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Non-alcohol-induced steatohepatitis (NASH) is char-Non-alcohol-induced steatohepatitis (NASH) is inacterized by elevated serum aminotransferase activities completely defined but may result in progressive liver with hepatic steatosis, inflammation, and occasionally disease with cirrhosis. NASH is a disease characterized fibrosis that may progress to cirrhosis. No established by the development of histopathological features comtreatment exists for this potentially serious disorder. parable to those findings induced by excessive alcohol Our aim was to conduct a pilot study to evaluate the intake, without clinical evidence of alcohol abuse. The pathogenesis of NASH is unknown but may rein mean serum levels of alkaline phosphatase, alanine late to excessive accumulation of lipids in the liver. transaminase (ALT), and g-glutamyl transpeptidaseSteatotic livers secondary to alcohol abuse or associ-(GGT) as well as histological grade of steatosis were significant. Among the patients treated with clofibrate, no ated with type II diabetes mellitus contain predomichange from baseline was found in mean ALT, aspartate nantly triglycerides and to a lesser extent cholesterol transaminase (AST), GGT, bilirubin, triglycerides, and esters.9 Elevated hepatic free fatty acids, products of cholesterol, or in histological grade of steatosis, inflam-triglyceride hydrolysis, have been identified in fatty mation, or fibrosis after 12 months of treatment as com-liver of pregnancy, 10 alcohol-induced hepatitis, 11 and pared with entry. Alkaline phosphatase activities de-morbid obesity 11,12 and have been shown to cause cellucreased significantly from baseline. Despite the known lar injury. PATIENTS AND METHODSFrom the Mayo Clinic and Foundation, Rochester, MN.

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To compare sensitivity, specificity and convenience, four indirect methods of detecting lactase deficiency were tested prospectively in 25 subjects with biopsy-proved lactase deficiency and in 25 with normal lactase activity. After ingestion of 50 g of lactose, containing 1-14Clactose, breath hydrogen was abnormally elevated in all 25 lactase-deficient subjects (greater than 0.30 ml per minute at two hours); breath 14CO2 was below the normal range in 23, and in 19 the plasma glucose increased by less than 20 mg per deciliter. When lactose and ethanol were given together, the rise in plasma galactose remained less than 5 mg per deciliter in 24 of the lactase-deficient subjects. The specificity of the four tests was excellent, with only one false-positive plasma glucose test. Measurement of breath hydrogen is sensitive and specific, and does not require ethanol or isotopes. It is noninvasive, and is not influenced by gastric emptying or metabolic factors. We believe it to be the most suitable test for population screening for lactase deficiency.

Nonalcoholic steatohepatitis (NASH) is a reasonably well-defined clinicopathological entity; it has been reported more commonly in women than in men or children of both sexes and it appears to be most closely associated with obesity, diabetes mellitus and related abnormalities, such as hyperlipidaemia and hyperglycaemia. However, the association with female gender, obesity and diabetes may not be as close as suggested by the literature and an underlying condition cannot be discerned in all cases. The natural history of the disease is poorly understood; the associated biopsy features span a wide spectrum, reaching from uncomplicated, clinically non-progressive fatty liver (not NASH in a strict sense) to a slowly progressive fatty liver with inflammation and fibrosis, to steatohepatitis with submassive hepatic necrosis, which has a subfulminant course and is often fatal. Non-progressive fatty liver appears to be very common but is of little clinical importance. The slowly progressive form of the disease represents NASH as encountered by most clinicians and pathologists. It is a common liver disease in current practice; patients may present with cirrhosis and even HCC arising from steatohepatitic cirrhosis. Subfulminant NASH has become exceedingly rare because many clinicians are now aware of the hazards of sudden weight loss, particularly in morbidly obese patients. Treatment options for NASH are still limited. The promotion of gradual weight loss in obese patients is the most widely recommended therapy but, unfortunately, this is very difficult to achieve. Avoidance of precipitous weight loss and careful control of diabetes mellitus are important and undisputed parts of patient management. Administration of UDCA as a treatment of NASH is still under study; it may be effective in some patients. The treatment of established steatohepatitic cirrhosis does not differ substantially from that of other types of cirrhosis and includes orthotopic liver transplantation.