Tumor Necrosis Factor Inhibitor Therapy Research Articles

The effect of tumor necrosis factor inhibitor therapy on the incidence of myocardial infarction in patients with psoriasis: a retrospective study

Background: Psoriasis has been shown to be associated with increased incidence of myocardial infarction (MI). The data on the effect of tumor necrosis factor (TNF) inhibitors on MI in psoriasis are scarce.Objective: To evaluate the effect of TNF inhibitors on the risk of MI in psoriasis patients compared with methotrexate (MTX) and topical agents.Methods: Data were obtained from the Electronic Health Records database of Farwaniya Hospital from psoriasis patients seen from January 2008 to December 2014. Patients were categorized into TNF inhibitor, MTX and topical cohorts.Results: The study included 4762 psoriasis patients. Both TNF inhibitor and MTX cohorts showed a statistically lower rate of MI compared with topical cohort. However, there was no statistically significant difference in MI rate between TNF inhibitor and MTX cohorts (P = .32). The probability of MI was lower in TNF inhibitor responders compared with non-responders (p = .001).Conclusions: The use of TNF inhibitors in psoriasis showed a significant reduction in the risk of MI compared with topical agents and a non-significant reduction compared with MTX. Responders to TNF inhibitor therapy showed a reduction in MI rate compared with non-responders.

Treatment patterns of biologics in US patients with ankylosing spondylitis: descriptive analyses from a claims database.

Examine treatment patterns among patients with active ankylosing spondylitis (AS) treated with a TNF inhibitor (TNFi). Patients with AS who initiated a TNFi between1January 2013, and 31January 2015, were identified in the Optum Research Database. Outcomes included adherence, persistence, discontinuation and therapy modifications of the index TNFi during 12-month follow-up. Of the 426patients included, 40.6% persisted on the index TNFi for ≥12months, 31.0% discontinued, 21.4% switched to a different TNFi, and 7.0% discontinued and then restarted. Of the 333patients who persisted on their TNFi for >90days, 44.7% received ≥1 add-on medication. A high proportion of patients with AS switched, discontinued or modified their TNFi therapy.

Rebound in Measures of Disease Activity and Symptoms in Corrona Registry Patients with Psoriatic Arthritis Who Discontinue Tumor Necrosis Factor Inhibitor Therapy after Achieving Low Disease Activity.

Rebound may occur in patients with psoriatic arthritis (PsA) who discontinue TNF inhibitor (TNFi) therapy in low disease activity (LDA). Using physician and patient reports, we quantified rebound following TNFi discontinuation [defined as Clinical Disease Activity Index (CDAI) score > 10 or TNFi restart] and time to rebound in adults with PsA in LDA (CDAI score ≤ 10) at TNFi discontinuation. Rebound occurred in 73% (69/94) of patients soon after discontinuation (median time to rebound 8.0 mos, 95% CI 6.0-12.0). Rebound occurred frequently in patients with PsA after TNFi discontinuation. TNFi discontinuation after achieving LDA should be carefully considered.

Association between NICE guidance on biologic therapies with rates of hip and knee replacement among rheumatoid arthritis patients in England and Wales: An interrupted time-series analysis.

To estimate the impact of NICE approval of tumor necrosis factor inhibitor (TNFi) therapies on the incidence of total hip replacement (THR) and total knee replacement (TKR) among rheumatoid arthritis (RA) patients in England and Wales. Primary care data [Clinical Practice Research Datalink (CPRD)] for the study period (1995-2014) were used to identify incident adult RA patients. The age and sex-standardised 5-year incidence of THR and TKR was calculated separately for RA patients diagnosed in each six-months between 1995-2009. We took a natural experimental approach, using segmented linear regression to estimate changes in level and trend following the publication of NICE TA 36 in March 2002, incorporating a 1-year lag. Regression coefficients were used to calculate average change in rates, adjusted for prior level and trend. We identified 17,505 incident RA patients of whom 465 and 650 underwent THR and TKR surgery, respectively. The modeled average incidence of THR and TKR over the biologic-era was 6.57/1000 person years (PYs) and 8.51/1000 PYs, respectively, with projected (had pre-NICE TA 36 level and trend continued uninterrupted) figures of 5.63/1000 PYs and 12.92 PYs, respectively. NICE guidance was associated with a significant average decrease in TKR incidence of -4.41/1000 PYs (95% C.I. -6.88 to -1.94), equating to a relative 34% reduction. Overall, no effect was seen on THR rates. Among incident RA patients in England and Wales, NICE guidance on TNFi therapies for RA management was temporally associated with reduced rates of TKR but not THR.

