Weeks Of Etanercept Treatment Research Articles

Effectiveness of Etanercept in Rheumatoid Arthritis: Real-World Data from the German Non-interventional Study ADEQUATE with Focus on Treat-to-Target and Patient-Reported Outcomes.

BackgroundFor rheumatoid arthritis (RA), the treat-to-target concept suggests attaining remission or at least low disease activity (LDA) after 12 weeks.ObjectivesThis German, prospective, multicenter, non-interventional study aimed to determine the proportion of patients with RA who achieved their treat-to-target aim after 12 and 24 weeks of etanercept (ETN) treatment in a real-life setting, as opposed to patients achieving their therapeutic target at a later timepoint (week 36 or 52).MethodsA total of 824 adults with a confirmed diagnosis of RA without prior ETN treatment were included. Remission and LDA were defined as DAS28 < 2.6 and DAS28 ≤ 3.2, respectively.ResultsThe proportion of patients achieving remission was 24% at week 12 and 31% at week 24. The proportion of patients achieving LDA was 39% at week 12 and 45% at week 24. The proportion of patients achieving remission or LDA further increased beyond week 24 up to week 52. Improvement in pain and reduction in concomitant glucocorticoid treatment were observed. Improvements in patient-reported outcomes were also seen in patients who did not reach remission or LDA. No new safety signals were detected.ConclusionsA considerable proportion of patients with RA attained the target of remission or LDA after 12 weeks of ETN treatment. Even beyond that timepoint, the proportion of patients achieving treatment targets continued to increase up to week 52.Trial RegistrationClinicalTrials.gov Identifier: NCT02486302.Supplementary InformationThe online version contains supplementary material available at 10.1007/s40744-021-00418-5.

OP0107 ETANERCEPT WITHDRAWAL AND RE-TREATMENT IN PATIENTS WITH INACTIVE NON-RADIOGRAPHIC AXIAL SPONDYLOARTHRITIS AT 24 WEEKS: RESULTS OF RE-EMBARK, AN OPEN-LABEL, PHASE IV TRIAL

Background:In the RE-EMBARK trial (NCT02509026), etanercept (ETN)-treated patients with non-radiographic axial spondyloarthritis (nr-axSpA) who achieved inactive disease (defined as Ankylosing Spondylitis Disease Activity Score with C-reactive protein [ASDAS CRP] &lt;1.3) in Period 1 (P1)1discontinued ETN for ≤40 weeks.Objectives:To assess the proportion of patients with inactive disease after P1 who experienced disease flare (ASDAS with erythrocyte sedimentation rate [ASDAS ESR] ≥2.1) within 40 weeks of ETN withdrawal and to estimate time to flare following ETN withdrawal.Methods:RE-EMBARK was a multicenter, open-label, Phase IV trial of ETN in patients with active nr-axSpA (meeting Assessment in SpondyloArthritis international Society criteria and with ASDAS CRP ≥2.1) and an inadequate response to ≥2 nonsteroidal anti-inflammatory drugs (NSAIDs) while taking a stable dose of 1 NSAID for ≥2 weeks before the first ETN dose. All patients received ETN (50 mg/week) plus NSAID for the first 24 weeks (P1). At week 24, patients with inactive disease discontinued ETN for ≤40 weeks (Period 2 [P2]). Those who experienced flare during P2 were re-treated with ETN for 12 weeks in Period 3 (P3). Kaplan-Meier (KM) analysis and Cox proportional hazard models were used to 1) estimate the probability of experiencing flare within a given time period, and 2) compare data between RE-EMBARK and the EMBARK trial (NCT01258738) of patients with nr-axSpA who met RE-EMBARK P2 entry criteria (achieved inactive disease after 24 weeks of ETN treatment) and continued treatment for a further ≤40 weeks.Results:Of the 209 patients in P1 (mean age, 33 years; women, 46%; white, 89%), 119 (57%) entered P2. The proportion of patients experiencing ≥1 flare increased from 22% (25/112) at P2 week 4 to 67% (77/115) at P2 week 40. Overall, 75% (86/115) of patients in P2 experienced flare and 50% experienced flare within 16 weeks (95% CI: 13-24 weeks, KM analysis). Conversely, data from the comparator EMBARK trial suggested that &lt;25% of patients receiving continuous ETN treatment over 40 weeks experienced flare. Cox proportional hazard model analysis showed an 85% relative risk reduction of experiencing flare during P2 in patients with inactive disease who continued ETN treatment vs those who discontinued. By P3 end 62% (54/87) of patients re-treated with ETN re-achieved inactive disease; 50% of patients who re-achieved inactive disease in P3 did so within 5 weeks (95% CI: 4-8 weeks, KM analysis). The observed trend of clinical improvement (P1), worsening (P2), and improvement (P3) was reflected in other clinical measures (Figure) plus measures of joint damage (Spondyloarthritis Research Consortium of Canada Sacroiliac Joint magnetic resonance imaging score) and quality of life (EQ-5D visual analog scale score); mean (standard deviation) score changes from each study period baseline–end were –6.1 (11.7) [P1], +1.5 (4.4) [P2], –2.0 (8.8) [P3] and +27.7 (26.7) [P1], –26.4 (30.5) [P2], +32.1 (26.3) [P3], respectively. There were no unexpected safety signals.Conclusion:For patients with nr-axSpA who achieved inactive disease with ETN and then discontinued treatment, a quarter maintained treatment-free inactive disease for 40 weeks and 50% maintained an ASDAS ESR score of &lt;2.1 for ≥16 weeks. Re-starting ETN allowed 62% of patients who flared to re-achieve inactive disease within 12 weeks.

