Dale C. Snover, Sally A. Weisdorf, Norma K. Ramsay, Philip Mcglave, John H. Kersey – 1 January 1984 – Ninety‐six liver biopsies [32 bone marrow transplant (BMT), 7 pre‐BMT, and 57 non‐BMT] are reviewed for histological evidence of graft versus host disease (GVHD), based on bile duct atypia and related inflammatory changes. In addition, the presence of cholestasis, piecemeal necrosis, and attachment of lymphocytes to vascular endothelium (endothelialitis) are evaluated.

Kunio Okuda, Hiroshi Obata, Yukio Nakajima, Toshio Ohtsuki, Nobuo Okazaki, Kunihiko Ohnishi – 1 January 1984 – Prognosis of 600 consecutive patients with hepatocellular carcinoma was analyzed in relation to treatment. They were divided into three stages based on four parameters of advanced disease: ascites, tumor greater than 50% of the two‐dimensional size of the liver, serum albumin below 3 gm per dl, and serum bilirubin above 3 mg per dl. Stage I had none of these signs; Stage II one or two signs, and Stage III three or all signs.

Rudolf Pichlmayr, CH. Brölsch, K. Wonigeit, P. Neuhaus, S. Siegismund, F.–W. Schmidt, M. Burdelski – 1 January 1984

Ruud A. F. Krom, Chris H. Gips, Hendrik J. Houthoff, Douglas Newton, Dirk V. D. Waaij, José Beelen, Elizabeth B. Haagsma, Maarten J. H. Slooff – 1 January 1984 – From March, 1979 to March, 1983, 26 orthotopic liver transplantations and 1 retransplantation were performed in our center. Sixteen patients are alive, 5 beyond22 years and 1 longer than 4 years after transplantation. The actuarial 1– and 2–year survival is 60%. Factors contributing to this result are patient selection and biliary anastomosis.

Stefan Lindgren, Anna‐Brita Laurell, Sten Eriksson – 1 January 1984 – Total complement activity was normal in 18 patients with primary biliary cirrhosis using two hemolytic assays capable of distinguishing between defects in classical and alternative pathways. Activation of the classical pathway was demonstrated in all patients by formation of complexes between C1r, C1s, and C1 inactivator. Large amounts of free C1q, not in complex with C1r and C1s, were demonstrated in the majority of patient sera. Furthermore, C4 levels were within the normal range or slightly subnormal.

Luigi E. Adinolfi, Riccardo Utili, Giovanni B. Gaeta, Charles O. Abernathy, Hyman J. Zimmerman – 1 January 1984 – Estradiol‐17β‐D‐glucuronide (E‐17G), a metabolite of natural estrogen, is a potent cholestatic agent in vivo. We, therefore, studied the mechanisms of E‐17G cholestasis using in vitro perfused rat liver system. Furthermore, since it has been postulated that sodium taurocholate (TC) may interfere with either uptake or biliary excretion of other steroid agents, we tested whether E‐17G cholestasis could be modified by TC administration.

Hosny W. M. Seda, Robin D. Hughes, Christopher D. Gove, Roger Williams – 1 January 1984 – Among the toxins accumulating in the circulation of patients with fulminant hepatic failure (FHF) are substances which inhibit leucocyte ouabain‐sensitive sodium transport. A similar inhibition of brain Na+,K+−ATPase could lead to both coma and cerebral edema found in these patients which are associated with high mortality. In this study, we have investigated the effect of sera from FHF on normal rat brain Na+,K+−ATPase activity in vitro.

JosÉ A. Solis‐Herruzo, Gregorio Castellano, Francisco Colina, Juan Diego Morillas, Maria Teresamuñoz‐Yagüe, Maria Del Carmen Coca, Dusko Jelavic – 1 January 1984 – We describe the clinico‐pathological characteristics of hepatic injury associated with the toxic‐epidemic syndrome caused by the consumption of adulterated rapeseed oil. Of 842 toxic‐epidemic syndrome patients admitted to our hospital between May, 1981, and January, 1982, 24.1% showed signs of liver involvement which was more frequent in women and in the fourth decade of life.

Raymond S. Koff, Rolf Teschke, Fernando Moreno, Edgarheinen, Jörg Herrmann, Hans‐Ludwig Krüskemper, Georg Strohmeyer – 1 January 1984

Joseph R. Bloomer, Harvey L. Sharp – 1 January 1984 – The liver may be involved in metabolic disorders in two ways, (i) Due to its critical role in several metabolic pathways, the liver may be the major site of expression of a biochemical abnormality. For example, in Type I Crigler‐Najjar syndrome, absence of hepatic bilirubin glucuronyl transferase activity causes severe unconjugated hyperbilirubinemia which invariably leads to death from kernicterus. (ii) The liver may also be structurally damaged by the metabolic disorder.