Editor,—The conclusions reached by Wigget al ((2001) Gut 48:206–11.OpenUrlAbstract/FREE Full Text) about the origin and importance of tumour necrosis factor α (TNF-α) in non-alcoholic steatohepatitis (NASH) patients have failed to take into account the relationship between even modest alcohol consumption and TNF-α production and function. The authors found a lack of correlation between obesity and TNF-α levels in NASH patients and concluded that TNF-α, which they see as central to the pathogenesis of the condition, must have other sources.

We first described the strong correlation between obesity and serum TNF-α in 1998.1 Adipose tissue synthesises a number of proinflammatory cytokines.2 The negative correlation found in the Adelaide study is surprising given the findings in larger studies of non-NASH subjects and may be due to the small study numbers and not correcting for modest alcohol intake.

Alcohol consumption is considered a risk factor for the development and progression of liver disease in patients with fatty livers. We previously showed a strong negative …

Dr AJ Wigg, Department of Gastroenterology and Hepatology, Flinders Medical Centre, Bedford Park, SA 5042, Australia.alan.wigg{at}flinders.edu.au