Association between C-reactive protein gene variant and treatment efficacy of etanercept in ankylosing spondylitis patients receiving hip arthroplasty.

BackgroundC‐reactive protein (CRP) level is one of the most widely used parameters to assess ankylosing spondylitis (AS), since CRP is associated with poor radiographic progression of AS patients. Recent studies have investigated the association between CRP gene variants and AS risk, but with conflicting findings.Material and MethodsWe enrolled 232 AS cases and 314 controls in this case‐control study. Next, we assessed the association of CRP gene rs3091244 polymorphism with the efficacy of etanercept for AS. Genotyping was done using a custom‐by‐design 48‐Plex SNP scanTM Kit.ResultsCRP gene rs3091244 polymorphism was associated with an increased risk of AS in this Chinese population. Clinical indicators of AS patients including morning stiffness time, Bath AS function index (BASFI), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Visual Analogue Scale (VAS), erythrocyte sedimentation rate (ESR), and CRP were significantly decreased after 12 weeks of etanercept treatment. Furthermore, AA genotype carriers showed higher values of VAS, BASDAI, BASFI, and CRP before etanercept treatment. AA genotype or A allele of rs3091244 polymorphism was associated with Ankylosing Spondylitis Assessment Study group response criteria 20 scores (ASAS20) and Assessment in SpondyloArthritis international Society 40 response (ASAS40) improvement. In addition, AA genotype carriers showed significantly higher CRP levels compared with genotype GG carriers (16.3 vs 8.8 mg/L).ConclusionCRP gene rs3091244 polymorphism is associated with an increased risk of AS. Additionally, rs3091244 polymorphism could serve as a biomarker for good response to etanercept treatment in AS.

Efficacy of an anti-TNF-alpha agent in refractory livedoid vasculopathy: a retrospective analysis

Background Livedoid vasculopathy is a recurrent thrombo-occlusive vasculopathy of cutaneous blood vessels and its standard or first-line therapy is still controversial. Besides hypercoagulability, inflammatory factors may also play a secondary role in the pathogenesis of this disease. Monotherapy of thrombolytics cannot achieve satisfactory results because of concomitant inflammation. Objective This pilot study aimed to determine the efficacy of an anti-TNF-alpha agent in patients with refractory livedoid vasculopathy. Methods We studied five patients with livedoid vasculopathy who were resistant to steroids, antiplatelets, or danazol therapy, and were treated with etanercept 25–50 mg once a week for 12 consecutive weeks. We assessed clinical characteristics, laboratory findings, and etanercept’s efficacy on skin lesions, pain, and quality of life. Results Etanercept therapy resulted in fast relief of pain in a mean time of 2 weeks. The median duration for the disappearance of erythema and ulcer healing was 8.8 weeks and 10.6 weeks, respectively. There was a reduction in pain by 34.3% after 12 consecutive weeks of etanercept treatment. Disease severity and quality of life significantly improved. Conclusions In refractory livedoid vasculopathy patients, etanercept therapy is efficient for skin lesions and pain, and improvement of quality of life, especially in rapid relief of pain.

HLA-Cw6 allele, NFkB1 and NFkBIA polymorphisms play no role in predicting response to etanercept in psoriatic patients.

