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Portal hypertension occurs in a number of disorders other than cirrhosis and they are collectively called non-cirrhotic portal hypertension (NCPH). The common causes of NCPH include idiopathic portal hypertension (IPH), non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal venous thrombosis (EHPVT). Other causes include schistosomiasis, hepatic venous outflow tract obstruction, veno-occlusive disease and congenital hepatic fibrosis. Patients with IPH and EHPVT present with upper gastrointestinal bleeding, splenomegaly, ascites after gastrointestinal bleeding, features of hypersplenism, growth retardation and jaundice due to portal biliopathy. The diagnosis is usually made by abdominal ultrasound, upper gastrointestinal endoscopy, normal liver function tests and normal liver histology. Variceal bleeding in NCPH has lower mortality as compared with cirrhosis because of better liver functions in NCPH. Treatment for NCPH includes primary prophylaxis for variceal bleeding and prevention of repeat bleeding using drugs like β-blockers, endoscopic sclerotherapy and endoscopic band ligation of varices. In patients with uncontrolled variceal bleeding or symptomatic hypersplenism, porto-systemic shunt surgery or splenectomy are required. [ABSTRACT FROM AUTHOR]

Abstract An attempt is made in this review to update the reader on recent developments and progress in the study of cholangiocarcinoma: a major primary carcinoma of the liver with a very poor prognosis. Knowledge of the cell biology and physiological functions of the cholangiocyte has recently so progressed that our understanding of cholangiocarcinogenetic mechanism is expected to follow. The first part of the review deals with semantic problems, temporal changes in the incidence of cholangiocarcinoma and geographic differences in epidemiology, etiologic factors (particularly opistorchiasis in Thailand and hepatolithiasis in the Far East), and discusses a recently disclosed role of hepatitis C virus infection (30% of cholangiocarcinoma patients have antibodies against hepatitis C virus in Japan). [ABSTRACT FROM AUTHOR]

Abstract Part 2 of this review discusses DNA damage in biliary epithelial cells in the development of cholangiocarcinoma, alterations in cell kinetics of biliary epithelial cells, biliary epithelial mitoinhibition, and apoptosis that includes the role of Bcl-2 , transforming growth factor-β, telomerase activities and deregulation of Ras and p53 , cancer-associated antigens in cholangiocarcinoma, precancerous lesions, stroma formation and angiogenesis, cancer invasion, cell–cell and cell–matrix interactions, and the mechanism of evasion from immune surveillance. These discussions are followed briefly by treatments such as photodynamic therapy, and surgical approaches comparing resection and liver transplantation. [ABSTRACT FROM AUTHOR]

Abstract Background and Aims: Studies of the hepatic artery are scarce. We have observed that hepatic artery calcification is very uncommon in patients with hyperparathyroidism that expedites calcification. Methods: Plain abdominal CT was studied in 221 patients on chronic hemodialysis. Control consisted of 442 sex- and age-matched patients with other diseases. Calcification was graded as a percentage of the entire wall circumference for the aorta, and as a percentage of the entire length of the hepatic and splenic arteries from the celiac trunk to the hilum of each organ. Results: Aortic calcification was seen in 79.2% of male dialysis patients, 22.1% of controls, 74.1% of female dialysis patients and 17.3% of controls (P < 0.0001). Hepatic artery calcification was seen in only 13 dialysis patients. The degree of calcification of the abdominal aorta was correlated with the length of hemodialysis period (P = 0.008), but not with serum calcium, serum phosphate or their product. Although serum parathormone levels were not correlated with calcification, seven of eight dialysis patients with hepatic artery calcification had very high parathormone levels. Conclusions: The hepatic artery is far less frequently calcified than are the abdominal aorta and splenic artery. This may be a teleologic phenomenon of the liver. [ABSTRACT FROM AUTHOR]

Editorial. Discusses why non-cirrhotic portal hypertension is common in India. Etiologic factors; Distinction between non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal obstruction; Problem related to whether idiopathic portal hypertension and NCPF represent undiagnosed intrahepatic portal thrombosis.

