Session Information
Date: Sunday, November 5, 2017
Title: Spondyloarthropathies and Psoriatic Arthritis – Pathogenesis, Etiology Poster I
Session Type: ACR Poster Session A
Session Time: 9:00AM-11:00AM
Background/Purpose: Psoriatic arthritis (PsA) is an inflammatory disease affecting the joints and connective tissue and is associated with psoriasis of the skin and nails. There is no reliable biomarker to identify psoriatic patients at risk of joint disease or disease progression. Eicosanoids, including prostaglandins and leukotrienes, are biological lipids that are implicated in various pathological processes including inflammation. We hypothesized that by defining more precisely the eicosanoid profile in PsA patients, we might identify novel diagnostic or prognostic biomarkers for disease activity and PsA pathogenesis.
Methods: Patients with PsA, diagnosed based on the CASPAR criteria, were recruited from the Rheumatology Outpatient Clinic at the University of California, San Diego. A thorough clinical examination, including joint and skin disease evaluations, was conducted. Patients completed a health assessment questionnaire. DAS28, Clinical Disease Activity Index (CDAI) and Simple Disease Activity Index (SDAI) scores and body surface area (BSA) of psoriasis were calculated. Serum eicosanoids were determined by mass spectrometry and were classified in groups according to the enzyme that participates in synthesis: cyclooxygenase (COX), 5-, 12- or 15-lipoxygenase (LOX), cytochrome P450, or non-enzymatic pathway. Inflammation markers were determined by ELISA. Statistical analysis included mean, standard deviation and Spearman correlation.
Results: 43 patients (average age 49.8, standard deviation 10.88) were recruited. Thirty-two (74.41%) had active skin disease with an average BSA of 4.25 (SD, 13.67). The means (SDs) of DAS28PCR was 2.25 (1.25) and CDAI was 10.69 (11.87). 48.83% of patients had nail disease, 20.93% had enthesitis, and 4.65% had dactylitis. Further, 65.11% received biological therapy (46.42% of them in association with a synthetic disease modifying drug, such as DMARD), 13.95% received sDMARD in monotherapy, and 20.9% had symptomatic treatment. Several eicosanoids, especially those in the 12-15-LOX pathway, significantly correlated with joint disease activity, but not with skin disease activity (Table 1). Several eicosanoids correlated with serum markers of (IL6, Resistin, EGF, IL1β and IL8), but not with CRP (Table 1). Of note, there was a weak correlation between CRP and SDAI that didn’t reach statistical significance (p=0.06).
Table 1. Correlation of Eicosanoids with clinical and serum parameters of inflammation |
|||||||||||
Eicosanoid |
CDAI |
SDAI |
DAS28 |
BSA |
CRP |
IL6 |
EGF |
Resistin |
IL1β |
IL8 |
|
COX |
PGE2 |
0.294* |
0.319** |
0.592*** |
|||||||
15-LOX |
15-HETE |
0.259* |
0.382*** |
0.333** |
0.392** |
0.499*** |
0.428*** |
0.399*** |
0.533*** |
||
15-HEPE |
0.380** |
0.364** |
0.478*** |
0.491*** |
0.484*** |
0.304** |
0.566*** |
||||
15HETrE |
0.317** |
0.489*** |
0.379** |
0.496*** |
0.579** |
0.638*** |
0.310** |
0.603*** |
|||
13HODE |
0.318** |
0.292* |
|||||||||
13HOTrE |
0.453*** |
0.471*** |
0.432*** |
0.276* |
0.290* |
0.342** |
0.441*** |
||||
12-LOX |
12-HETE |
0.260* |
0.383** |
0.391** |
0.472*** |
||||||
12-HEPE |
0.266* |
0.317** |
0.539*** |
0.501*** |
0.512*** |
||||||
Tetranor 12-HETE |
0.399*** |
0.365** |
0.373** |
0.386** |
0.530*** |
0.547*** |
|||||
HXB3 |
0.350** |
0.284* |
0.366** |
0.440*** |
0.485*** |
0.290* |
0.552*** |
||||
PGE2-Prostaglandin E; HETE- hydroxyeicosatetraenoic acid; HETrE- hydroxyeicosatrienoic acid; HODE- Hydroxyoctadecadienoic acid; HOTrE- hydroperoxyoctadecatrienoic acid; HXB3-Hepoxilin B3.* p<0.1, ** p<0.05, *** p<0.01 |
Conclusion: Eicosanoids, especially in the 12- and 15- LOX pathways, correlated with joint disease activity better than the CRP, but not with skin disease, suggesting that they may be potential biomarkers of joint activity in psoriatic and PsA patients. Further studies are needed to determine whether 12- and 15-LOX pathways also play a role in the pathogenesis of joint inflammation in PsA.
To cite this abstract in AMA style:
Coras R, Kavanaugh A, Huynh DH, Shadyab A, Marsal S, Quehenberger O, Guma M. Role of Eicosanoids As Biomarkers in Psoriatic Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/role-of-eicosanoids-as-biomarkers-in-psoriatic-arthritis/. Accessed .« Back to 2017 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/role-of-eicosanoids-as-biomarkers-in-psoriatic-arthritis/