This retrospective study aimed to evaluate the role of NFKB1-94 insertion/deletion ATTG (rs28362491) and NFkBIA 2758 A>G (rs696) polymorphisms and HLA-Cw6 allele in predicting the response to etanercept, a TNF-α blocker, in a population of psoriatic patients naive to biologics. Genomic DNA was extracted from whole blood in a series of 96 psoriatic patients who received etanercept for at least 3 months. Patients were classified as responders if they achieved a Psoriasis Area and Severity Index improvement of at least 75% after 12 weeks of etanercept treatment and as nonresponders if Psoriasis Area and Severity Index improvement was less than 75%. Genotyping was performed using the PCR-restriction fragment length polymorphism (PCR-RFLP) method. We did not find any significant role of NFKB1-94 insertion/deletion ATTG (rs28362491) and NFkBIA 2758 A>G (rs696) polymorphisms and the HLA-Cw6 allele in predicting the response to etanercept. Our findings suggest that NFKB1 and NFkBIA polymorphisms are not related to the response to etanercept. They also indicate that the therapeutic response to etanercept is not influenced by the presence of the HLA-Cw6 allele, in contrast with previous evidence on ustekinumab, suggesting that such an association is related more to drug than to disease characteristics.

Combination therapy with etanercept in psoriasis: Retrospective analysis of efficacy and safety outcomes from real-life practice.

ObjectiveTo investigate the efficacy and safety outcomes of combination therapy used to optimize etanercept treatment in patients with psoriasis treated in real-life clinical practice.MethodsData from patients presenting with psoriasis, treated initially with etanercept monotherapy, were analysed retrospectively. Patients subsequently treated with combination therapy were further analysed. The Psoriasis Area and Severity Index (PASI) score was recorded for all patients receiving comedication; a subjective pain score was recorded in those with psoriatic arthritis receiving comedication after 12, 24 and 48 weeks’ treatment and thereafter at 6-month intervals.ResultsFrom the database of 400 patients treated with etanercept, 37 patients (18 male; 19 female; mean age 59.43 years) underwent combination therapy due to lack of efficacy. Patients received mostly short-term (range 4–34 weeks) comedication with corticosteroids, cyclosporine, methotrexate, nonsteroidal anti-inflammatory drugs, acitretin or sulphasalazine. There were significant reductions in the mean PASI score from baseline at all timepoints. There were also significant reductions in the mean pain VAS score from baseline at all timepoints in patients with psoriatic arthritis. The drug survival rate was 59.6% over a mean duration of 323 weeks of etanercept treatment. The safety profile of combination therapy was satisfactory.ConclusionsShort-term comedication in combination with etanercept may optimize treatment options and improve long-term drug survival in patients with psoriasis.

TNF-alpha gene polymorphisms can help to predict response to etanercept in psoriatic patients.

Genetic factors might have a role for lack of therapeutic response to anti-TNF-alpha agents, as previously suggested in patients with rheumatoid arthritis and inflammatory bowel disease. We evaluated the role of the main TNF-alpha polymorphisms (-238G>A, -308G>A, -857C>T) in predicting the response to etanercept, an anti-TNF-alpha fusion protein. Genomic DNA was extracted from buccal epithelial cells in a series of 97 psoriatic patients who received etanercept for at least 3 months. Patients were classified as responders, if they achieved a PASI improvement ≥ 75% after 12 weeks of etanercept treatment, and non-responders, if PASI improvement was <75%. Single-nucleotide polymorphisms (SNPs) in TNF-alpha gene (-238G>A, -308G>A, -857C>T) were genotyped by PCR restriction fragment length polymorphism (RFLP) assays. We found that patients heterozygous (GA) for the -238G>A polymorphism were more likely not responsive to therapy compared to the GG genotype. In fact, the GA genotype was found in 5/59 (8.5%) responders and in 14/38 (36.8%) non-responders (P = 0.001). A significant relationship with therapy was also observed for the -308G>A polymorphisms. In fact, the GG, GA and AA genotypes were detected in 48 (81.4%), 9 (15.3%) and 2 (3.4%) of the 59 responders and in 22 (57.9%), 11 (28.9%) and 5 (13.2%) of the 38 non-responder patients (P = 0.03). No association with therapy was observed for the -857C>T polymorphisms. Our study supports the role of TNF-alpha polymorphisms in predicting the response to anti-TNF-alpha agents. In particular, we found that the presence of -238G>A and -308G>A polymorphisms is associated with poor response to a 3-month therapy with etanercept. However, our data have yet to be validated in larger cohorts.

