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AN ARTIFICIAL HEART

aspect of liver function can only detect severe damage. The absence of jaundice or of significant increase in the level of serum bilirubin, the slight increase in the level of serum alkaline phosphatase, and the negative result attending the colloidal gold test all bear witness to the lack of help in diagnosis afforded by these tests in fatty liver disease. Bromsulphthalein clearance was impaired only when liver damage was of sufficient severity to endanger life. Liver biopsy was of value in confirming the diagnosis of fatty liver and in following the course of recovery. The outstanding feature of the disease is, of course, the fat accumulation in the liver, and still more remarkable is its failure to respond to methionine and choline, the usual lipotrophic substances, the lack of which produces gross fat accumulation in the liver in laboratory animals. Chemical poisons and infectious hepatitis have been carefully excluded in these cases. It is pointed out that the fat accumulation is not specific of the disease, because fat accumulation is a feature of many conditions, including those due to chemical poisons, infections and starvation; and it is also emphasized that the problem of fat in the liver is highly complex. In starvation and after injections of pituitary extract fat in the liver comes from the depots and in choline deficiency from the food. In choline deficiency therefore the caloric intake bears a direct relationship to the quantity of fat in the liver. Animals in an active growth phase may use their essential amino acids for building body tissue, so that a relative deficiency is produced, and methionine-supplied methyl groups for the synthesis of choline are unavailable for this purpose. Waterlow considers that this particular fatty liver disease of infants differs from the bulk of human fatty liver disease in that the source of fat is exogenous, a point supported by the relatively high caloric intake on a background of all otherwise deficient diet. This high carbohydrate accompanied by low protein intake is also important in the determination of wdema. The failure to respond to very large doses of methionine or choline is difficult to explain, but the response to milk suggests that, although Iipotrophic activity of casein is related to its methionine content, there is a possibility of an active factor other than methionine. Waterlow, however, does not favour the view that fatty liver disease is a deficiency of some substance yet unknown, but lays emphasis on three factors, namely, the metabolic demands of the growing organism, prolonged depletion of protein, and carbohydrate overloading. Protein deficiency may, by virtue of the loss of certain labile components of enzyme systems intimately associated with fat metabolism, accelerate a fat accumulation which will remain unaffected by the lipotrophic components of the protein.