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Liver Disease and Home Parenteral Nutrition

TO THE EDITOR: Cavicchi and colleagues reported on end-stage liver disease (ESLD) in patients with intestinal failure who were receiving long-term home parenteral nutrition (HPN) (1). One important finding was that patients with extremely short bowel had an increased risk for ESLD. We recently described 42 patients who had received a total of 283 patient-years of HPN (2). A relevant finding from our studynot examined by Cavicchi and coworkerswas a subgroup of young patients with extremely short bowel and normal serum albumin concentrations but no inflammatory disorders. These patients, who received HPN for a mean (SD) of 13.6 6.7 years, did not develop cholestasis. This finding suggests that an underlying inflammatory disorder, rather than the remaining length of small intestine, poses the risk for ESLD. Cavicchi and colleagues also identified a link between the amount of lipid in the nutrition solution and risk for ESLD. We (3) and others (4) have described the contribution of lipid emulsions to a proinflammatory state in patients receiving HPN. In patients with severe malabsorption, those receiving HPN containing lipid had elevated plasma membrane arachidonic acid (AA) concentrations compared with healthy controls and patients who received fat-free HPN (3, 4). Arachidonic acid is principally derived by hepatic desaturation and elongation of the essential fatty acid linoleic acid (LA), the main component of lipid emulsions. Production of AA from LA is tightly controlled because AA is a precursor of eicosanoids that modulate proinflammatory responses (5). Therefore, in patients with the short-bowel syndrome receiving parenteral lipid to prevent essential fatty acid deficiency, enhanced conversion of LA to AA probably promotes production of proinflammatory mediators; this might contribute to hepatic dysfunction in a susceptible host with underlying inflammation. Therefore, Cavicchi and associates' paper supports suggestions that long-term parenteral presentation of nutrients to the liver (plus limited enteral absorption) may worsen hepatic functionin this case, by exacerbating inflammatory stimuli. Dietary fish oil supplementation might therefore be considered in patients at particular risk for ESLD, because eicosapentaenoic acid inhibits production of AA from LA and yields fewer proinflammatory eicosanoids. However, the absorption of fish oil in the short-bowel syndrome is uncertain.