Confusion prevails throughout the world regarding the definition and classification of the Budd-Chiari syndrome. The original patients (Budd and Chiari) described had hepatic vein thrombosis, but this syndrome now encompasses various hepatic venous outflow blocks, of which membranous obstruction of the inferior vena cava (IVC) is the most common. This author has been suggesting that the classical Budd-Chiari syndrome or hepatic vein thrombosis and membranous obstruction of IVC or primary thrombosis of IVC at its hepatic portion are epidemiologically, pathologically and clinically different, and that they should be treated as two clinical entities that are not to be mixed. The two diseases have a different onset, different clinical manifestations and a different natural history. Whereas hepatic vein thrombosis is a severe disease with an acute onset, IVC thrombosis presents mildly at onset, but it recurs and eventually turns into a fibrous occlusion of IVC of varying thickness or stenosis of a various degree. The fibrous IVC occlusion is found as a mysterious thin membrane, but is more often much thicker than a membrane, and therefore 'membrane' is a misnomer. Although the genesis is not established, formation of a thin membrane may be an outcome of recurrent thrombosis. The past congenital vascular malformation theory no longer holds, because the disease occurs mostly in adulthood, and transformation of thrombosis into a membrane has now been well documented pathologically as well as clinically. This author suggests that a term 'obliterative hepatocavopathy' replace membranous obstruction of IVC, the term 'Budd-Chiari syndrome' be abandoned, and that primary hepatic venous outflow block be divided into primary hepatic vein thrombosis and primary IVC thrombosis (obliterative hepatocavopathy). [ABSTRACT FROM AUTHOR]

AbstractBackground: The TT virus (TTV), a new DNA virus found in Japan from a patient with post-transfusion hepatitis non-A–non-G, is frequently positive in the sera of patients with liver disease. It is not established whether this virus causes liver damage. We studied the frequency of superinfection of this virus and hepatitis C virus (HCV) known to be endemic among haemodialysis patients, and the possible deleterious effect of TTV on HCV-induced chronic liver disease. Methods: We used primers from a conservative region in the TTV genome (Okamoto, 1998) to detect TTV. Sera from 163 dialysis patients positive for anti-HCV and 77 dialysis patients negative for anti-HCV (control) were tested. Results: TT Virus positivity was 35% among HCV antibody (anti-HCV)-positive patients and 45.4% among anti-HCV-negative patients. TT Virus positivity was unrelated to the length of haemodialysis or amounts of blood the patients had received in the past. More anti-HCV-positive patients had a history of transfusion, but TTV positivity was not as closely associated with transfusion as anti-HCV positivity. The severity of chronic liver disease was estimated from peak serum alanine aminotransferase levels in the preceding 6 months. Among anti-HCV positives, TTV-positive patients tended to have less active disease; at least there was no indication that TTV superinfection aggravated chronic hepatitic C in long-term dialysis patients. Four of 35 anti-HCV-negative, TTV-positive patients had chronic active liver disease, while none of the anti-HCV-negative and TTV-negative patients did. Conclusions: TT Virus infection is prevalent among haemodialysis patients. Its transmission occurs not only by blood transfusion, but also by non-parenteral infection. Superinfection of TTV does not exert deleterious effects on the liver disease induced by HCV. However, it may cause chronic hepatitis in a limited number of patients, but remains dormant most of the time. Triple infection, HCV and TTV plus HBV or HGV (one case each), did not cause severe liver disease. [ABSTRACT FROM AUTHOR]

This review describes the early chronological events in the pursuit of a treatment for pernicious anaemia, and the subsequent discovery of vitamin B[sub 12] and the intrinsic factor. It details Castle’s experiments which established the theory of extrinsic and intrinsic factors as hemopoietic principles, and describes the studies on purification of the anti-pernicious anaemia principle from liver tissue that terminated in the crystallization of vitamin B[sub 12] and identification of its coenzyme forms. Biochemical purification and characterization of the intrinsic factor secreted by the gastric parietal cells, and two other vitamin B[sub 12] proteins, R-binder (transcobalamin I, haptocorrin), and transcobalamin II, are discussed in detail. The biochemical reactions in micro-organisms and humans in which vitamin B[sub 12] is involved are then briefly reviewed, and finally and briefly the immunological basis of pernicious anaemia is discussed. [ABSTRACT FROM AUTHOR]

Editorial. Examines the peripheral type of cholangiocarcinoma (CC) treated surgically. Differences in clinical features between hilar and peripheral CC; Association of hepatolithiasis with peripheral CC; Relationship between intrahepatic and extrahepatic cholethiasis.