Early effects of tumor necrosis factor inhibition on bone homeostasis after soluble tumor necrosis factor receptor use.

Background/AimsOur aim was to assess whether short-term treatment with soluble tumor necrosis factor (TNF) receptor affects circulating markers of bone metabolism in rheumatoid arthritis (RA) patients.MethodsThirty-three active RA patients, treated with oral disease-modifying antirheumatic drugs (DMARDs) and glucocorticoids for > 6 months, were administered etanercept for 12 weeks. Serum levels of bone metabolism markers were compared among patients treated with DMARDs at baseline and after etanercept treatment, normal controls and naive RA patients not previously treated with DMARDs (both age- and gender-matched).ResultsBone-specific alkaline phosphatase (BSALP) and serum c-telopeptide (CTX)-1 levels were lower in RA patients treated with DMARDs than in DMARD-naive RA patients. After 12 weeks of etanercept treatment, serum CTX-1 and sclerostin levels increased. In patients whose DAS28 improved, the sclerostin level increased from 1.67 ± 2.12 pg/mL at baseline to 2.51 ± 3.03 pg/mL, which was statistically significant (p = 0.021). Increases in sclerostin levels after etanercept treatment were positively correlated with those of serum CTX-1 (r = 0.775), as were those of BSALP (r = 0.755).ConclusionsRA patients treated with DMARDs showed depressed bone metabolism compared to naive RA patients. Increases in serum CTX-1 and sclerostin levels after short-term etanercept treatment suggest reconstitution of bone metabolism homeostasis.

IL-17 and TNF Synergistically Modulate Cytokine Expression while Suppressing Melanogenesis: Potential Relevance to Psoriasis

Inflammation-associated pigmentation changes are extremely common, but the etiology behind this clinical observation remains elusive. Particularly, it is unclear how the myriad of cytokines known to be involved in inflammatory skin processes affect epidermal melanocytes. We sought to determine how IL-17 and TNF influence normal human melanocytes, as these two cytokines have been implicated in various skin diseases. IL-17 and TNF jointly stimulated broad inductions of cytokines , including melanoma mitogens CXCL1 and IL-8. Moreover, IL-17 and TNF synergistically inhibited pigmentation-related signaling and melanin production, and induced keratinocytes production of β-defensin 3, an antagonist for melanocortin-receptor 1. When analyzing psoriasis lesions that are known to over express IL-17 and TNF, we observed an increase in melanocyte number and a simultaneous decrease in pigmentation signaling. Furthermore, therapeutic neutralization of TNF and IL-17 with mAbs results in a rapid recovery of pigment gene expression in psoriasis lesions. These results demonstrate that IL-17 and TNF can impact both the growth and pigment production of melanocytes, which may contribute to the pigmentation changes associated with psoriasis. These findings may allow the development of novel therapeutics for pigmentary disorders and bring new insights into the immune milieu surrounding melanocytes and related neoplasms.

Which subgroup of rheumatoid arthritis patients benefits from switching to tocilizumab versus etanercept after previous infliximab failure? A retrospective study

A retrospective study of 39 rheumatoid arthritis (RA) patients with an inadequate response to infliximab was conducted. The responses of subjects switching from infliximab to tocilizumab (n = 23) were compared to those of subjects switching to etanercept (n = 16). Disease activity was assessed by the Disease Activity Score 28-CRP ([C-reactive protein] DAS28-CRP), the Simplified Disease Activity Index (SDAI), and the Clinical Disease Activity Index (CDAI). Twenty-two patients completed 48 weeks of tocilizumab treatment, and 15 patients completed 48 weeks of etanercept treatment. In both treatment groups, 1 patient each discontinued treatment because of lack of efficacy. No serious adverse events occurred during the study, and no patients in either group withdrew due to adverse events. At week 48, there was a significant reduction from baseline in DAS28-CRP, SDAI, and CDAI values after switching to either tocilizumab or etanercept, and there was no significant difference in efficacy, as measured by the DAS28-CRP, SDAI, and CDAI, between the two treatment groups (p = 0.12, 0.76, and 0.86, respectively). These results suggest that safety and tolerability were similar for both treatments. A switch from infliximab to either tocilizumab or etanercept in patients with RA who have not responded to infliximab is a feasible, well-tolerated treatment option.

