PARENTERAL NUTRITION WITH OMEGA-3 FATTY ACIDS RESULTS IN HIGH ENDOGENOUS EPA/DHA LEVELS IN SHORT BOWEL SYNDROME PATIENTS

Introduction:

Long-term parenteral nutrition (PN) of short bowel syndrome (SBS) patients bears an increased risk of intestinal failure associated liver disease (IFALD). The antiinflammatory properties of long-chain omega-3 polyunsaturated fatty acids (n-3 LC-PUFA) attracted attention for preventing IFALD. However, the relative impact and mechanisms of this approach have not been fully established yet, as required for recommending general use of n-3 LC-PUFA containing PN solutions in SBS patients.

Objectives:

A prospective pilot study was performed in adult IFALD-free SBS patients to investigate the effects of n-3 LC-PUFAs on endogenous fatty acid (FA) profiles, inflammatory markers, and liver function tests.

Methods:

8 SBS-patients (mean age 50 ± 24 years; pretreated with PN containing n-3 LC-PUFA) received n-3 LC-PUFA-free Lipovenös® MCT 20% (Fresenius Kabi AG) during an 8- week washout, followed by 8 weeks PN, wherein 25% of fat was replaced by the n-3 LC-PUFA-rich Omegaven® (Fresenius Kabi AG). 1538 ± 275 kcal per infusion were applied on 5.3 ± 1.4 days/week. Blood samples were taken every 4 weeks. The FA profile of erythrocytes yielded the HS-omega-3 index, which represents the sum of eicosapentaenoic acid and docosahexaenoic acid (EPA + DHA) as percentage of total FA.

Results:

At baseline SBS patients demonstrated an HS-omega-3 index of 12 ± 1.8. During wash-out this value declined continuously to 9 ± 0.8. Subsequent re-supplementation during additional 8 weeks resulted in significantly increased n-3 PUFAs (C20:5n3, C22:5n3, and C22:6n3) and decreased saturated and n-6 FA (C14:0, C18:2n6, C18:3n6, C20:2n6, C20:3n6, C20:4n6, and C22:4n6) leading to a raised the HS-omega-3 index of 13 ± 1.1. These changes in endogenous FA profiles were accompanied by stable laboratory parameters and a clinically stable course.

Conclusion:

A high baseline HS-omega-3-index did exclude n-3 LC-PUFA deficiency on pre-study PN, however, a specific reduction of n-3 LC-PUFA on wash-out and reversible increase on re-supplementation could be demonstrated and was associated with clinical and paraclinical stability indicating exceptionally effective n-3 LC-PUFA supplementation. Thus, n-3 LC-PUFA-rich PN results in extraordinarily high endogenous EPA/DHA levels compared to oral supplementation (HS-omega-3 indices 4 to 8). Future studies are needed to determine the appropriate dose range of n-3 LC-PUFA to exert the potential for protective modification of inflammation and/or metabolism in SBS patients.

Disclosure of Interest:

None declared.