“…Therefore, management of CVD risk factors is recommended . In addition, an association has been suggested between peripheral joint inflammation and lipid dysregulation in PsA .The magnitude and dose dependency of increases in lipid levels to month 6 in patients with psoriatic arthritis (PsA) receiving tofacitinib were consistent with findings in patients with rheumatoid arthritis (RA) and psoriasis.As increases in low‐density lipoprotein cholesterol were paralleled by increases in high‐density lipoprotein cholesterol (HDL‐c), no meaningful changes in the total cholesterol:HDL‐c ratio were observed.The incidence of major adverse cardiovascular events in patients with active PsA was within the range reported in prior tofacitinib studies in RA and psoriasis, and was generally consistent with data reported in the literature for other PsA treatments.There is no evidence at this time that treatment of PsA with tofacitinib is associated with increased cardiovascular risk.…”
Objective.
The risk of cardiovascular (CV) disease is higher in patients with psoriatic arthritis (PsA) versus the general population. Tofacitinib is an oral Janus kinase inhibitor for the treatment of PsA. As tofacitinib increases circulating lipid levels in some patients, we evaluated CV risk factors and major adverse cardiovascular events (MACE) in patients with active PsA receiving tofacitinib 5 or 10 mg twice daily plus conventional synthetic disease-modifying antirheumatic drugs.
Methods.
Data were pooled from two Phase 3 studies (OPAL Broaden [NCT01877668] and OPAL Beyond [NCT01882439]) and one ongoing long-term extension (OPAL Balance [NCT01976364]; data cut-off January 2017; database not locked). Outcomes included fasting lipid levels, blood pressure (BP), hypertension-related adverse events (AEs; including ‘hypertension’, ‘high blood pressure’, and ‘increased blood pressure’), and MACE.
Results.
Overall, 783 tofacitinib-treated patients were included. Percentage increases from baseline in low-density and high-density lipoprotein cholesterol levels (LDL-c and HDL-c, respectively) ranged from 9–14% for tofacitinib 5 and 10 mg at 3 and 6 months; no meaningful changes in LDL-c/HDL-c or total cholesterol/HDL-c ratios were observed. BP remained stable over 24 months. Fifty-eight (7.4%) patients had hypertension-related AEs; none were fatal (incidence rate [IR] per 100 patient-years: 4.81; 95% confidence interval [CI]: 3.65–6.22). Five (0.6%) patients had MACE (IR: 0.24; 95% CI: 0.05–0.70); two were fatal.
Conclusion.
Serum lipid level increases at month 3 following tofacitinib treatment in PsA were consistent with observations in rheumatoid arthritis and psoriasis. The incidence rate of hypertension-related AEs and MACE was low; long-term follow-up is ongoing.
“…Therefore, management of CVD risk factors is recommended . In addition, an association has been suggested between peripheral joint inflammation and lipid dysregulation in PsA .The magnitude and dose dependency of increases in lipid levels to month 6 in patients with psoriatic arthritis (PsA) receiving tofacitinib were consistent with findings in patients with rheumatoid arthritis (RA) and psoriasis.As increases in low‐density lipoprotein cholesterol were paralleled by increases in high‐density lipoprotein cholesterol (HDL‐c), no meaningful changes in the total cholesterol:HDL‐c ratio were observed.The incidence of major adverse cardiovascular events in patients with active PsA was within the range reported in prior tofacitinib studies in RA and psoriasis, and was generally consistent with data reported in the literature for other PsA treatments.There is no evidence at this time that treatment of PsA with tofacitinib is associated with increased cardiovascular risk.…”
Objective.
The risk of cardiovascular (CV) disease is higher in patients with psoriatic arthritis (PsA) versus the general population. Tofacitinib is an oral Janus kinase inhibitor for the treatment of PsA. As tofacitinib increases circulating lipid levels in some patients, we evaluated CV risk factors and major adverse cardiovascular events (MACE) in patients with active PsA receiving tofacitinib 5 or 10 mg twice daily plus conventional synthetic disease-modifying antirheumatic drugs.
Methods.
Data were pooled from two Phase 3 studies (OPAL Broaden [NCT01877668] and OPAL Beyond [NCT01882439]) and one ongoing long-term extension (OPAL Balance [NCT01976364]; data cut-off January 2017; database not locked). Outcomes included fasting lipid levels, blood pressure (BP), hypertension-related adverse events (AEs; including ‘hypertension’, ‘high blood pressure’, and ‘increased blood pressure’), and MACE.
Results.
