Commentary
See article on page 206Is bacterial ash the flash that ignites NASH?
| The first 150 words of the full text of this article appear below. |
As obesity creeps in epidemic proportions through increasingly inert and affluent "developed" societies, metabolic imbalance has become the commonest cause of liver disease. Fatty liver, although itself benign, predisposes the liver to NASH or non-alcoholic steatohepatitis, a chronic disorder characterised by steatosis, mixed cell type inflammation, focal hepatocyte degeneration, and perivenular or pericellular fibrosis.1 2 NASH is slowly progressive, occasionally resulting in cirrhosis with the potentially fatal complications of portal hypertension, liver failure, and hepatocellular carcinoma.2 3
Most cases of NASH appear to have a multifactorial
aetiopathogenesis. The predisposing factors include obesity, type II
diabetes, insulin resistance, hypertriglyceridaemia, and rapid weight
loss, each of which can cause hepatic steatosis. The trigger that sets off injury and inflammation against this background of oxidisable fatty
acid excess, and the mechanisms that perpetuate steatohepatitis and
fibrogenesis are less clear.4 A focus of recent
experimental studies has been on biochemical processes that reduce
oxygen to reactive
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- A J Wigg, I C Roberts-Thomson, R B Dymock, P J McCarthy, R H Grose, and A G Cummins
Gut 2001 48: 206-211.[Abstract] [Full Text] [PDF]
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[Abstract] [Full Text]
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