Dwain L. Thiele – 1 March 1989

Ernest Urban, Vincent J. Dindzans, David H. Van Thiel – 1 March 1989 – This is a report of six patients with cirrhosis of the liver in whom primary hyperparathyroidism occurred due to a solitary parathyroid adenoma 3 months to 9 years after undergoing emergency portacaval shunt for hemorrhage from esophageal varices. The presenting symptoms in all six patients were weakness and bone pain. Three patients had a bone fracture after insignificant trauma, one and probably two passed kidney stones, and a duodenal ulcer developed in two.

Owen Epstein – 1 March 1989

Richard Moreau, Samuel S. Lee, Antoine Hadengue, Yves Ozier, Christian Sicot, Didier Lebrec – 1 March 1989 – To elucidate the relationship between oxygen transport and uptake in cirrhosis, we studied the effects of three vasoactive drugs that change O2 transport. Systemic hemodynamics, blood gases and lactate concentration were measured in patients with alcoholic cirrhosis before and after intravenous dobutamine, propranolol and nitroglycerin. Nine patients received successively dobutamine and then propranolol. Ten patients received nitroglycerin.

Melchor Hoyos, José V. Sarrión, Teresa Pérez‐Castellanos, Martín Prieto, María L. Marty, Vicente Garrigues, Joaquín Berenguer – 1 March 1989 – The relationship between donor status for antibody to hepatitis B core antigen and the occurrence of non‐A, non‐B posttransfusion hepatitis in the recipient was prospectively studied in 112 patients undergoing open‐heart surgery who were followed for 6.5 months after surgery.

Toshiji Saibara, Saburo Onishi, Hiroshi Sakaeda, Yasutake Yamamoto – 1 March 1989 – Lymphokine‐activated killer activity and natural killer activity in hepatocellular carcinoma patients were assessed. Maximum lymphokine‐activated killer activity was induced at 3 to 5 days of incubation, and lymphokine‐activated killer activity tended to increase in a manner dose dependent of recombinant interleukin‐2. However, the maximum increase of lymphokine‐activated killer activity in hepatocellular carcinoma was not as high as that of normal subjects or liver cirrhosis patients.

Philip J. Snodgrass – 1 March 1989 – We produced moderately severe, inactive micronodular cirrhosis in rats using CCl4 and measured the urea cycle enzyme activities in liver after feeding a 15% casein diet for 1 week and again after a 60% casein diet for 1 week. There was no deficiency of any of the five urea cycle enzymes in cirrhotic livers of rats pair‐fed the 15% casein diet. Argininosuccinate synthetase and carbamyl phosphate synthetase activities were lower than in non‐pair‐fed controls by some baselines.

Peter F. Whitington, Beat H. Kehrer, Susan H. Whitington, Benjamin Shneider, Dennis D. Black – 1 March 1989 – A major factor in poor bioavailability of cyclosporine in children undergoing orthotopic liver transplantation appears to be poor absorption of the drug. Our hypothesis is that the Roux‐en‐Y choledochojejunostomy used for biliary drainage in these children causes cyclosporine malabsorption by reducing the length of bowel available for absorption and by distally displacing the entry of bile into the intestine.

J. Marc Shabot – 1 March 1989 – Chlamydia trachomatis as an etiological agent in the Fitz‐Hugh‐Curtis syndrome has recently been reported; however, the condition has not been typically associated with ascites. We report a case of Chlamydia trachomatis perihepatitis in a young woman who had exudative ascites as a predominant clinical feature of her disease. Laparoscopy revealed characteristic “violin string” adhesions which were also identified on abdominal computerized scan.

James P. Knochel – 1 March 1989 – This is the first record of hypophosphataemia in acute liver failure induced by paracetamol; it occurred in most of the patients and was severe (<0.3 mmol/l) in more than one third. At this level hypophosphataemia produces impaired oxygen transport and tissue hypoxia, abnormal leucocyte function, depressed platelet numbers and function, generalised muscle weakness, and disorder of the central nervous system; these are frequent complications of acute liver failure.