Disease activity in axial spondyloarthritis after discontinuation of TNF inhibitors therapy.

ObjectiveUse of tumour necrosis factor inhibitors (TNFi) has proved to be an important step forward in the treatment of axial spondyloarthritis (axSpA), but the duration of the therapy as well as the management in case of low disease activity (LDA) or remission are not clearly established. Currently, the identification of potential predictors associated with the treatment discontinuation is the basic purpose of many clinical studies. The aim of this study was to analyze the influence of the discontinuation of TNFi therapy on the disease activity in patients with low disease activity.Material and methodsThe study included 65 patients; 47 of patients (72%) were treated with etanercept, 16 (2%) with adalimumab and 2 (3%) with infliximab.ResultsThe mean age of the patients was 45 years, the mean BASDAI score was 6.8 and VAS for low back pain was 76 mm at baseline. 54 patients with axSpA (83%) achieved LDA after 9 months of anti-TNF therapy. During follow-up 40 patients (74% of patients with LDA) had an increase of the disease activity after mean 14 weeks and needed to restart the treatment with TNFi. After restart of the therapy LDA was regained in all patients after mean 7 weeks. 11 patients (17%) have never achieved LDA and 14 patients (22%) had LDA longer than 6 months without relapse. At baseline higher levels of CRP and ESR were observed in patients with relapse of the disease at the end of treatment and with LDA shorter than 6 months.ConclusionsChanges in the values of disease activity indicators (CRP, ESR) correlated with more stable response to TNFi therapy. Over 50% of patients who were treated with TNFi needed to restart the therapy. Treatment resumption allowed to regain a good clinical effect among affected patients.

Long-term follow-up of secondary amyloidosis patients treated with tumor necrosis factor inhibitor therapy: A STROBE-compliant observational study.

There are no treatment modalities, which were proven to prevent the deposition of amyloid, proteinuria, and loss of renal function due to amyloidosis. Anti-tumor necrosis factor agents (anti-TNFs) were shown to decrease the production of serum amyloid A protein.We aimed to evaluate the long-term efficacy and safety of anti-TNFs in secondary (AA) amyloidosis patients treated in a single center.Thirty-seven patients with AA amyloidosis were started an anti-TNF for AA amyloidosis between March 2001 and June 2008 and followed until May 2016 unless deceased. They were surveyed for the endpoints of death, development of end-stage renal disease (ESRD), switch to another agent due to worsening of amyloidosis and adverse events.Among the 37 patients, 12 (32%) had died, 9 (24%) had ESRD, and 8 (22%) had started another group of biologic due to worsening of amyloidosis indicated by an increase in proteinuria, 5 (14%) patients are still doing well with anti-TNFs, and 3 (8%) are off treatment at the end of a median follow-up of 10 (interquartile range [IQR]: 5.5–10.5) years since the start of anti-TNFs and 10 (IQR: 8–13) years since the diagnosis of AA amyloidosis. Most common serious adverse events were sepsis and thrombotic events observed in 8 and 4 patients, respectively.Treatment with anti-TNFs may be associated with a higher survival rate compared with historic cohorts of AA amyloidosis, especially when started early with a lower serum creatinine level at baseline. Caution is needed regarding serious adverse events, especially infections.

Development of paradoxical inflammatory disorders during treatment of psoriasis with TNF inhibitors: a review of published cases.

