Harold O. Conn – 1 May 1986

Emanuel Sikuler, Roberto J. Groszmann – 1 May 1986 – It is not known whether the hyperdynamic state which has been observed in several experimental models and in patients with portal hypertension reflects a temporary phase during the evolution of the portal hypertensive syndrome or is an expression of a permanent steady state. A hemodynamic study was performed in a group of rats with long‐standing portal hypertension induced by portal vein constriction performed 6.2 ± 0.1 months earlier.

Burton Combes – 1 May 1986

Michel Doffoel, Marie M. Tongio, Jean‐Pierre Gut, Guy Ventre, Alain Charrault, Denis Vetter, Marc Ledig, Marie L. North, Simone Mayer, René Bockel – 1 May 1986 – In order to study the genetic risk of alcoholic cirrhosis, the frequency of 26 HLA‐A and ‐B antigens was compared in 184 normal controls, 175 alcoholic cirrhotic patients and 83 alcoholic patients with hepatic steatosis of carefully selected ethnic origin. Eight HLA‐DR antigens were also determined in 95 subjects of the normal control group and 63 patients of the alcoholic cirrhosis group.

Edward Penner, Hans Goldenberg, Siegfried Meryn, Julian Gordon – 1 May 1986 – A dot‐immunobinding assay was established for the detection of antimitochondrial antibodies. Nitrocellulose strips were coated with sonicated rat liver mitochondria and incubated in the presence of human sera. The resulting immune complexes were visualized with an enzyme‐linked second antibody. Antimitochondrial antibodies were found in the sera of 96% of patients with primary biliary cirrhosis, 17% of patients with autoimmune hepatitis and 4% of patients with progressive systemic sclerosis.

D. Neil Granger, Dale A. Parks – 1 May 1986 – We have investigated the possible protective effect of superoxide dismutase and allopurinol in a rat model of mild and severe hepatic necrosis produced by Corynebacterium parvum with or without endotoxin. Histology showed a sinusoidal mononuclear cell infiltrate with multiple granulomata but variable degrees of hepatic necrosis. In the severe hepatic injury model there was a reduction in mortality, associated with a decrease in histologic and biochemical evidence of hepatic necrosis, after treatment with superoxide dismutase.

Francesco M. Cetta – 1 May 1986 – Findings in two patients having brown pigment bile stones, recurrent 18 and 36 months after cholecystectomy, are reported. Present data suggest that bile infection precedes rather than follows the formation of brown stones. The present data are part of a prospective study of 600 consecutive patients who underwent operation for gallstones and in whom clinical and laboratory findings, intra‐ and postoperative bile culture and bile pH were related to the analysis of stone composition by X‐ray diffractometry and infrared spectroscopy.

Yang‐Te Tsai, Chii‐Shyan Lay, Kwok‐Hung Lai, Wai‐Wah Ng, Yeong‐Shyan Yeh, Jiin‐Yu Wang, Teun‐Tzong Chiang, Shou‐Dong Lee, Benjamin N. Chiang, Kwang‐Juei Lo – 1 May 1986 – Thirty‐nine patients admitted during a 16‐month period for acute bleeding from varices confirmed by emergency endoscopy were randomized to receive either continuous intravenous infusions of vasopressin alone (0.66 units per min) (Group I: 19 patients) or vasopressin plus sublingual nitroglycerin (0.6 mg every 30 min for 6 hr) (Group II: 20 patients).

Shou‐Dong Lee, Kwang‐Juei Lo, Jaw‐Ching Wu, Yang‐Te Tsai, Jiin‐Yu Wang, Ling‐Pai Ting, Myron J. Tong – 1 May 1986 – Sera from 108 HBsAg carrier mothers at delivery and their respective offspring at birth and at 6 months of age were examined for hepatitis B virus DNA by the dot‐blot hybridization technique. Hepatitis B virus DNA was detected in 83% of 88 carrier mothers who were HBeAg positive, and in 10% of 20 carrier mothers who were HBeAg negative.

Leo Ranek – 1 May 1986 – We studied susceptibility to halothane hepatitis with an in vitro test that detects cell damage from electrophilic drug intermediates. Metabolites of phenytoin were generated by incubation of phenytoin with rat hepatic microsomes in the presence of the epoxide hydrolase inhibitor 1,1,1‐trichloropropene oxide (TCPO), which prevents the further metabolism of phenytoin to an inert metabolite.