Intrahepatic cholestasis and phospholipidosis associated with the use of trimethoprim‐sulfamethoxazole

Santiago J. Muñoz, Antonino Martinez‐Hernandez, Willis C. Maddrey – 1 August 1990 – Although liver injury after administration of the trimethoprim‐sulfamethoxazole combination is rare, hepatocellular necrosis and cholestasis have developed in a few cases. We describe a patient who developed a severe, prolonged cholestatic reaction after trimethoprim‐sulfamethoxazole administration. The findings from serial liver biopsy samples showed characteristic abnormalities of phospholipidosis that have not been previously described for trimethoprimsulfamethoxazole–related hepatic injury.

Abnormal hepatic uptake of low doses of sulfobromophthalein in Gilbert's syndrome: The role of reduced affinity of the plasma membrane carrier of organic anions

Sandro Gentile, Marcello Persico, Claudio Tiribelli – 1 August 1990 – The plasma disappearance rate of sulfobromophthalein (VBSP; μmol/kg/min) was measured in 15 Gilbert's syndrome patients and 12 control subjects after intravenous injection of two different doses (0.59 and 5.90 μmol/kg) of the dye. Plasma disappearance rate was significantly reduced in Gilbert's syndrome patients after administration of 0.59 μmol sulfobromophthalein/kg (0.119 ± 0.016 vs. 0.146 ± 0.018 μmol/kg/min; mean ± S.D.; p < 0.001), whereas no difference was found with the higher dose (0.754 ± 0.040 vs.

Partial portal decompression: Two approaches to the management of portal hypertension

Eric B. Rypins, I. James Sarfeh – 1 August 1990 – To test the hypothesis that partial portal decompression in the treatment of variceal hemorrhage will diminish subsequent encephalopathy, 50 consecutive patients were studied after construction of a small‐stoma (10 to 12 mm) side‐to‐side portacaval shunt, with the goal of a postoperative portacaval pressure gradient of 10 mm Hg. During follow‐up averaging 26 months, six patients (12 percent) died. Four patients (8 percent) had episodes of rebleeding, only one from varices.

Benign recurrent intrahepatic cholestasis: Failure of S‐adenosylmethionine therapy

Harold O. Conn, C. N. Ghent – 1 August 1990 – S‐Adenosylmethionine (800 mg i.v. per day) was used to treat two brothers and a brother and sister from each of two kindreds with benign recurrent intrahepatic cholestasis. Symptoms, routine tests of liver function, concentrations of total bile acids, and the oral clearances of [11,12‐2H]chenodeoxycholic acid and [24‐13C]cholic acid were determined before and after treatment with S‐adenosylmethionine. S‐Adenosylmethionine did not ameliorate symptoms or biochemical parameters of cholestasis but reduced bile acid clearances in 3 of 4 subjects.

Microscopic incipient hepatocellular carcinoma found incidentally in a routine liver biopsy specimen

Noboru Hirooka, Yoshiro Nitta, Takabumi Tsunoda, Eiji Kitazawa, Junichi Sato, Akira Machii, Yoshitsugu Murakami, Manabu Takahashi, Fukuo Kondo – 1 August 1990 – A microscopic atypical focus suggestive of hepatocellular carcinoma is reported. The lesion, 0.3 mm in diameter, was found by chance in a liver biopsy specimen taken from a cirrhotic patient; it was characterized histologically by cytoplasmic basophilia, hypercellularity (high nucleus‐to‐cell ratio) and microacinar structures.

Lack of metabolic effects of cholecystokinin on hepatocytes

Louis J. Kost, Gregory J. Gores, John M. Sayles, Laurence J. Miller, John J. Lemasters, Brian Herman, Nicholas F. Larusso – 1 August 1990 – We previously reported that the liver was the major organ that extracts small, biologically active, circulating forms of cholecystokinin. Although our work indicated extensive degradation of cholecystokinin extracted from plasma during its transit across the hepatocyte, it was unclear whether cholecystokinin might also have a physiological effect on this cell before its intracellular degradation.

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