Fulminant hepatitis in patients undergoing liver transplantation: Evidence for a non‐A, non‐B, non‐C, non‐D, and non‐E syndrome

M. Lucia Ferraz, A. Eduardo Silva, Graeme A. Macdonald, Sergei A. Tsarev, Adrian M. Di Biscelgie, Michael R. Lucey – 1 January 1996 – Fulminant hepatic failure (FHF) in the absence of serum markers of hepatitis A (HAV) or B (HBV) infection or another cause is called non‐A, non‐B (NANB) FHF. The pathogenetic role of viral infection in NANB FHF remains controversial. To better define this relationship, we studied patients who underwent orthotopic liver transplantation (OLT) for FHF. Thirty‐six patients with FHF underwent transplantation between 1987 and 1992.

Autoantibodies from patients with primary biliary cirrhosis recognize a region within the nucleoplasmic domain of inner nuclear membrane protein LBR

F Lin, C M Noyer, Q Ye, J Courvalin, H J Worman – 1 January 1996 – Autoantibodies from rare patients with primary biliary cirrhosis (PBC) recognize LBR, or lamin B receptor, an integral membrane protein of the inner nuclear membrane. Human LBR has a nucleoplasmic, amino‐terminal domain of 208 amino acids followed by a carboxyl‐terminal domain with eight putative transmembrane segments. Autoantibodies against LBR from four patients with PBC recognized the nucleoplasmic, amino‐terminal domain but not the carboxyl‐terminal domain.

Impaired bile flow and disordered hepatic calcium homeostasis are early features of halothane‐induced liver injury in guinea pigs

L Frost, J Mahoney, J Field, G C Farrell – 1 January 1996 – To characterize the early events in liver injury produced by halothane, experiments were performed in genetically susceptible guinea pigs 19 hours after halothane exposure. Serum bile acid concentrations were fourfold increased in halothane‐exposed animals compared with controls. In isolated perfused liver experiments, livers from halothane‐exposed animals did not differ in hepatic oxygen uptake or in perfusion pressure at the end of experiments, but bile flow and biliary bile salt concentrations were reduced.

Selective inhibition of the reverse transcription of duck hepatitis B virus by binding of 2′,3′‐dideoxyguanosine 5′‐triphosphate to the viral polymerase

A Y Howe, M J Robins, J S Wilson, D L Tyrrell – 1 January 1996 – Hepatitis B virus (HBV) replication is mediated by the viral polymerase that possesses three functional domains: primer, DNA polymerase/reverse transcriptase, and RNase H. Using the Pekin duck as an animal model, we demonstrate a novel mechanism of inhibition of duck hepatitis B virus (DHBV) by 2,6‐diaminopurine 2′,3′‐dideoxyriboside (ddDAPR), a prodrug of 2′,3′‐dideoxyguanosine (ddG).

Bacterial translocation in acute liver injury induced by D‐ galactosamine

F B Kasravi, L Wang, X Wang, G Molin, S Bengmark, B Jeppsson – 1 January 1996 – Acute liver injury is associated with a high rate of infectious and septic complications. Most of these infections are produced by gram negative enteric bacteria. We evaluated bacterial translocation, intestinal permeability, blood flow, portal pressure, and intestinal microflora after induction of liver injury and 70% liver resection in the rat.

Prostaglandins modulate the responsiveness of the gastric microcirculation of sodium nitroprusside in cirrhotic rats

J Geraldo, P Ferraz, J L Wallace – 1 January 1996 – Cirrhotic rats have an increased susceptibility to ethanol‐induced gastric injury, related to an inability to mount a defensive gastric hyperemic response to luminal irritants, and associated with an impaired reactivity of the gastric microcirculation to nitric oxide (NO)/cyclic guanosine monophosphate (cGMP)‐dependent vasodilators. Whether this hyporesponsiveness is in some way related to depressed prostaglandin synthesis by the stomach of cirrhotic rats is not clear.

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