Haemodynamic changes in ischaemic vs. anhepatic pig experimental model of acute liver failure.

BACKGROUND AND OBJECTIVE: The removal of the non-functioning liver in cases of fulminant liver failure has been advocated by some authors as a means of improving haemodynamic instability and acid-base disturbances associated with acute liver failure. METHODS: The aim of the present experimental study was to investigate whether maintaining a non-functioning liver is preferable over removing it in terms of haemodynamic variables, after acute hepatic failure has been surgically induced. Twenty Landrace pigs were used in the study. All of them underwent portocaval anastomosis and ligation of the hepatic artery. After an 18-h period and with biochemical indices of fulminant hepatic failure clearly demonstrated, the animals were randomly assigned to one of two groups: in 10 pigs (Group A) the ischaemic liver was left in situ and no further surgical intervention was undertaken. The other 10 (Group B) underwent total hepatectomy. Haemodynamic monitoring was the same in both groups. No inotropes were administered throughout the whole period of observation. RESULTS: Haemodynamic deterioration was observed in the hepatectomized pigs (Group B) whereas the group with the ischaemic liver in situ (Group A) remained stable in terms of the haemodynamic variables evaluated until the end of the experiment. (Cardiac index in Group A 7.59 +/- 1.25 L min(-1) m(-2) vs. 2.92 +/- 0.68 L min(-1) m(-2) in Group B, P < 0.05.) CONCLUSIONS: The concept of salvage hepatectomy in cases of acute liver failure should be redefined since there seems to be some experimental evidence that it may not be as beneficial as originally thought.

Extrahepatic manifestations of chronic viral hepatitis.

Hepatitis B (HBV) and C (HCV) viruses are well-recognized causes for chronic hepatitis, cirrhosis, and even for hepatocellular carcinoma. Apart from liver disease, these viral infections are known to be associated with a spectrum of extrahepatic manifestations. The prevalence of clinically significant extrahepatic manifestations is relatively low, but it can be associated with significant morbidity and even mortality. An awareness and recognition of these manifestations is of paramount importance in facilitating early diagnosis and in offering treatment. However, treatments are not necessarily effective, and patients may continue with disabling extrahepatic manifestations. Hepatitis B virus has been well recognized as causing a variety of manifestations that include skin rash, arthritis, arthralgia, glomerulonephritis, polyarteritis nodosa, and papular acrodermatitis. More recently, infection with hepatitis C virus has elicited considerable interest for its role in a spectrum of extrahepatic manifestations. Among the best-reported are cryoglobulinemia, glomerulonephritis, high titer of autoantibodies, idiopathic thrombocytopenic purpura, lichen planus, Mooren's corneal ulcer, Sjögren's syndrome, porphyria cutanea tarda, and necrotizing cutaneous vasculitis. The precise pathogenesis of these extrahepatic complications has not been determined, although the majority represent the clinical expression of autoimmune phenomena.