TNF inhibitors have proven to be effective and relatively safe in the management of psoriasis. While infections and certain malignancies are established as acknowledged side effects, paradoxical inflammatory, non-neoplastic, noninfectious adverse events are being recognized less frequently. We aimed to identify published, peer-reviewed cases of paradoxical inflammatory, non-neoplastic, noninfectious adverse events in psoriasis patients during TNF inhibitor therapy. A literature search in MEDLINE was performed for articles published from inception through the 8th of June 2016 that reported suspected incidents fulfilling a predefined search strategy. In addition, articles identified by reference lists were added. A total of 295 cases from various organ systems among 13 269 patients were identified: 91 cases were related to infliximab, 101 cases were related to etanercept, and 102 cases were related to adalimumab. One case report was related to both etanercept and adalimumab. Induction of paradoxical non-neoplastic noninflammatory adverse events in psoriasis patients treated with a TNF inhibitor is worth recognizing. The amount of cases identified by this study suggests that continuous surveillance and research into these adverse effects is relevant. Nondermatologic paradoxical inflammatory reactions may be underreported.

Treatment Persistence and Clinical Outcomes of Tumor Necrosis Factor Inhibitor Cycling or Switching to a New Mechanism of Action Therapy: Real-world Observational Study of Rheumatoid Arthritis Patients in the United States with Prior Tumor Necrosis Factor Inhibitor Therapy.

IntroductionTo examine treatment persistence and clinical outcomes associated with switching from a tumor necrosis factor inhibitor (TNFi) to a medication with a new mechanism of action (MOA) (abatacept, anakinra, rituximab, tocilizumab, or tofacitinib) versus cycling to another TNFi (adalimumab, certolizumab pegol, etanercept, golimumab, or infliximab) among patients with rheumatoid arthritis.MethodsThis retrospective, longitudinal study included patients with rheumatoid arthritis in the JointMan® US clinical database who received a TNFi in April 2010 or later and either cycled to a TNFi or switched to a new MOA therapy by March 2015. Cox proportional hazards models were used for time to non-persistence (switching or discontinuing). An ordinary least squares regression model compared 1-year reduction from baseline for the Clinical Disease Activity Index (CDAI).ResultsThere were 332 (54.2%) TNFi cyclers and 281 (45.8%) new MOA switchers. During a median follow-up of 29.9 months, treatment persistence was 36.7% overall. Compared with new MOA switchers, TNFi cyclers were 51% more likely to be non-persistent (adjusted hazard ratio, 1.511; 95% CI 1.196, 1.908), driven by a higher likelihood of switching again (adjusted hazard ratio, 2.016; 95% CI 1.428, 2.847). Clinical outcomes were evaluable for 239 (53.3%) TNFi cyclers and 209 (46.7%) new MOA switchers. One-year mean reduction in CDAI from baseline to end of follow-up was significantly higher for new MOA switchers than TNFi cyclers (−7.54 vs. −4.81; P = 0.037), but the difference was not statistically significant after adjustment for baseline CDAI (−6.39 vs. −5.83; P = 0.607).ConclusionIn this study, TNFi cycling was common in clinical practice, but switching to a new MOA DMARD was associated with significantly better treatment persistence and a trend toward greater CDAI reduction that was not significant after adjustment for baseline disease activity.FundingSanofi and Regeneron Pharmaceuticals.

Switching tumor necrosis factor inhibitors in the treatment of axial spondyloarthritis.