Presents a letter to the editor about a case reporting investigated fat droplets around the liver and spleen of a patient who developed acute renal failure, published in the October 1, 2003 issue of the Journal of Gastroenterology and Hepatology.

Focuses on hepatitis studies in Japan. History of epidemics of catarrhal jaundice; Separation of catarrhal jaundice and homologous serum jaundice.

Abstract The natural history of hepatocellular carcinoma (HCC) varies greatly with the global region, because the carcinogenic factors are not the same among countries. Besides the clinicopathological factors such as tumor characteristics, sex, and age, background liver disease is a major determinant of prognosis. Hepatocellular carcinoma, mainly associated with chemical carcinogens such as aflatoxin, does not have severe background cirrhosis, and grows quickly, whereas HCC developing in association with a virus in a cirrhotic liver generally grows more slowly, and the severity of cirrhosis is the major prognostic factor. The median survival of untreated sub-Saharan African patients is less than 1 month from diagnosis, contrasted by an average survival of 4 months in virus-induced HCC associated with cirrhosis. Tumor characteristics, such as size, number, and growth speed, which vary considerably from case to case, affect the prognosis. Vascular (portal) invasion portends a poor prognosis, and α-fetoprotein levels also correlate with prognosis. Several distinct clinical types of HCC occur, namely diffuse-type HCC caused by rapid portal spread of cancer cells, febrile-type caused by poorly differentiated sarcomatoid cancer cells, and cholestatic HCC caused by intraductal invasion; all have a short survival. There are several histological variant forms: combined hepato-cholangiocarcinoma behaves like HCC, with a poorer prognosis because of more frequent lymph node metastases; fibromellar carcinoma, which is relatively common in young Caucasian adults, has a good prognosis if diagnosed early, permitting resection; and cholangiolocellular carcinoma, which derives from the canalicular epithelium, is indistinguishable from HCC, with a similar prognosis. © 2002 Blackwell Publishing Asia Pty Ltd. [ABSTRACT FROM AUTHOR]

Abstract Aims: The early stage of hepatocarcinogenesis is not well understood pathologically and clinically. The present study was designed to define small (early) hepatocellular carcinoma (HCC) angiographically using the angio-helical computed tomography (CT) system. Methods: Arterial portography CT and hepatic arteriography CT were carried out in 29 patients in whom small HCC ≤ 20 mm was detected during follow-up. Results: There were 17 males and 12 females, aged 47 to 85 years. The offending virus was hepatitis B in four, hepatitis C in 24 and no virus marker in one case. The follow-up period varied from less than a year to 17 years, averaging 6.4 years. The underlying disease was cirrhosis in 12 and chronic hepatitis in 17 cases. The mass was solitary in 16 and multiple in 13 cases, while the size of the mass ranged from 8-20 mm. All lesions were low in attenuation on arterial portography CT, and in 23 of 30 lesions hepatic arteriography CT showed high attenuation, suggesting arterial blood supply. In the remaining 7 cases, lesions were perhaps in the transition from portal to arterial. Conclusions: It was concluded that HCC develops frequently in a liver with chronic hepatitis, often muticentrically, and that early HCC lesions are more often overt HCC already with arterial blood supply, rather than extremely well-differentiated supplied by the portal vein as generally believed. [ABSTRACT FROM AUTHOR]

