Berend Mets, Rosemary Hickman, Rosemary Allin, Jean van Dyk, Zoe Lotz – 1 April 1993 – The metabolism of lidocaine to monoethylglycinexylidide has been found useful as an indicator of liver function in association with liver transplantation. It has been postulated that this is due to the common effect of hypoxic damage on liver function and lidocaine metabolism. The effects of hypoxia on the elimination of lidocaine and the formation of mono‐ethylglycinexylidide and on indexes of liver function were investigated with the isolated perfused pig liver preparation.

1 April 1993

Yong‐Yuan Zhang, Bengt Göran Hansson, Lin Sheng Kuo, Anders Widell, Erik Nordenfelt – 1 April 1993 – Sera from 410 patients from the Wuhan area in the central part of China with the diagnosis of chronic liver disease were analyzed for markers of hepatitis B, C and D virus infections. All sera, plus liver biopsy specimens from 188 of the patients, were also tested for hepatitis B virus DNA by polymerase chain reaction. Sixty‐eight percent were HBsAg positive in serum, whereas 29% showed markers of past hepatitis B virus infection.

Renée E. Poupon, Khadija Ouguerram, Yves Chrétien, Claudine Verneau, Eveline Eschwège, Thierry Magot, Raoul Poupon – 1 April 1993 – We have previously shown in a 2‐yr controlled trial that hypercholesterolemia, frequent in primary biliary cirrhosis, is lowered by ursodeoxycholic acid (13 to 15 mg daily). To further investigate this effect, we analyzed the influence of long‐term ursodeoxycholic acid administration on serum lipids, lipoproteins and bile acids.

Christine H. Janes, Douglas B. McGill, Jurgen Ludwig, Ruud A. F. Krom – 1 April 1993 – A 3‐yr‐old child underwent biopsy of a nonresectable liver cell adenoma. She was well thereafter, but at the age of 22 yr, she underwent orthotopic liver transplantation because the lesion had grown. The α‐fetoprotein level was 4,300. The specimen showed poorly differentiated hepatocellular carcinoma in a noncirrhotic liver. At this writing, the patient is well 32 mo after transplantation. (HEPATOLOGY 1993;17:583–585.)

Martina Greeve, Linda Ferrell, Michael Kim, Connie Combs, John Roberts, Nancy Ascher, Teresa L. Wright – 1 April 1993 – To examine whether unknown viruses or autoimmune processes contribute to the development of cryptogenic liver disease, we studied 48 patients undergoing liver transplantation who had non‐A, non‐B cirrhosis; non‐blood‐borne cirrhosis of unknown etiology; or autoimmune cirrhosis.

Sylvie Grimbert, Bernard Fromenty, Cecile Fisch, Philippe Letteron, Alain Berson, Anne Marie Durand‐Schneider, Gerard Feldmann, Dominique Pessayre – 1 April 1993 – Severe impairment of the β‐oxidation of fatty acids, as a consequence of a single factor or a combination of different causes, leads to microvesicular steatosis of the liver. In an effort to understand the mechanism(s) leading to the development of acute fatty liver of pregnancy in some women, we determined the effects of pregnancy on the mitochondrial oxidation of fatty acids in mice.

Roger D. Soloway – 1 April 1993

Ned Ballatori – 1 April 1993 – We determined the trans effects of extracellular reduced glutathione (GSH) on the rate of efflux of endogenous labeled GSH from freshly isolated rat hepatocytes. The presence of GSH (10 mM) in the medium significantly stimulated the fractional rate of efflux of [35S]GSH from 5.2 to 12.6%/15 min (p < 0.01). This effect was concentration‐dependent, had sigmoid type of kinetics (D50 of 0.32 mM), and was reversible upon removal of external GSH.

Masahito Minami, Takeshi Okanoue, Etsuro Nakajima, Koichiro Yasui, Keizo Kagawa, Kei Kashima – 1 April 1993 – A defective form of the hepatitis B virus has been found in a patient with chronic type B hepatitis. Sequence analysis of the viral DNA after polymerase chain reaction amplification revealed a 117–base pair deletion (nucleotides 3129–53, subtype adr). This deletion includes the initiation codon of the pre‐S2 region and a newly created in‐frame stop codon in the pre‐S1 region (nucleotide 3055) located 230 base pairs downstream from the pre‐S1 initiation codon.