obstructive jaundice in which preoperative histologic diagnosis of villous adenoma played a critical role in managing this patient. Herein, we present a case report of bile duct villous adenoma and a review of the reported cases in korea to help define and manage this rare disease entity in the bile ducts. In addition, confusing nomenclature of bile duct adenomas is discussed.
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2/85. Mucobilia in association with a biliary cystadenocarcinoma of the caudate duct: a rare cause of malignant biliary obstruction.

    Mucobilia is a rare condition characterized by the accumulation of abundant mucus within the intra- or extrahepatic biliary tree. A variety of hepatobiliary and pancreatic neoplasms are mucin producing and have been associated with the development of mucobilia including biliary mucinosis, biliary papillomatosis, mucin-producing cholangiocarcinoma (MPCC), or cystic neoplasms of the pancreas or biliary tree (cystadenoma or cystadenocarcinoma). We report the case of 46 year-old male with a biliary cystadenocarcinoma of the caudate lobe which resulted in chronic biliary obstruction and relapsing cholangitis. A review of the literature for both mucobilia and biliary cystadenocarcinoma is provided along with a discussion addressing the clinical presentation, diagnosis, treatment, and prognosis for this rare entity.
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3/85. Obstructive jaundice caused by hepatocellular carcinoma: detection by endoscopic sonography.

    Tumor thrombus in the extrahepatic biliary tree is a rare mechanism of obstructive jaundice. We present a patient with a minute hepatocellular carcinoma in the caudate lobe that invaded the common hepatic duct and caused biliary obstruction. Endoscopic sonography showed a tumor thrombus with central echogenicity and a "nodule-in-nodule" pattern and suggested the correct diagnosis.
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4/85. Pseudoaneurysm of the gastroduodenal artery as a cause of obstructive jaundice.

    A 35-year-old man presented to our emergency room with asymptomatic jaundice. A physical exam revealed a palpable mass with audible bruit in the epigastrium. Total serum bilirubin was 21.7 mg%. A real time sonography/Doppler examination showed widening of the biliary tree (common bile duct diameter of 13 mm) and a mass in the pancreatic head with turbulent flow. Arteriography of the celiac axis revealed a pseudoaneurysm of the gastroduodenal artery. A ligation of the gastroduodenal artery was performed surgically, and the aneurysmal cavity was explored and emptied. An intraoperative cholangiography showed slight stenosis of the common bile duct distally, and so a choledochojejunostomy was performed. The patient's recovery was uneventful. A follow-up angiogram revealed the short stump of the gastroduodenal artery and no aneurysm or extravasation of dye. A follow-up ultrasound showed the common bile duct measuring 5.5 mm. The bilirubin level dropped to normal values. The patient was discharged on 12 days after surgery. Ten months following surgery he was doing well. The pathology, diagnosis, and treatment of such cases are briefly discussed.
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5/85. Endoscopic removal of ascaris lumbricoides from the biliary tract as emergency treatment for acute suppurative cholangitis.

    ascariasis is the most common intestinal helminthiasis worldwide. Heavily infected individuals are prone to develop bowel obstruction or perforation as well as biliary disease. Nevertheless, the presence of roundworms in the biliary tree outside endemic areas is very uncommon. The migration of these worms to the biliary system can cause biliary colic, pancreatitis, or even acute suppurative cholangitis with hepatic abscesses and septicemia.We report here on 2 infants with 14 and 15 months and a 9-year-old boy who suffered from massive biliary ascariasis and who presented with acute suppurative cholangitis. All cases were successfully treated by endoscopic retrograde cholangiopancreatography with worm extraction and adjuvant medical therapy.physicians should be aware of ascariasis in patients with pancreatobiliary symptoms who have traveled to endemic areas or in immigrants from these areas.
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6/85. Portal biliopathy.

