The effect of tauroursodeoxycholic acid and taurine supplementation on biliary bile acid composition

Ashok K. Batta, Gerald Salen, Sarah Shefer, G. Steven Tint, Bishambar Dayal – 1 November 1982 – The biliary bile acid conjugation patterns were determined by high‐performance liquid chromatography in five subjects after 6 months of 500 mg per day of free ursodeoxycholic acid feeding. Prior to bile acid therapy, approximately 35% of the biliary bile acids were conjugated with taurine and approximately 65% were glycine conjugated, and ursodeoxycholic acid was either absent or, when present, accounted for less than 5% as the glycine conjugate.

Interferon production by peripheral lymphocytes in HBsAg‐positive liver diseases

Yasuhiro Kato, Hirohito Nakagawa, Kenichi Kobayashi, Nobu Hattori, Kiichi Hatano – 1 November 1982 – Interferon production by lymphocytes was normal in HBsAg carriers with normal liver function tests and normal liver histology, whereas it was significantly decreased in HBsAg‐positive patients with chronic active hepatitis and cirrhosis. It is possible that an impaired interferon system is causally related to the development of chronic liver disease in hepatitis B virus infection.

Valproate‐induced hepatic steatogenesis in rats

James H. Lewis, Hyman J. Zimmerman, Carlton T. Garrett, Elliot Rosenberg – 1 November 1982 – The administration of high‐dose valproic acid (VPA) (750 mg per kg) consistently produced significant microvesicular steatosis in mature Sprague‐Dawley rats after 48 hr. Similar changes occurred in animals pretreated with phenobarbital which received a lower dose of VPA (350 mg per kg), but no steatosis was seen in animals treated with the low‐dose VPA alone. The steatogenic effect of VPA is most likely mediated by a toxic metabolite.

H2‐receptor antagonists and hepatic drug disposition

George W. Mihaly, Richard A. Smallwood, Jeanette D. Anderson, D. Brian Jones, Lorraine K. Webster, Frank J. Vajda – 1 November 1982 – The effect of four H2‐receptor antagonists (Cimetidine, burimamide, oxmetidine, and ranitidine) on antipyrine elimination was studied in the isolated perfused rat liver. The first three drugs are substituted imidazoles, whereas ranitidine contains a furanyl nucleus. Isolated livers were perfused using a 100‐ml, recycling, constant flow circuit for 4 hr. Antipyrine elimination was studied with or without an H2‐receptor antagonist present.

Adenine arabinoside 5′‐monophosphate treatment of chronic type B hepatitis

Jay H. Hoofnagle, Gerald Y. Minuk, Geoffrey M. Dusheiko, Daniel F. Schafer, Rodney Johnson, Stephen Straus, E. Anthony Jones, John L. Gerin, Kamal Ishak – 1 November 1982 – Six patients with chronic type B hepatitis were treated with adenine arabinoside 5′‐monophosphate at a dosage of 10 to 15 mg per kg per day for 10 days. All demonstrated an immediate and marked decrease in serum hepatitis B virus DNA and DNA polymerase, and 5 of the 6 became negative for both markers by the end of the period of therapy.

Changes of the golgi apparatus induced by diethylmaleate in rat hepatocytes

Anne‐Marie Jezequel, Patrizia Bonazzi, Piera Amabili, Cinzia Venturini, Francesco Orlandi – 1 November 1982 – Ultrastructural studies of the liver of rats given diethylmaleate (DEM) (0.7 ml per kg body, i.p.) weight revealed marked alterations of the configuration of the Golgi complex in all hepatocytes. This consisted in dilatation of the cisternae leading to the formation of large cysts. The alteration was more prominent 15 min after administration of the drug, coincident with a 2‐fold increase of bile flow and a decrease of hepatic glutathione to 15% of controls.

Effect of hematin administration to patients with protoporphyria and liver disease

Joseph R. Bloomer, Claus A. Pierach – 1 November 1982 – Hepatic damage in protoporphyria appears to be caused by a toxic effect of excess protoporphyrin. Therapy which reduces the formation of excess protoporphyrin may, therefore, be helpful. We examined the effects of hematin administered i.v. to two patients with protoporphyria and decompensated cirrhosis. Neither patient had side effects from the compound or manifested signs of toxicity. The vascular disappearance of hematin in one patient was similar to that in patients with porphyria who do not have structural liver disease.

Spontaneous disappearance of viral replication and liver cell inflammation in HBsAg‐positive chronic active hepatitis: Results of a placebo vs. interferon trial

Solko W. Schalm, Rudolf A. Heijtink – 1 November 1982 – In 20 patients with HBsAg‐and HBeAg‐positive chronic active hepatitis, we determined the long‐term effect of human leukocyte interferon as well as placebo treatment. During the 2‐year follow‐up period, HBsAg remained present in all patients, but the Dane particle markers HBeAg and DNA polymerase disappeared in two of 10 patients who had received interferon, and in 4 of 10 patients from the placebo group.

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