The role of granulomatous phlebitis and thrombosis in the pathogenesis of cirrhosis and portal hypertension in sarcoidosis

F Moreno‐Merlo, I R Wanless, K Shimamatsu, M Sherman, P Greig, D Chiasson – 30 December 2003 – Sarcoidosis often involves the liver with mild elevation of serum enzymes and granulomas histologically. Rarely, chronic cholestasis, portal hypertension, cirrhosis, or nodular hyperplasia may be found. The pathogenesis of the portal hypertension and of the cirrhosis are not understood, in part because large samples of tissue have seldom been described.

A new rat bile ductular epithelial cell culture model characterized by the appearance of polarized bile ducts in vitro

A E Sirica, T W Gainey – 30 December 2003 – The rat treated with bile duct ligation (BDL) and furan is a unique animal model of massive bile ductular hyperplasia in which normal liver parenchyma is largely replaced with well‐differentiated proliferated bile ductules. We have now developed a simple cell isolation procedure to obtain and culture viable bile ductular epithelial cells in high numbers and with a high degree of purity from the livers of BDL/furan‐treated rats.

Effect of lamivudine on morphology and function of mitochondria in patients with chronic hepatitis B

P Honkoop, R A De Man, H R Scholte, P E Zondervan, J W Van Den Berg, L H Rademakers, S W Schalm – 30 December 2003 – Nucleoside analogues can induce mitochondrial dysfunction leading to severe clinical syndromes. Lamivudine, a new nucleoside analogue, is an active inhibitor of hepatitis B viral replication without apparent clinical toxicity. To assess subclinical mitochondrial toxicity, we studied the morphology and function of the mitochondrial system in 15 patients treated with lamivudine.

Association of a tumor necrosis factor promoter polymorphism with susceptibility to alcoholic steatohepatitis

J Grove, A K Daly, M F Bassendine, C P Day – 30 December 2003 – Twin concordance studies suggest that genetic factors play a role in determining why only a minority of heavy drinkers develop hepatitis and cirrhosis. Tumor necrosis factor α (TNF‐α) has emerged as the “final common pathway” in the pathogenesis of alcohol‐related hepatic necro‐inflammation. We have examined the frequency of the two recently described polymorphisms of the TNF‐α promoter in 150 patients with biopsy‐proven alcoholic liver disease and 145 healthy volunteers.

A mutation in the human canalicular multispecific organic anion transporter gene causes the Dubin‐Johnson syndrome

C C Paulusma, M Kool, P J Bosma, G L Scheffer, F ter Borg, R J Scheper, G N Tytgat, P Borst, F Baas, R O Elferink – 30 December 2003 – The human Dubin‐Johnson syndrome (DJS) is a rare autosomal recessive liver disorder characterized by chronic conjugated hyperbilirubinemia. Patients have impaired hepatobiliary transport of non‐bile salt organic anions. A highly similar phenotype has been described for a mutant Wistar rat strain, the transport‐deficient (TR‐) rat, which is defective in the canalicular multispecific organic anion transporter (cmoat).

Effects of the Japanese herbal medicine “Sho‐Saiko‐To” (TJ‐9) on in vitro interleukin‐10 production by peripheral blood mononuclear cells of patients with chronic hepatitis C

M Yamashiki, A Nishimura, H Suzuki, S Sakaguchi, Y Kosaka – 30 December 2003 – “Sho‐saiko‐to” (TJ‐9) consists of 7 herbal components. In Japan, it is widely prescribed to patients with chronic viral liver disease. TJ‐9 is known to suppress liver cancer development and possess macrobiotic effects, but its mode of action is not fully understood.

Early antibody response against hypervariable region 1 is associated with acute self‐limiting infections of hepatitis C virus

A Zibert, H Meisel, W Kraas, A Schulz, G Jung, M Roggendorf – 30 December 2003 – Antibodies directed to hypervariable region 1 (HVR1) of hepatitis C virus (HCV) have recently been shown to neutralize the corresponding HCV isolate in vitro. We analyzed the appearance of antibodies directed to HVR1 during the course of infection in a large group of patients who have been infected by the same isolate of a HCV contaminated anti‐D immunoglobulin (HCV‐AD78).

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