Effect of cholestyramine on bile acid kinetics in patients with portal cirrhosis of the liver

1978 ◽  
Vol 23 (12) ◽  
pp. 1115-1120 ◽  
Author(s):  
B. Angelin ◽  
K. Einarsson ◽  
K. Hellstrom
Keyword(s):  
Bile Acid ◽  
Cirrhosis Of The Liver ◽  
Portal Cirrhosis

scholarly journals Secondary Hemochromatosis

Blood ◽  
1953 ◽  
Vol 8 (9) ◽  
pp. 824-836 ◽  
Author(s):  
ARTHUR C. AUFDERHEIDE ◽  
HOWARD L. HORNS ◽  
ROBERT J. GOLDISH
Keyword(s):  
Iron Content ◽  
Iron Absorption ◽  
Oral Iron ◽  
Cirrhosis Of The Liver ◽  
Iron Therapy ◽  
Etiologic Factor ◽  
Blood Transfusions ◽  
Portal Cirrhosis ◽  
Oral Iron Therapy ◽  
Total Body

Abstract 1. Secondary hemochromatosis has been sharply separated from simple hemosiderosis by defining the former as "a condition acquired as a consequence of anemia, blood transfusions, or both, and characterized by increased hepatic and total body iron content and unequivocal portal cirrhosis of the liver." 2. Previously reported cases are critically reviewed in the light of this definition. 3. Two new cases of secondary (exogenous) hemochromatosis are reported. 4. Anemia is postulated as the basic etiologic factor in secondary hemochromatosis by causing increased iron absorption; iron introduced in the form of blood transfusions probably only accelerates a process already in progress. 5. Prolonged futile oral iron therapy may be harmful. 6. A plea is made for a strict concept of secondary hemochromatosis as well as for thorough documentation of future reports.

scholarly journals OBSERVATIONS ON THE CONDITIONS OF DIETARY HEPATIC INJURY (NECROSIS, CIRRHOSIS) IN RATS

1942 ◽  
Vol 75 (4) ◽  
pp. 355-368 ◽  
Author(s):  
Paul György ◽  
Harry Goldblatt
Keyword(s):  
Pericardial Effusion ◽  
Hepatic Injury ◽  
Basal Diet ◽  
Dietary Factors ◽  
Cirrhosis Of The Liver ◽  
Portal Cirrhosis ◽  
Fat Infiltration ◽  
Focal Necrosis ◽  
Combined Administration ◽  
Frequent Accompaniment

Experimental dietary hepatic injury (diffuse or focal necrosis and cirrhosis in rats, with or without ascites and pleural and pericardial effusion) is determined by the dietary factors instrumental also in the production of fat infiltration of the liver and thus opposed to the lipotropic activity of casein. Accordingly, rats maintained on a diet low in casein with a moderately high or high content of fat and without choline regularly exhibited hepatic injury after between 100 and 150 days. Supplements of l-cystine had an aggravating effect on the production of cirrhosis of the liver, whereas a supplement of choline alone reduced the severity and the incidence of hepatic injury, although not decisively. The combined administration of l-cystine plus choline or of dl-methionine in adequate doses, however, proved to be highly effective in preventing injury to the liver. These conclusions have been corroborated by the use of different modifications of the basal diet. Rats with dietary hepatic injury exhibit, in sequence, changes that vary from diffuse necrosis resembling human acute or subacute yellow atrophy to advanced portal cirrhosis. Diffuse necrotizing nephrosis was a frequent accompaniment of the hepatic injury. Cystine again, proved to be a factor which aggravated this condition.

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