Margaret F. Bassendine, S. J. Yeaman – 1 March 1992

Satoru Todo, Thomas E. Starzl, Andreas Tzakis, Keith J. Benkov, Frantisek Kalousek, Takeyori Saheki, Kyuichi Tanikawa, Wayne A. Fenton – 1 March 1992 – Hyperammonemia, abnormalities in plasma amino acids and abnormalities of standard liver functions were corrected by orthotopic liver transplantation in a 14‐day‐old boy with carbamyl phosphate synthetase‐I deficiency and in a 35‐yr‐old man with argininosuccinic acid synthetase deficiency. The first patient had high plasma glutamine levels and no measureable citrulline, whereas citrulline values were markedly increased in Patient 2.

Patricia Sheiner, Wilfred de Majo, Gary A. Levy – 1 March 1992 – Background. When administered early after an overdose of acetaminophen, intravenous acetylcysteine prevents hepatic necrosis by replenishing reduced stores of glutathione. How acetylcysteine improves the survival of patients with established liver damage induced by acetaminophen, however, is unknown. This study was undertaken to determine whether the beneficial effect of acetylcysteine under such circumstances could be due to enhancement of oxygen delivery and consumption.

P. Aiden McCormick, Graham L. Kaye, Lynda Greenslade, Fabrizio Cardin, Kenneth E. F. Hobbs, Neil McIntyre, Andrew K. Burroughs – 1 March 1992 – It is not clear which therapy should be used in patients with bleeding esophageal varices that are not controlled by emergency sclerotherapy. This is a high‐risk group with reported mortality rates of between 70% and 90%. We report our 7‐yr experience with staple transection of the esophagus in this patient group. Of 168 patients (280 bleeding episodes) treated with sclerotherapy, 22 had emergency staple transection for failure to control bleeding.

1 February 1992

Hiroaki Okamoto, Fumio Tsuda, Atsuhiko Machida, Eisuke Munekata, Yoshihiro Akahane, Yoshiki Sugai, Kazuo Mashiko, Takehiro Mitsui, Takeshi Tanaka, Yuzo Miyakawa, Makoto Mayumi – 1 February 1992 – Immunoassays were developed to detect antibodies against oligopeptides deduced from the putative core gene of hepatitis C virus, and their performances were compared with that of the commercial immunoassay for antibodies against the product of nonstructural regions of hepatitis C virus (anti‐C100‐3).

J. Michael Henderson, Gregory J. Mackay, Michael Hooks, Judith L. Chezmar, John R. Galloway, Thomas F. Dodson, Michael H. Kutner – 1 February 1992 – This study measured cardiac output before and 1 or 2 yr after orthotopic liver transplantation in 23 patients. Cardiac output was measured by thermodilution before transplantation and by first‐pass radionuclide angiocardiography at follow‐up.

Sun‐Mee Lee, Mark G. Clemens – 1 February 1992 – This study was done to determine the relationship between microsomal lipid peroxidation during hepatic ischemia/reperfusion and alteration in cytochrome P‐450–dependent drug metabolism. Rats were pretreated with α‐tocopherol to inhibit lipid peroxidation or with vehicle (soybean oil) and then subjected to 60 min no‐flow hepatic ischemia in vivo. Control animals were time‐matched sham‐ischemic animals. After 1, 5 or 24 hr of reperfusion, liver microsomes were isolated and cytochrome P‐450 and mixed function oxidases were studied.

David E. Milov, Wou‐Seok Jou, Rachel B. Shireman, Paul W. Chun – 1 February 1992 – Bile salts are potent inhibitors of bovine carbonic anhydrase and human carbonic anhydrase I and human carbonic anhydrase II. To further characterize the binding of bile salts to carbonic anhydrase, rate constants for the CO2 hydration reaction in the presence of deoxycholate, cholate, glycocholate and taurocholate were determined using stop‐flow experments.

James H. Kelly, Tarek Koussayer, Da‐Er He, Maria G. Chong, Thomas A. Shang, Hartwell H. Whisennand, Norman L. Sussman – 1 February 1992 – We have established an improved model of fulminant hepatic failure in dogs. Buthionine sulfoximine is used to inactivate glutathione synthesis, and small increments of acetaminophen are given intravenously to maintain the plasma level at approximately 200 μg/ml for 20 hr. This regimen produces severe liver injury along with many of the features seen in humans with acetaminophen poisoning. The first sign of impending liver failure is hypoglycemia.