Which subgroup of rheumatoid arthritis patients benefits from switching to tocilizumab versus etanercept after previous infliximab failure? A retrospective study

A retrospective study of 39 rheumatoid arthritis (RA) patients with an inadequate response to infliximab was conducted. The responses of subjects switching from infliximab to tocilizumab (n = 23) were compared to those of subjects switching to etanercept (n = 16). Disease activity was assessed by the Disease Activity Score 28-CRP ([C-reactive protein] DAS28-CRP), the Simplified Disease Activity Index (SDAI), and the Clinical Disease Activity Index (CDAI). Twenty-two patients completed 48 weeks of tocilizumab treatment, and 15 patients completed 48 weeks of etanercept treatment. In both treatment groups, 1 patient each discontinued treatment because of lack of efficacy. No serious adverse events occurred during the study, and no patients in either group withdrew due to adverse events. At week 48, there was a significant reduction from baseline in DAS28-CRP, SDAI, and CDAI values after switching to either tocilizumab or etanercept, and there was no significant difference in efficacy, as measured by the DAS28-CRP, SDAI, and CDAI, between the two treatment groups (p = 0.12, 0.76, and 0.86, respectively). These results suggest that safety and tolerability were similar for both treatments. A switch from infliximab to either tocilizumab or etanercept in patients with RA who have not responded to infliximab is a feasible, well-tolerated treatment option.

Etanercept can induce resolution of renal deterioration in patients with amyloid A amyloidosis secondary to rheumatoid arthritis

The benefit of biological therapies in rheumatoid arthritis (RA) treatment is well known, but their role in amyloid A (AA) amyloidosis secondary to RA is unclear. The aim of this study was to clarify the clinical benefit of etanercept in RA patients with AA amyloidosis. We treated 14 RA patients who had serum amyloid A protein (SAA) 1.3 allele, with biopsy-confirmed AA amyloidosis with etanercept and investigated the efficacy of etanercept treatment, focusing on renal function retrospectively. The AA amyloidosis improved and stabilized after 89.1 ± 27.2 weeks. Proteinuria decreased from 2.24 ± 0.81 to 0.57 ± 0.41 g/day (P < 0.01) and SAA fell from 250 ± 129 to 26 ± 15 μg/ml (P < 0.01), respectively. Diarrhea secondary to gastrointestinal AA amyloidosis was less. Overall, the serum creatinine levels did not benefit with treatment, but in those with a creatinine values <2.0 mg/dl the creatinine level continued to fall (P = 0.021). Serum albumin increased following 96 weeks of etanercept treatment (P = 0.003). Etanercept treatment led to clinical improvement in proteinuria and serum albumin levels accompanied by a fall in SAA levels.

Psoriatic arthritis

In a chronic inflammatory disease, such as rheumatoid arthritis (RA), the hypothalamic-pituitary-adrenal axis is altered in three ways: (1) the inflammation-related spontaneous and stimulated secretion of cortisol is inadequate; (2) the inflammation-related secretion of adrenocorticotropic hormone (ACTH) is low; and (3) the levels of adrenal androgens decrease. In patients with RA, long-term therapy with anti-TNF therapy sensitizes the pituitary gland and improves adrenal androgen secretion. We have recently found that the mean serum levels of ACTH, cortisol, 17-hydroxyprogesterone (17OHP), and androstenedione (ASD) in 11 prednisolone-naïve patients with psoriatic arthritis did not markedly change during 12 weeks of etanercept treatment, nor did the serum cortisol/ACTH ratio. However, the greater increase in serum cortisol in comparison with serum 17OHP or ASD was related to clinical improvement, which indicates that the improvement was more related to the higher cortisol levels.

Effects of 14 weeks of TNF alpha blockade treatment on lipid profile in ankylosing spondylitis