Overall, 783 tofacitinib-treated patients were included. Percentage increases from baseline in low-density and high-density lipoprotein cholesterol levels (LDL-c and HDL-c, respectively) ranged from 9–14% for tofacitinib 5 and 10 mg at 3 and 6 months; no meaningful changes in LDL-c/HDL-c or total cholesterol/HDL-c ratios were observed. BP remained stable over 24 months. Fifty-eight (7.4%) patients had hypertension-related AEs; none were fatal (incidence rate [IR] per 100 patient-years: 4.81; 95% confidence interval [CI]: 3.65–6.22). Five (0.6%) patients had MACE (IR: 0.24; 95% CI: 0.05–0.70); two were fatal.
Conclusion.
Serum lipid level increases at month 3 following tofacitinib treatment in PsA were consistent with observations in rheumatoid arthritis and psoriasis. The incidence rate of hypertension-related AEs and MACE was low; long-term follow-up is ongoing.
“…Psoriatic arthritis (PsA) is a chronic condition associated with psoriasis (PsO), spondylitis and peripheral arthritis, and comorbidities, including cardiovascular disorders with an increased risk of death [1][2][3]. PsA has been classified as a form of spondyloarthritis (SpA), and it shares some similar proinflammatory pathways with other SpAs [4][5][6][7] and similar metabolic burden with psoriasis [7,8].…”
Section: Introductionmentioning
confidence: 99%
“…PsA has been classified as a form of spondyloarthritis (SpA), and it shares some similar proinflammatory pathways with other SpAs [4][5][6][7] and similar metabolic burden with psoriasis [7,8]. However, PsA seems to have a different cardiovascular risk profile and higher cardiovascular risk (CVR) than other SpAs and cutaneous psoriasis (PsO) [1,2]. So, one can assume that cardiovascular risk in PsA is not only a sum of risk factors associated with PsO and SpA but may result from different pathogenic factors.…”
Objective: To investigate the associations of IL-18 serum levels with serum lipids, cardiovascular risk, and disease activity in patients with ankylosing spondylitis (AS) and psoriatic arthritis (PsA) with axial (axPsA) and peripheral (perPsA) joint involvement. Methods: 155 adult patients (PsA 61/AS 94) were enrolled in the study. Standard disease activity indices, BASDAI, and ASDAS, were calculated for AS and PsA and DAPSA for PsA. Sera from peripheral blood samples were obtained after night fasting. Serum concentrations of cytokines (IL-18, IL-17) were measured by ELISA, while lipid profile with total cholesterol (TC), triglycerides (TG), low-density cholesterol-(LDL), high-density cholesterol (HDL), and C-reactive protein (CRP) concentrations were determined using routine procedures. The atherogenic index was calculated using the standard formula AI = TC/HDL. Results: Patients with PsA and peripheral joint involvement (perPsA) had significantly higher IL-18 serum levels than axial PsA and AS patients (medians 160 vs. 116 vs. 80 pg/mL). In patients with PsA and in the subgroup with PsA+ ischemic heart disease (IHD), IL-18 positively correlated with atherogenic index (AI) (rho = 0.46 and rho = 0.67, respectively) and TG serum concentrations (rho = 0.4 and rho = 0.675), while negatively with HDL levels (rho= −0.37 and rho= −0.608). In PsA + IHD subgroup IL-18 serum levels correlated positively also with disease activity (DAPSA) (rho = 0.613). Importantly, in patients with perPsA, characterized by the highest IL-18 serum levels, cardiovascular risk, and frequency of both hypertriglyceridemia and IHD, positive correlations between IL-18 and IL-17 (rho = 0.47, p = 0.002), TG (rho = 0.45 p = 0.01) levels and AI (rho = 0.63 p = 0.021) were found. Whereas linear regression models revealed that IL-17, TG concentrations and the tender joint count had an impact on IL-18 Conclusions: We confirmed that patients with perPsA are characterized by a more pronounced proinflammatory and proatherogenic cardiovascular risk profile than patients with axPsA and AS. Importantly our study indicates that in PsA, but not in AS, elevated serum concentration of IL-18 is associated with higher disease activity and proatherogenic lipid profile, leading to a higher cardiovascular risk. Thus, our results point out IL-18 as a critical contributor in these pathological processes and possible therapeutic targets.
“…Анализ сопутствующих заболеваний показал, что, по сравнению с пациентами с РА, больные ПсА имеют больший риск развития дислипидемии, ожирения и сахарного диабета 2-го типа. Выявлена ассоциация между дислипидемией и периферическим артритом у больных ПсА [39][40][41].…”
Observational cohort investigations are an effective way to study chronic diseases, including psoriatic arthritis, in clinical practice. One of the tools to support such research is registers that collect data related to various aspects of the disease and pharmacotherapy. This review provides information on the main registers of patients with psoriatic arthritis.
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