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American Journal of Clinical Nutrition, Vol. 73, No. 3, 661-662, March 2001
© 2001 American Society for Clinical Nutrition


Letter to the Editor

Abnormal fatty acid status in patients with Crohn disease

Maria Esteve-Comas and Miquel Angel Gassull

Department of Gastroenterology Hospital Universitari Germans Trias i Pujol Ctra de Canyet, s/n 08916 Badalona Catalonia Spain E-mail:mgassull{at}ns.hugtip.scs.es

Dear Sir:

We read with interest the article by Jeppesen et al (1) that assessed the influence of administration of enteral or parenteral nutrition on plasma phospholipid essential fatty acid (EFA) concentrations in patients with malabsorption. This was a well-designed study that included 4 groups of patients; 2 groups received parenteral nutrition (groups C and D), group A had fat malabsorption of <50% of fat intake, and group B had fat malabsorption of >50% of fat intake. Group C received parenteral nutrition containing lipids and EFA and group D received fat-free parenteral nutrition. EFA absorption was negligible in groups C and D and EFA supplementation in group C was not enough to completely reverse biochemical EFA deficiency. The authors concluded that EFA requirements in patients receiving parenteral nutrition are higher than the amounts recommended to patients with preserved intestinal absorption.

However, as McCowen et al (2) pointed out in a letter to the Journal, a major concern with the study is that most of the patients had Crohn disease. In fact, an abnormal fatty acid profile has been described in patients with active (3) and inactive (4) Crohn disease and in both plasma (3, 4) and intestinal mucosa (5). Plasma long-chain n-3 polyunsaturated fatty acids (PUFAs) were significantly elevated in patients with Crohn disease (3) and a similar but nonsignificant trend was observed for n-6 long-chain PUFAs in patients with inactive disease (4). This finding is consistent with results of the study by Jeppesen et al that showed higher values of both 20:3n-6 and 20:4n-6 in all the groups studied (including most patients with Crohn disease) than in the control group (1).

In addition, elevated concentrations of long-chain n-6 PUFAs were observed in the intestinal mucosa of patients with Crohn disease (5). Similar findings were observed in patients with ulcerative colitis and in experimental colitis, suggesting that there is a common biochemical response to intestinal inflammation (5).

Enteral nutrition has a primary effect on the course of Crohn disease, inducing remission in 60% of patients (6). It is not known which component or components of the diet are responsible for the control of inflammation, but there are some data suggesting that the lipid composition of the diet may play a crucial role (6, 7).

Thus, the authors should be cautious before recommending high doses of parenteral EFAs in patients with Crohn disease because these patients have increased amounts of products of these fatty acids, especially in intestinal mucosa (5). This maneuver might exacerbate the activity of the disease (8). This nutritional recommendation would probably be more useful in patients with short-bowel syndrome and EFA deficiency due to another non-immune–mediated disease.

REFERENCES

  1. Jeppesen PB, Høy C-E, Mortensen PB. Differences in essential fatty acid requirements by enteral and parenteral routes of administration in patients with intestinal malabsorption. Am J Clin Nutr 1999; 70:78–84.[Abstract/Free Full Text]
  2. McCowen K, Ling PR, Bistrian BR. Arachidonic acid concentrations in patients with Crohn disease. Am J Clin Nutr 2000;71:1008–9.[Free Full Text]
  3. Esteve-Comas M, Ramírez M, Fernández-Bañares F, et al. Plasma polyunsaturated fatty acid pattern in active inflammatory bowel disease. Gut 1992;33:1365–9.[Abstract/Free Full Text]
  4. Esteve-Comas M, Núñez MC, Fernández-Bañares F, et al. Abnormal polyunsaturated fatty acid pattern in non-active inflammatory bowel disease. Gut 1993;34:1370–3.[Abstract/Free Full Text]
  5. Fernández-Bañares F, Esteve-Comas M, Mañé J, et al. Changes in mucosal fatty acid profile in inflammatory bowel disease and in experimental colitis: a common response to bowel inflammation. Clin Nutr 1997;16:177–83.
  6. Fernández-Bañares F, Cabré E, Esteve-Comas M, Gassull MA. How effective is enteral nutrition in inducing clinical remission in active Crohn's disease? A meta-analysis of the randomized clinical trials. JPEN J Parenter Enteral Nutr 1995;19:356–64.[Abstract]
  7. Gassull MA, Fernández-Bañares F, Cabré E, et al. Fat composition is the differential factor to explain the primary therapeutic effect of enteral nutrition in Crohn's disease. A double blind randomized multicenter European trial. Gastroenterology 2000;118(suppl): A117 (abstr).
  8. Takahashi K, Kato T, Schreiner GF, Ebert J, Badr KF. Essential fatty acid deficiency normalizes function and histology in rat nephritis. Kidney Int 1992;41:1245–53.[Medline]



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