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Published on: February 27, 2014
Abnormal plasma polyunsaturated fatty acid pattern in non-active inflammatory bowel disease
M Esteve-Comas1, M C Núñez, F Fernández-Bañares
1Department of Gastroenterology, Hospital Universitari Germans Trias i Pujol, Badalona, Spain.
Inactive inflammatory bowel disease (IBD) patients show abnormal polyunsaturated fatty acid (PUFA) patterns, with elevated n3 PUFAs. This suggests a primary metabolic defect in PUFA metabolism persists even in remission.
Area of Science:
- Gastroenterology
- Biochemistry
- Nutritional Science
Background:
- Abnormal plasma polyunsaturated fatty acid (PUFA) patterns, characterized by increased n3 and decreased n6 PUFAs, are observed in active inflammatory bowel disease (IBD).
- A hypothesis suggests a primary defect in PUFA metabolism may underlie IBD.
Purpose of the Study:
- To investigate plasma PUFA patterns in patients with inactive IBD.
- To compare PUFA patterns in ulcerative colitis (UC) patients who underwent colectomy versus those without colectomy and in Crohn's disease (CD) patients.
Main Methods:
- Plasma fatty acids were analyzed using semi-capillary column gas-liquid chromatography.
- Three groups of inactive IBD patients were studied: UC without colectomy (n=24), UC with colectomy (n=15), and CD (n=27).
- Comparison was made against control groups.
Main Results:
- Patients with inactive UC (both operated and non-operated) and CD exhibited significantly higher plasma concentrations and percentages of C22:6n3 and higher unsaturation indices compared to controls (p < 0.0001).
- These elevated n3 PUFA markers were more pronounced in remission due to the absence of confounding factors like malnutrition, steroids, and active inflammation.
- The persistence of these abnormalities in both operated and non-operated UC groups was noted.
Conclusions:
- Inactive IBD is associated with an altered plasma PUFA profile, notably increased n3 fatty acids, suggesting enhanced PUFA biosynthesis.
- The findings indicate a potential primary abnormality in PUFA metabolism in IBD, which is evident even during remission and across different disease phenotypes and surgical histories.
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