    Herein we describe a case of obstructive jaundice and cholangitis originating from choledochal lithiasis secondary to a stricture of the common bile duct in a patient with cavernous transformation of the portal vein. In fact, portal cavernous transformation gives rise to many dilated pericholedochal and periportal collaterals that bypass the portal vein obstruction. Extrinsic compression of the common duct by dilated venous collaterals together with pericholedochal fibrosis from the inflammatory process causing portal thrombosis may lead to biliary stricture and dilatation of the proximal biliary tree. This condition sometimes causes the formation of secondary biliary stones and cholangitis. Treatment in our case could not be accomplished by a biliodigestive anastomosis because the patient suffered from a short bowel syndrome subsequent to extensive ileal resection for splanchnic venous thrombosis. We repeatedly attempted stone removal during endoscopic retrograde cholangiopancreatography (ERCP) but finally resorted to a percutaneous transhepatic approach, which permitted removal of the stones and treatment of the stricture by pneumatic dilatation. The patient remains well 3 years after the procedure and has shown no signs of jaundice or cholangitis.
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7/85. Acute cholestatic hepatitis associated with celecoxib.

    OBJECTIVE: To report a case of acute cholestatic hepatitis associated with the selective cyclooxygenase-2 inhibitor celecoxib. CASE SUMMARY: A 41-year-old white man was hospitalized for jaundice after 2 doses of celecoxib 200 mg for pain associated with right-knee trauma. Laboratory workup showed hyperbilirubinemia, mildly elevated serum transaminase concentrations, and cholestasis. Abdominal imaging showed no dilation of the biliary tree. histology showed cholestasis, with bile plugs in dilated bile canaliculi and a mild portal infiltrate that are highly suggestive of drug-induced cholestasis. DISCUSSION: This is the fourth report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient. CONCLUSIONS: Cholestatic hepatitis is a well-recognized adverse effect of several drugs. Although celecoxib is considered to have a very low potential for hepatic toxicity, well-documented reports of adverse reactions can contribute significantly to the definition of more accurate safety profiles for new drugs introduced into clinical practice.
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8/85. Surgical management of a hydatid cyst of the hepatic dome ruptured into the biliary tree.

    Hydatid disease of the liver remains an important and challenging medical problem. Although surgery is considered the treatment of choice for hydatid disease of the liver, controversies still exist about the preferred operative technique. We report the case of a patient with obstructive jaundice caused by rupture of a hydatid cyst of the hepatic dome into the biliary tract. He was managed by a new surgical approach of myoplasty of the right hemidiaphragm combined with preoperative decompression of the bile duct by an endoscopic sphincterotomy. The postoperative course of the patient was uneventful, and he remains well 3 years later. This procedure is simple, requires less time, and has the advantage of avoiding a thoracoabdominal incision, which makes any abdominal reoperation easier.
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9/85. Idiopathic cholangiopathy in a biliary cast syndrome necessitating liver transplantation following head trauma.

    The development of total biliary casts is very unusual, especially in patients who have not undergone liver transplantation. The aetiology of these casts is uncertain but several factors are believed to play a role, including periods of fasting, haemolysis, cholangitis and recent surgery. Resultant bile stasis and/or gallbladder hypocontractility promote sludge and subsequent stone formation. Here we present the case of a previously well 66-year-old woman who developed a total biliary cast several weeks after being involved in a road traffic accident during which she sustained head injuries but no obvious liver insult. This cast was removed at laparotomy but the patient had resultant diffuse biliary tree abnormalities and persistent cholestasis and subsequently required a liver transplant. The possible aetiologies of biliary cast formation and subsequently cholangiopathy necessitating transplantation in this patient are described.
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10/85. Complete bile duct sequestration after liver transplantation, caused by ischemic-type biliary lesions.

    Ischemic-type biliary lesions (ITBLs) are the most frequent cause of nonanastomotic biliary strictures in liver grafts, affecting about 2-19 % of patients after liver transplantation. ITBL is characterized by bile duct destruction, subsequent stricture formation, and sequestration. We report here the case of a patient affected by extremely severe ITBL, with sequestration and disintegration of the entire bile duct system, in which it was possible to extract the complete biliary tree endoscopically in a single piece. Histological examination revealed that all cells of the bile duct wall had been destroyed within 3 months after liver transplantation and replaced by connective tissue. Subsequently, biliary stricture formation occurred at the hepatic hilum, as well as the adjacent large bile ducts. It may be hypothesized that cellular rejection of small bile ducts leads to the vanishing bile duct syndrome, whereas cellular rejection of large bile ducts results in ITBL. The strictures were repeatedly dilated by endoscopic means, allowing successful control of stricture formation, as well as maintenance of liver function. At the time of writing, the grafted organ and the patient had survived for more than 3 years in good health. This is the first detailed report on a sequestration of the entire bile duct system caused by ITBL, successfully treated for several years by endoscopic means.
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