Abstract Background and Aim: Gastric varices, the rupture of which can be a fatal complication of portal hypertension, have not been well documented histopathologically. While cardiac varices develop in continuity with esophageal varices, fundic varices develop independently, having characteristic pathophysiology. Elucidation of the angioarchitecture of fundic varices will facilitate future improvement of treatment. Methods: Twelve stomachs with fundic varices, either resected or autopsied, were examined by injecting a barium-gelatin solution into the vein that was forming varices, soft X-rayed for the study of the vessel course, and then the stomach made into transparent preparations for stereoscopic study. Five fundic varices with a recognizable rupture site were studied histologically. Results: Fundic varices could be classified into two types: Type I, single vein forming the supplying vessel, varix and draining vessel without changing caliber (eight cases) or plural veins supplying the varix (one case) and; Type II, many branching vessels existing beside the main supplying and draining vessels (three cases). Fundic varices exist in the submucosa with no enlarged vein in the lamina propria, and rupture occurs through the portion of the varix that protrudes into the stomach lumen penetrating the muscularis mucosae and lamina propria. Conclusions: Fundic varices form with the supplying vessel, mostly singular, and the draining vessel is frequently a gastrorenal collateral. Fundic varices form in the submucosa, unlike esophageal varices, and perforate through the overlying muscularis mucosae and lamina propria. [ABSTRACT FROM AUTHOR]

Presents a diagnostic image of an enhanced lesion in the liver of a 61-year-old woman with a history of cirrhosis due to chronic hepatitis C virus infection. Location of the hepatocellular carcinoma upon initial detection; Laboratory findings.

Information on several conference papers are presented from the International Symposium on Hepatology in Beijing, China from December 5-9, 1999. Extrahepatic manifestations of cholestasis include pruritus, fatigue, osteoporosis, and cholangiocellular carcinoma, which develops when the epithelium of the intrahepatic bile duct invades the liver. Transplantation of patients with cholestatic liver disease showed good results with few chances to recurring in the graft.

Chronic hepatitis B infection is a serious health threat in the Asia–Pacific area. A consensus meeting on the treatment of chronic hepatitis B infection was conducted in Hong Kong, in August 1997. It was generally agreed that treatment of chronic hepatitis B infection should be based on the understanding of the natural history of chronic hepatitis B infection. To date, interferon α is the only Food and Drug Administration (FDA)-approved form of therapy for chronic hepatitis B infection. The overall response in Asian patients is unsatisfactory: approximately 15–20% will clear hepatitis B e antigen, but less than 5% will clear hepatitis B surface antigen. Newer immunomodulatory therapies are under trial. In contrast, nucleoside analogues, such as lamivudine (pending FDA approval) and famciclovir, have been shown to be potent suppressors of hepatitis B viral replication; however, their role as monotherapy in the treatment of chronic hepatitis B infection remains to be defined. Also, the issues of resistance to nucleoside analogues and withdrawal rebound need to be carefully studied. The future direction of therapy in chronic hepatitis B infection is probably a combination of nucleoside analogues or nucleoside analogues with immunomodulatory therapy. [ABSTRACT FROM AUTHOR]

To study the effects of habitual alcohol intake and cigarette smoking on the latency period for the development of hepatocellular carcinoma (HCC), 455 patients with HCC were analyzed with respect to age at diagnosis. They were divided into hepatitis B virus (HBV) positive and negative patients based on HbsAg and high titer anti-HBc in serum. HBV-positive and negative HCC patients were further subdivided into four subgroups based on the history of drinking more than one small bottle of Japanese 'sake' or its equivalent per day for more than 10 yr and the history of smoking more than one cigarette per day for more than 10 yr. Among HBV-positive HCC patients, the average age of those with a drinking and a smoking habit (50 ± 10 yr) was younger compared with that of patients with a drinking habit but without a smoking habit (56 ± 14 yr, not significant, NS), of those who were smokers and nondrinkers (55 ± 10 yr, NS) and of those who did not drink nor smoke (59 ± 8 yr, p < 0.005). Among HBV-negative HCC patients, patients with drinking and smoking habits (57 ± 9 yr) were younger compared with those with a drinking habit without smoking (59 ± 9 yr, NS), those who were smokers and nondrinkers (62 ± 9 yr, p < 0.005), and those who were nondrinkers and nonsmokers (63 ± 12 yr, p < 0.005). These data suggest that habitual alcohol intake may promote the development of HCC if the patients smoke cigarette regardless of the status of HBV seromakers. [ABSTRACT FROM AUTHOR]

Focuses on the proposal of the International Association for the Study of the Liver Subcommittee on changes in classification of liver failure. Benefits of the proposal; Definition of fulminant hepatic failure; Reasons for the need for modifications; Details of the proposed nomenclature and classification.