Session Type: ACR Poster Session C
Session Time: 9:00AM-11:00AM
It is well established that psoriatic arthritis is associated with increased cardiovascular disease risk. The use of statins may impart anti-inflammatory effects, possibly through blocking mevalonate production, thereby preventing induction of trained immunity. Mevalonate activates mammalian target of rapamycin (mTOR) and other mediators, subsequently modifying inflammatory pathways. Several studies confirm beneficial effects of statins on C-reactive protein (CRP) in patients with rheumatoid arthritis and lupus. CRP enhances mTOR signaling. Therefore, we aimed to evaluate whether statin therapy affects psoriatic arthritis disease activity by evaluating the degree of systemic inflammation, using CRP elevation as a marker, in an outpatient population at a hospital based clinic.
A retrospective analysis was performed on the University of Tennessee Knoxville Patient Database for all patients with an ICD-10 code corresponding to psoriatic arthritis that had a CRP checked in the last 10 years. From the selected patients, we divided them into two separate groups: the first group of 54 patients were on statin therapy, and the second group of 152 were not on a statin. We also recorded the most recent CRP concentration, as well as other parameters including ESR, BMI, and specific treatments for psoriatic arthritis including any DMARD, biologic, or steroid use in each of these patients. Non-parametric Mann-Whitney U tests were used for between-subject comparisons using CRP concentration and other parameters with either the presence or absence of statin therapy. The association between CRP level and patient’s BMI was tested using Spearman’s rho correlation.
Out of a total of 220 patients with an ICD-10 code corresponding to psoriatic arthritis in our system over the last 10 years, 206 had CRP levels on record. In this group of 206, significant beneficial role of statin medication on CRP level was found when prescribed with or without conventional DMARDs or biologic agents. CRP level was found to be significantly lower in the patients on adjunct statin medication compared to the non-statin group (p = 0.003), with the statin group of 54 patients demonstrating lower median CRP level of 0.2 (IQR = 0.4) compared to non-statin group of 152 patients with median CRP of 0.4 (IQR = 0.6). ESR elevation was not significantly different between the groups though there was a trend, with lower levels seen in the statin group compared to the non-statin group (p = 0.07). The statin group demonstrated lower median ESR level of 5 (IQR = 8.0) compared to the non-statin group median ESR of 7 (IQR = 13.0). There was a statistically significant positive correlation between CRP and BMI with rs = 0.35, p < 0.001.
These results suggest a potentially beneficial role of statin therapy in patients with psoriatic arthritis. Statins produced significant biochemical improvement based on CRP level. More studies are needed to further characterize the effect of statins on clinical outcomes. These results also suggest that the pathogenesis of psoriatic arthritis may involve alterations in trained immunity.
To cite this abstract in AMA style:Jackson L, Bieber J, Heidel RE. Effect of Statins on CRP Elevation in Patients with Psoriatic Arthritis [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/effect-of-statins-on-crp-elevation-in-patients-with-psoriatic-arthritis/. Accessed October 27, 2020.
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