To assess the impact of switching tumor necrosis factor (TNF)-alpha inhibitors on patients with axial spondyloarthritis (axSpA). PubMed literature searches were conducted using combinations of search terms including ankylosing spondylitis, spondyloarthropathy, spondyloarthritis, switch/switching, drug survival, and TNF/tumor necrosis factor to identify published articles with data on outcomes related to switching biologic therapies in patients with axSpA. Of the 134 studies screened, 21 were identified as reporting data on switching TNF inhibitors in patients carrying a diagnosis of axSpA or ankylosing spondylitis. The most common reasons for switching from the first TNF inhibitor were lack of efficacy (14-68%), loss of efficacy (13-61%), and adverse events/poor tolerability (13-57%). Switching TNF inhibitors was beneficial for a substantial proportion of patients with axSpA who failed to respond to initial or even second TNF inhibitor therapy and adverse effects were not enhanced. Drug survival rates were generally lower for the second (47-72% at 2 years) or third TNF inhibitor (49% at 2 years) than for the first TNF inhibitor (58-75% at 2 years). Predictors of responses in TNF-naïve patients included HLA-B27 positivity, absence of enthesitis, age ≤40 years, elevated C-reactive protein level, good functional status, and shorter disease duration. Predictors of drug survival included male sex and peripheral arthritis. Common characteristics of patients who switched TNF inhibitors included female sex, older age, more severe disease, greater symptom burden, higher erythrocyte sedimentation rate, complete ankyloses, and enthesitis. When the first or even the second TNF inhibitor fails, switching to an alternate one is not an unreasonable clinical therapeutic decision.

Spondyloarthritis: Matrix Metalloproteinasesas Biomarkers of Pathogenesis and Response to Tumor Necrosis Factor (TNF) Inhibitors.

The term spondyloarthritis (SpA) is used to describe a group of multifactorial chronic inflammatory diseases characterized by a predisposing genetic background and clinical manifestations typically involving the sacroiliac joint. The absence of pathognomonic clinical and/or laboratory findings generally results in a delay in diagnosis and, consequently, in treatment. In addition, 20–40% of SpA patients are non-responders to tumor necrosis factor (TNF) inhibitor therapies. Given these considerations, it is important to identify biomarkers that can facilitate the diagnosis and assessment of disease activity. As inflammation plays a key role in the pathogenesis of SpA, inflammatory mediators have been investigated as potential biomarkers for diagnosing the disease and predicting response to therapy. Some investigators have focused their attention on the role of matrix metalloproteinases (MMPs), which are known to be markers of synovial inflammation that is generated in the joint in reaction to inflammatory stimuli. Several studies have been carried out to verify if serum MMPs levels could be useful to diagnose SpA, to assess disease severity, and to predict response to TNF inhibitor therapy. The current review focuses on MMPs’ role in SpA pathogenesis, diagnosis and therapeutic implications.

Lipid profile and comorbidities in patients with psoriasis vulgaris

Background and Aim: Psoriasis is an inflammatory skin disorder with important influence on the lipid profile, insulin resistance and cardiovascular disease. The aim of this study is to compare the lipid profile of classical therapy versus anti-TNFs patients and asses the associated diseases. Methods: We conducted a prospective study. Patients’ data were collected from two Romanian Dermatology Clinics, during the period January 2015 – June 2016. The patients were divided into two groups: study group (on TNF inhibitors) and control group (on classical treatment). Results: The subjects in the study group had more associated diseases and much more patients suffered from dyslipidemia. There were not statistically significant differences in the lipid profile between the two groups. But eliminating patients treated with Acitretin and Methotrexate, a p- value of 0.0259 (significant statistically) was observed when comparing the values of triglycerides in the two groups. Conclusions: We did not observe a beneficial effect of the TNF inhibitors therapy in psoriatic patients on the lipid profile. Subjects on biological treatment suffer from a more severe form of psoriasis vulgaris and associate much more comorbidities.

Transcriptional profiling of leukocytes from rheumatoid arthritis patients before and after anti-tumor necrosis factor therapy: A comparison of anti-nuclear antibody positive and negative subsets.

