Hiroki Taoka

S4a + S5 with caudate lobe (S1) resection using the Taj Mahal liver parenchymal resection for carcinoma of the biliary tract.

Recently we have been performing S4a + S5 with total resection of the caudate lobe (SI) by using a dome-like dissection along the root of the middle hepatic vein at the pinnacle, which we refer to as the Taj Mahal liver parenchymal resection, for carcinoma of the biliary tract. This procedure offers the following advantages: (1) It allows total resection of the caudate lobe, including the paracaval portion (S9), and (2) because the cut surface of the liver is large, it allows intrahepatic jejunostomy to be performed more easily with a good field of view. The indications for this procedure include hilar bile duct carcinoma, gallbladder carcinoma, and choledochal cyst (type IVA). Because of the high rate of hilar liver parenchyma and caudate lobe invasion associated with hilar bile duct carcinoma, the liver must be resected. The Taj Mahal procedure is indicated in cases where extended liver resection is impossible. The dissection limits of this procedure are, on the left side, the B2 + 3 bifurcation at the right margin of the umbilical portion of the portal vein and, on the right side, the B8 of the anterior branch and the B6+7 bifurcation of the right posterior branch. This procedure could also be described as a reduced form of extended right hepatectomy and extended left hepatectomy. For gallbladder carcinoma, this procedure is indicated to ensure an adequate surgical margin and eradicate transvenous liver metastasis, particularly in cases of pT2 lesions. Hilar and caudate lobe invasion also occurs in liver bed-type gallbladder carcinoma, and bile duct resection and caudate lobe resection are required for the surgery to be curative. We performed this procedure in four cases of hilar bile duct carcinoma, five cases of gallbladder carcinoma, and one case each of choledochal cyst (type IVA) with carcinoma of the bile duct and gallbladder adenomyomatosis. Curative resection was possible in all except the patient with adenomyomatosis, and all of the patients are alive and recurrence free 10 to 37 months postoperatively. This procedure, in addition to preserving liver function, provides a wide field of view and facilitates reconstruction of multiple intrahepatic bile ducts. Thus it can be said to be a curative operation not only in patients considered high risk but also in those whose hilar bile duct carcinoma is limited to the bifurcation area (Bismuth type IIIa and IIIb) and in gallbladder carcinoma up to pT2 with slight extension on the hepatic side.

Experimental study on the pathogenesis of acute acalculous cholecystitis, with special reference to the roles of microcirculatory disturbances, free radicals and membrane-bound phospholipase A2.

SummaryTo elucidate the pathogenesis of acute acalculous cholecystitis, the gallbladder was subjected to ischemia-reperfusion by simultaneously occluding the middle hepatic artery and the superior mesenteric vein in dogs, and the degree of inflammation and biochemical changes in the gallbladder mucosa were studied by varying the duration of ischemia or reperfusion. Ischemia alone did not induce cholecystitis either macroscopically and histologically, although it increased phospholipase A2 (PIA2) activity, content of lipid peroxide, and Superoxide dismutase (SOD) activity in the mucosa with prolongation of the ischemic time. Cholecystitis was produced in all animals by 45-min ischemia followed by 90-min reperfusion as the shortest ischemia and reperfusion times. In this model, prolongation of the ischemic time increased the area of mucosal inflammation horizontally with increases of the PIA2 activity, content of lipid peroxide, and SOD activity, whereas by prolonging the reperfusion time the inflammation area spread deeper vertically toward the serosal side with significant increase in the mucosal PIA2 activity, content of lipid peroxide, and SOD activity. These results revealed that ischemia-reperfusion plays an important role in the pathogenesis of acute acalculous cholecystitis, causing the generation of free radicals and the activation of membrane-bound PIA2.

Surgical Treatment of Hilar Bile Duct Carcinoma: Experience With 25 Consecutive Hepatectomies

To evaluate our recent surgical policy regarding hilar bile duct carcinoma, we evaluated 62 cases treated between 1976 and 1993, and 25 cases treated between 1994 and 2000. In the late period we used percutaneous transhepatic portal vein embolization (PTPE) before extended right hepatectomy; S4a + S5 + S1 hepatectomy for elderly patients and those with poor liver function; and routine total caudate lobectomy including the paracaval portion and resection of the inferior portion of the medial segment (S4a). Sixtyfive (74.7%) of the 87 patients underwent hepatectomy: 40 in the early period and 25 in the late period. Bile duct resection alone was performed in 22 patients, all in the early period. Resection was curative in 54.8% in the early period and 88.0% in the late period. The 3- and 5-year survival rates in the early period were 27.1% and 20.2%, respectively, as compared to 59.9% and 49.9% in the late period. Analysis of the 25 hepatectomies in the late period revealed improved survival times compared to patients treated by PTPE with extended right hepatectomy. No complications occurred after extended left hepatectomy or S4a + S5 + S1 hepatectomy, but four patients (16%) who underwent extended right hepatectomy plus PTPE died postoperatively. Our policy has resulted in improved outcome in patients with hilar bile duct carcinoma.

