Elevated ALT and GGT levels were the most common findings with LFTs. In the patients with known glucose intolerance, increased glycogen within hepatocyte cytoplasm and nuclei was noted. In adults, NASH follows a relatively benign clinical course compared with alcoholic steatohepatitis. Although follow-up data in the paediatric age group are limited, the finding of evolving cirrhosis in one of our patients highlights the view that NASH may be a progressive disease. 10-12 Rashid and Roberts have speculated that at least some patients with cryptogenic cirrhosis occurring in adulthood may have had NASH since childhood.
Septal fibrosis occurs frequently in overweight adult patients with abnormal LFTs.
The pathogenesis of NASH is still being determined. A recent study 15 based on data from the National Health and Nutrition Examination Survey concluded that reduced serum levels of fat-soluble antioxidants are present in obese children. TNF antagonises insulin receptors, leading to glucose intolerance, hyperlipidaemia and steatosis. Another study 17 suggests that fatty livers are vulnerable to liver ATP depletion and necrosis, indicating that altered hepatic energy homoeostasis may be involved. Increased lipid peroxidation may increase hepatic stellate cell activation.