Objective Cardiovascular morbidity and mortality seem to be increased in ankylosing spondylitis, perhaps as the result of biological inflammation and consecutive dyslipidemia. This study aims to investigate the impact of TNF alpha-inhibitors, an effective treatment, on lipid profile. Methods Thirty-four ankylosing spondylitis (AS) patients with active disease undergoing anti-TNF alpha therapy ( n = 20, infliximab; n = 7, etanercept; n = 7, adalimumab) were recruited. Disease activity parameters, total cholesterol, LDL-cholesterol, HDL-cholesterol and triglycerides were assessed at baseline and after 14 weeks of treatment. Results After 14 weeks of TNF alpha blockade treatment, there was a significant increase in levels of total cholesterol (5.08 ± 1.20 vs. 4.73 ± 1.12 mmol/l; p = 0.01) and HDL-cholesterol (1.61 ± 0.47 vs. 1.47 ± 0.35 mmol/l; p = 0.008), but no resulting change in the atherogenic index (3.43 ± 1.13 vs. 3.35 ± 0.93; p = 0.87). There was also no change in concentrations of triglycerides (1.33 ± 1.22 vs. 1.27 ± 0.98 mmol/l; p = 0.794) and LDL-cholesterol (3.15 ± 0.99 vs. 2.91 ± 0.93 mmol/l; p = 0.24). TNF alpha inhibitor treatment was followed by a significant improvement in all disease activity parameters: VAS pain or VAS disease activity, BASDAI or BASFI and systemic inflammation. Sub-group analysis showed that monoclonal antibodies increased total and LDL-cholesterol levels but did not change the atherogenic index. Conversely, 14 weeks of etanercept treatment was followed by no change in lipid profile. Conclusion TNF alpha inhibitors may be successful in reducing cardiovascular risk in AS, as in RA, but not by affecting lipid profile. However, there is insufficient documented evidence, and long-term investigations are needed to define the possible protective mechanisms of TNFalpha inhibitor treatment in spondylarthropathies.

Tumor Necrosis Factor-α Blockade Leads to Decreased Peripheral T Cell Reactivity and Increased Dendritic Cell Number in Peripheral Blood of Patients with Ankylosing Spondylitis

To study the effect of tumor necrosis factor-alpha (TNF-alpha) antagonist (etanercept) treatment on the peripheral T cell reactivity of patients with ankylosing spondylitis (AS). Peripheral blood mononuclear cells were collected from 40 patients with AS at baseline, after 2 and 6 weeks of etanercept treatment or placebo treatment, and from healthy controls. The number of cells secreting various cytokines was detected by enzyme linked immunospot. Serum soluble interleukin 2 (IL-2) receptor level was measured by ELISA. T cell proliferation was assayed with the WST-1 live cell-staining method. The myeloid dendritic cell (mDC) and regulatory T cell (Treg) levels were analyzed by fluorescence activated cell sorting. . After 2 and 6 weeks of etanercept treatment, the number of TNF-alpha-secreting monocytes decreased. Although the T cell proliferation rate remained stable, the number of T cells secreting IL-2 and interferon-gamma under anti-CD3/anti-CD28 stimulation was significantly decreased. The level of serum soluble IL-2R (sIL-2R), a T cell activation marker, also declined. The changes in T cell reactivity were correlated with a significant increase in MHC Class II-positive mDC cells in circulation. An increase in Treg cell numbers was also observed. . The anti-TNF-alpha therapy blockaded MHC Class II-positive mDC maturation, enhanced regulatory T cell levels, and suppressed the functions of effector T cells. The reduced T cell reactivity could contribute to the efficacy of the TNF-alpha antagonist therapy in patients with AS.

Effects of etanercept on C-reactive protein levels in psoriasis and psoriatic arthritis

C-reactive protein (CRP), an inflammation biomarker, indicates cardiovascular risk and is elevated in psoriasis. The effect of etanercept on CRP in psoriasis has not been previously examined. The primary objective was to examine the effect of etanercept on CRP levels from baseline to week 12 compared with placebo. Secondary objectives included assessment of baseline CRP and relationships between CRP and body mass index (BMI), statin drug use, and Psoriasis Area and Severity Index (PASI) scores. A retrospective analysis was conducted of CRP levels from patients with psoriasis who participated in a randomized, double-blind, placebo-controlled, U.S. registrational study. Data were analysed separately if patients self-reported psoriatic arthritis. Baseline CRP levels were elevated in patients with psoriasis with and without psoriatic arthritis. CRP was significantly reduced in both groups after 12 weeks of etanercept treatment. Patients with psoriasis with psoriatic arthritis and patients with higher BMIs had higher median baseline CRP values and greater reduction of CRP values compared with those without psoriatic arthritis and those with lower BMIs. Etanercept lowered CRP levels in statin users and nonusers. Regression analyses revealed an association between baseline PASI score and baseline CRP independent of BMI in patients with psoriasis. Patients with moderate to severe plaque psoriasis, with or without psoriatic arthritis, have increased systemic inflammation demonstrated by elevated CRP levels. In psoriasis without psoriatic arthritis, skin disease activity is associated significantly with CRP elevation, independent of BMI, age and sex. Etanercept reduced CRP levels in all but the normal weight psoriasis group without psoriatic arthritis.