Non-steroidal anti-inflammatory drugs (NSAIDs) are the basic treatment of pain and stiffness in patients with ankylosing spon- dylitis (AS). NSAIDs act by blocking the synthesis of eicosanoids which are derived from 20-carbon long-chained polyunsaturated fatty acids (LCPUFAs). LCPUFAs in the body are obtained from the diet or from endogenous elongation of shorter dietary poly- unsaturated fatty acids.In a cross-sectional design, dietary intake of LCPUFAs, com- position of LCPUFAs in plasma and adipose tissues and disease activity were assessed among patients with AS who were not on treatment with biologics. Blood samples and gluteal fat biopsy were drawn from sixty-six patients (51 male, 15 female,mean age 48 years, range 26-65) with AS fulfilling the modified New York criteria. Dietary intake of LCPUFAs were calculated on the ba- sis of a semi-quantitative food frequency questionnaire. Plasma and adipose tissue content of LCPUFAs were assessed using gas chromatography. Disease status was measured with erythrocyte sedimentation rate (ESR, Westergren), high sensitive C-reactive protein (hiCRP) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI).The phospholipid plasma level of Arachodonic Acid (AA) correlated significantly with disease activity according to both the total BASDAI score (Rs=0.39, p<0.01), and five of its six sub-scores. Levels of other long-chained fatty acids in plasma phospholipids such as dihomo gammalinolenic acid and eicosa- pentaenoic acid did not correlate with BASDAI. Neither did con- tents of LCPUFAs in gluteal adipose tissue and dietary intake correlate with BASDAI.The plasma phospholipid content of AA correlated with BAS- DAI, and may be regarded as a biomarker for disease activity. The lack of correlation between BASDAI and LCPUFAs in diet and adipose tissue, suggests that the endogenous production and incorporation of AA in phospholipids may be involved in the pathogenesis of AS.