Anti-nuclear antibodies (ANAs) may be induced in patients with rheumatoid arthritis (RA) receiving anti-tumor necrosis factor (TNF) therapy with TNF inhibitors (TNFi), etanercept, infliximab or adalimumab. In the present study, 11 patients who were TNFi drug naive were started on TNFi at a time of high disease activity. Of these, all cases were positive for rheumatoid factor and 9 cases tested were positive for anti-citrullinated peptide (anti-CCP) antibodies prior to TNFi treatment. Peripheral blood mononuclear cells (PBMCs) and serum were collected from all patients before and after TNFi therapy. Serum was assayed for ANAs over time. Total cellular RNA was extracted from PBMCs and assessed using Illumina arrays. Gene expression profiles were examined for alterations in key effector pathways. After 3 or more months on TNFi, 6 patients converted to ANA-positivity. Analysis of transcripts from patients with RA who converted to ANA-positivity after 3 months on TNFi identified complex gene expression profiles that reflected a reduction in cell adhesion, cell stress and lipid metabolism transcripts. In summary, unique transcriptional profiles in PBMCs from patients with RA were observed after TNFi therapy. This pilot study suggests that transcriptional profiling is a precise method of measuring the impact of TNFi therapies and reveals novel pathways that likely influence the immune response.

Isoniazid treatment for latent tuberculosis infection is tolerable for rheumatoid arthritis patients receiving tumor necrosis factor inhibitor therapy.

Background/AimsTo evaluate the impact of isoniazid (INH) treatment for latent tuberculosis infection (LTBI) on the development of liver function test (LFT) abnormality and the persistence of tumor necrosis factor (TNF) inhibitors in rheumatoid arthritis (RA) patients.MethodsWe retrospectively enrolled patients with RA who were treated with TNF inhibitors at a university hospital between December 2000 and November 2011. After dividing the patients into two groups based on the occurrence of LFT abnormality during follow-up, we compared demographic and clinical features between the two groups. A multivariable logistic regression analysis was performed to identify the impact of INH treatment on LFT abnormality. The impact of INH treatment on the persistence of TNF inhibitors was also evaluated with the log-rank test and the Cox-proportional hazards model.ResultsA total of 312 RA patients including 96 patients (30.9%) who took INH for LTBI were included in this analysis. Thirty-nine patients (12.5%) experienced LFT abnormalities while using TNF inhibitors. The use of INH was associated with LFT abnormalities (odds ratio, 3.01; 95% confidence interval [CI], 1.39 to 6.48) after adjusting for covariates, including methotrexate use. However, the persistence of TNF inhibitors over 5 years did not differ between patients receiving or not receiving INH treatment (49.4 vs. 54.6%, p = 0.79). INH treatment was not a risk factor for discontinuation of TNF inhibitors (hazard ratio, 1.01; 95% CI, 0.66 to 1.57).ConclusionINH treatment for LTBI in RA patients who started TNF inhibitors is associated with the occurrence of LFT abnormality; however, it does not lead to discontinuation of TNF inhibitors.

Impact of prior biologic use on persistence of treatment in patients with psoriatic arthritis enrolled in the US Corrona registry

Psoriatic arthritis (PsA) is a chronic condition characterized by a diverse set of symptoms, from swollen joints to nail disease to skin disease. A variety of treatment options are available, including tumor necrosis factor inhibitors (TNFis). Little is known about treatment persistence in patients with PsA who initiate TNFi therapy, with and without prior biologic use. This study assessed persistence in these subgroups of patients with PsA and identified factors associated with persistence. This retrospective study utilized data from the Corrona registry of patients with PsA—with or without prior biologic experience—who initiated TNFi therapy between October 1, 2002, and March 21, 2013. Kaplan-Meier curves estimated median time to nonpersistence (discontinuation or switch to another biologic). Cox proportional hazards models identified factors associated with TNFi nonpersistence. A total of 1241 TNFi initiations were identified: 549 by biologic-naïve and 692 by biologic-experienced patients. Through 4 years of follow-up, more biologic-naïve than biologic-experienced patients remained persistent. Biologic-naïve patients had a greater mean time to nonpersistence compared with biologic-experienced patients: 32 vs 23 months (p = 0.0002). Moderate and high disease activities based on clinical disease activity index and disease duration were associated with persistence in both biologic-naïve and biologic-experienced patients. Additionally, in the biologic-experienced patients, the number of prior medications and skin disease were associated with persistence. The majority of patients with PsA in this study were persistent with their TNFi therapy; biologic-naïve patients had greater persistence compared with biologic-experienced patients. Predictors of persistence differed slightly between biologic-naïve and biologic-experienced patients.

