Assessment of lidocaine metabolite formation as a quantitative liver function test in children

David A. Gremse, Hassan H. A‐Kader, Timothy J. Schroeder, William F. Balistreri – 1 September 1990 – Lidocaine, an aminoethylamide, undergoes deethylation in the liver after intravenous injection, resulting in the formation of monoethylglycinexylidide. Serum monoethylglycinexylidide concentration can be measured by a simple, rapid fluorescent polarization immunoassay. We sought to determine whether lidocaine metabolism, as indicated by monoethylglycinexylidide formation, could be used as a quantitative index of hepatic function.

Alveolar echinococcosis of the liver: A parasitic disease in search of a treatment

Dominique Vuitton – 1 September 1990 – The efficacy of albendazole (50 mg/kg/d), mebendazole (50 mg/kg/d) and praziquantel (500 mg/kg/d) against established intraperitoneal infections of Echinococcus multilocularis in gerbils was compared by monitoring parasite weight and making ultrastructural observations on treated and untreated material. Praziquantel was the most active protoscolicidal agent, reducing protoscolex viability to <2%, although it did not inhibit cyst growth.

The response of atrial natriuretic factor and sodium excretion to dietary sodium challenges in patients with chronic liver disease

Leonard C. Warner, Peter J. Campbell, Gilles A. Morali, Alexander G. Logan, Karl L. Skorecki, Laurence M. Blendis – 1 September 1990 – Despite intensive investigation, the pathogenesis of sodium retention in patients with chronic liver disease is not fully known. We have studied 19 chronic liver disease patients, 13 without (group 1) and six with (group 2) histories of clinical sodium retention (ascites or edema) by varying dietary sodium intake.

What does “reduced central blood volume in cirrhosis” really mean?

G. A. Morali, L. M. Blendis – 1 September 1990 – The pathogenesis of ascites formation in cirrhosis is uncertain. It is still under debate whether the effective blood volume is reduced (underfilling theory) or whether the intravascular compartment is expanded (overflow theory). This problem has not yet been solved because of insufficient tools for measuring the central blood volume. We have developed a method that enables us to determine directly the central blood volume, i.e., the blood volume in the heart cavities, lungs, and central arterial tree.

Plexiform neurofibromatosis of the liver and mesentery in a child

Jacqueline S. Partin, Bernard P. Lane, John C. Partin, Lawrence R. Edelstein, Cedric J. Priebe – 1 September 1990 – Plexiform neurofibromatosis of the liver was recognized by needle biopsy of the liver in an 11‐yr‐old boy who had a 2‐yr history of diarrhea, intermittent abdominal pain, failure to gain weight and progressive abdominal distention. Imaging studies demonstrated a large retroperitoneal mass; a laparotomy was performed. At surgery, the mesentery was greatly thickened by neurofibromas, and plexiform neurofibroma extended through the hilum of the liver.

A hypercoagulable state follows orthotopic liver transplantation

Robert L. Stahl, Alexander Duncan, Michael A. Hooks, J. Michael Henderson, William J. Millikan, W. Dean Warren – 1 September 1990 – Orthotopic liver transplantation may be associated during the postoperative period with hepatic artery thrombosis, a catastrophic occurrence generally necessitating emergency retransplantation. To assess the contribution of the coagulation mechanism to this complication, the levels of procoagulant and anticoagulant proteins were followed in 41 liver transplant patients during the first 10 postoperative days.

Mitochondrial structure and function in CCl4‐induced cirrhosis in the rat

Stephan Krählenbühl, Jürg Reichen, Arthur Zimmermann, Peter Gehr, Jörg Stucki – 1 September 1990 – To investigate whether the impairment of mitochondrial function in cirrhosis is due to a reduction in liver cell mass or whether mitochondrial function is altered specifically, we analyzed mitochondrial volume and surface density of mitochondrial membranes in control and cirrhotic rats by stereological means. Cirrhosis was induced by long‐term exposure to phenobarbital and CC14.

Subscribe to