A report of 5 cases of cystic bile duct carcinoma of the liver and proposal of a new classification.

SummaryPrimary biliary cystadenocarcinoma of the liver is rare. Among 239 patients with primary liver cancer admitted to our service during the last 13 years, there were 5 cases of cystic bile duct carcinoma of the liver. Three of these were cystadenocarcinoma, one was adenocarcinoma arising from a liver cyst, and one was carcinoma of the intrahepatic bile ducts with cystic dilatation. A better classification of these entities seems necessary, and it is suggested that malignant cystic tumors of the liver should be divided into 3 groups: Group A is cystic adenocarcinoma, group B is bile duct carcinoma with primary or secondary intrahepatic bile duct, and group C is degenerative cyst formation by other types of malignant tumors. Cystic adenocarcinoma (Group A) can then be further subdivided into cystadenocarcinoma, cystadenocarcinoma with cystadenoma, and carcinoma in a simple cyst of the liver.

A new classification of cystic malignant tumours of the liver: classification of 65 cases reported at the 26th annual meeting of the Liver Cancer Society of Japan.

Reports of liver cancers which appear cystic have increased recently. However, the term ‘cystadenocarcinoma’ has sometimes been misused, and reports have included both carcinomas occurring in a simple cyst of the liver and bile duct carcinomas with intrahepatic bile duct dilatation. Some have also been confused with cystadenocarcinoma originating from a cystadenoma. Therefore, an improved classification of these tumours is necessary. Our new classification of cystic malignant turnours of the liver was used to classify 65 cases, including our own 5, that were reported at the 26th Annual Meeting of the Liver Cancer Society of Japan in June 1990.’’* Cystic malignant liver tumours were one of the main themes of this meeting, at which most papers were presented as posters.

Histopathological studies of mucin-producing carcinoma of the bile duct

Mucin-producing carcinoma (MPC) of the bile duct produces large amounts of mucin. As many aspects of the characteristic biological pattern of invasion and origin of this tumor are unclear, we investigated its pathological molecular biology and association with peribiliary glands. Molecular biologically, MPC with multiple tumors had a higher tumor proliferation potency than MPC consisting of a single tumor. Even multiple tumors with high malignant potential showed little evidence of lymphatic invasion, and there was little venous or perineural invasion. Findings in regard to the peribiliary glands (PGs) suggested that PGs are involved in the origin and extension of MPC. Mucinous PGs under the main tumor were exhibited beneath the dysplasia and non-neoplastic epithelium, whereas mucinous PGs under MPC with multiple tumors contained neoplastic cells. PGs secreted large quantities of mucin. We conclude that neoplastic cells in PGs caused cell proliferation toward the bile duct lumen.

Administration of branched chain amino acids prevents bacterial translocation after liver resection in the cirrhotic rat

After major liver resection, bacterial infectious complications, including sepsis and endotoxemia, can be at least in part, attributed to translocation of enteric bacteria and endotoxin. We evaluated the effectiveness of the enteral and parenteral administration of branched-chain amino acids (BCAA) in preventing bacterial translocation after 70% liver resection in rats with thioacetamide-induced-cirrhosis. Bacterial translocation after hepatectomy was induced by a disturbance of protein metabolism in intestinal epithelial cells. However, the administration of BCAA, particularly via the enteral route, improved amino acid metabolism in the gut and stimulated the synthesis of nonsecreted protein and the proliferation of crypt cells, thereby preventing bacterial translocation after liver resection. Improvement in this cascade of metabolic reactions is believed to have been responsible for the improved outcome after extensive resection of the cirrhotic liver.

Abstracts of Selected Papers Presented at the 31st Annual Meeting of the Japanese Society of Gastroenterology

S OF SELECTED PAPERS PRESENTED AT THE 31ST ANNUAL MEETING OF THE JAPANESE SOCIETY OF GASTROENTEROLOGY October 5-7, 1989, Asahikawa, Japan Chairman: Masayoshi NAMIKI, M.D.