Dose relationship between oral glucocorticoids and tumor necrosis factor inhibitors and the risk of hospitalized infectious events among patients with rheumatoid arthritis

The objective of this study was to evaluate the impact of oral glucocorticoid (GC) dose on rates of hospitalized infectious events (HIEs) among RA patients newly exposed to tumor necrosis factor inhibitor (TNFi) therapy. This retrospective cohort study used data from the MarketScan claims database. Incident and prevalent adult RA patients newly exposed to TNFi therapy were identified and assigned to three cohorts: no GC, low-dose GC (≤7.5 mg), and high-dose GC (>7.5 mg); patients could contribute exposure time to multiple cohorts if they changed dose or discontinued GC. The primary outcome was estimated incidence rate (IR) of HIEs per 100 patient-years of GC exposure. A total of 40,933 eligible patients were identified (mean age 53.0 years; 77.4% female). HIE risk increased with increasing GC dose: the IR [95% confidence interval (CI)] was 3.9 (3.63–4.13) for no GC; 6.4 (5.68–7.16) for low-dose GC; and 13.3 (11.9–15.5) for high-dose GC. Adjusted rate ratios (95% CI) were 1.4 (1.21–1.60) for low-dose vs no GC; 2.8 (2.32–3.34) for high-dose vs no GC, and 2.0 (1.66–2.45) for high-dose vs low-dose GC. The risk of HIEs increased with increasing age. HIE risk did not increase with longer exposure to GCs. Oral GCs, regardless of dose, significantly increased the risk of HIEs among RA patients newly initiating TNFi therapy. Steroid dosing must be considered when assessing infection risk in treatment decisions for RA patients.

Ustekinumab in the Treatment of Guttate Psoriasis and Crohn's Disease: A Case Report

Psoriasis and Crohn's disease are autoimmune diseases believed to share a similar pathogenesis. Ustekinumab is FDA-approved for treatment of psoriasis in 45 mg and 90 mg dosages and is undergoing phase III trials for Crohn's disease in higher dosages. Data on ustekinumab in guttate psoriasis (GP) are limited. We report the case of a 21-year-old female with Crohn's disease on adalimumab who developed severe, generalized GP 2 months after a streptococcal infection. Her GP did not regress after discontinuation of adalimumab. She began ustekinumab 45 mg every 12 weeks, which led to complete regression of her psoriasis. Due to persistent bowel symptoms, ustekinumab was increased to 135 mg every 8 weeks, with improvement. In this case, GP may have been related to recent streptococcal infection, or a complication of TNF-inhibitor therapy. Here, we show ustekinumab has potential as a therapeutic option for both GP and Crohn's disease.

Rates of Serious Infections in HIV-Infected Patients Receiving Tumor Necrosis Factor Inhibitor Therapy for Concomitant Autoimmune Diseases.

To estimate the incidence of serious infections in patients with HIV infection and autoimmune disease who were treated with tumor necrosis factor (TNF) inhibitors, and to compare these rates by stratified viral load levels. Using a unified search strategy, 4 centers identified HIV-infected patients exposed to TNF inhibitors. Patient characteristics and infection data were assessed via chart review in all patients who were ≥18 years old and who received TNF inhibitor therapy after HIV diagnosis, between January 1999 and March 2015. We studied 23 patients with 26 uses of TNF inhibitor therapy (86.7 person-years of followup). Two (8.7%) experienced at least 1 serious infection episode, for an overall incidence rate of 2.55 per 100 patient-years (95% confidence interval [95% CI] 0.28-9.23). The incidence rate per 100 patient-years was 3.28 (95% CI 0.04-18.26) among patients with a viral load >500 copies/ml at therapy initiation and 2.09 (0.03-11.65) among patients with a viral load ≤500 copies/ml. This study suggests that the rate of serious infections in patients with HIV infection under active care who have received treatment with TNF inhibitors may be comparable to the rates observed in registry databases.

Switching biologics in the treatment of psoriatic arthritis.

Psoriatic arthritis (PsA) is a heterogeneous inflammatory disorder that requires targeted treatment based on clinical manifestations, symptom severity, comorbidities, and other factors. Moderate or severe peripheral arthritis symptoms are typically treated with disease-modifying antirheumatic drugs (DMARDs) or biologic DMARDs (bDMARDs), and early and aggressive treatment is recommended in order to prevent permanent damage. Although rheumatologists are now able to choose between several bDMARDs for PsA that have different chemical structures, pharmacokinetic properties, dosing regimens, immunogenicity, safety profiles, and mechanisms of action, there is a lack of typical patient profiles or detailed treatment algorithms that can be followed when patients require alterations in their therapeutic regimens. PsA treatment recommendations were evaluated to identify consensus guidelines on switching between bDMARD therapies. PubMed literature searches were then conducted using the terms psoriatic arthritis, switch/switching, biologic, and TNF/tumor necrosis factor. Articles were deemed relevant if they presented data on switching between different bDMARDs in patients with PsA. Data from the clinical literature on switching bDMARD therapies in PsA are limited. Evidence suggests that response to adalimumab, etanercept, and ustekinumab is lower after previous tumor necrosis factor inhibitor (TNFi) therapy and the efficacy of infliximab is independent of previous bDMARD treatment. Trials of ustekinumab and secukinumab showed efficacy responses were greater compared with placebo in patients who failed to respond to ≥1 TNFi. Switching bDMARD therapies is a recommended strategy for patients who experience treatment failure. Many factors must be considered for determining which agent to switch to including PsA disease characteristics, comorbidities, cardiometabolic risk factors, treatment history, and patient preference. Switching between TNFis can be effective for many patients, but bDMARDs with different mechanisms of action may be superior alternatives.

Changes in Treatment Patterns in Patients with Psoriatic Arthritis Initiating Biologic and Nonbiologic Therapy in a Clinical Registry.

Treatment options for psoriatic arthritis (PsA) have increased and improved in the past decade; treatment patterns in PsA remain poorly understood. Understanding current practices would aid in treatment management of patients with PsA. This observational study was based on data from the Corrona registry of adult patients with PsA in North America collected between January 1, 2004, and December 31, 2012. Patients were divided among 3 therapy cohorts: tumor necrosis factor inhibitor (TNFi) monotherapy, methotrexate (MTX) monotherapy, and TNFi and MTX combination therapy. Patients were further divided among 3 study periods to understand changes over time: 2004-2006, 2007-2009, and 2010-2012. Data were collected on persistence, discontinuation, restarting, switching, adding/dropping therapy, and dose stretching. This study included 520 patients: 190 TNFi monotherapy, 217 MTX monotherapy, and 113 combination therapy; 110 from 2004 to 2006, 192 from 2007 to 2009, and 218 from 2010 to 2012. Over time, the proportion of patients initiating TNFi monotherapy decreased, while the proportion initiating combination therapy remained constant. The percentage of patients who were persistent decreased over time across all therapy cohorts, but remained higher in TNFi monotherapy than in other cohorts. Duration of persistence decreased over time. Patients initiating MTX monotherapy were more likely than their TNFi counterparts to add therapy. Treatment patterns in patients with PsA have changed from 2004 to 2012. Physicians are not more likely to initiate TNFi monotherapy, although clinical evidence supporting its effectiveness has increased over this study period, and patients remain more persistent with it.

Relationship between exposure to tumour necrosis factor inhibitor therapy and incidence and severity of myocardial infarction in patients with rheumatoid arthritis

ObjectivesPatients with rheumatoid arthritis (RA) are at increased risk of myocardial infarction (MI) compared with subjects without RA, with the increased risk driven potentially by inflammation. Tumour necrosis factor inhibitors...