No abstract

Objective. Numerous reports of the induction or worsening of psoriasis in patients treated with tumor necrosis factor (TNF) antagonists indicate that this is not a rare phenomenon. The etiology of this paradoxical clinical response remains unclear. The aim of this study was to describe similar cases, conduct a comprehensive analysis of the literature, explore possible immunologic mechanisms of action of this perplexing reaction, and recommend management options. Methods. A systematic literature review was performed using the PubMed and Medline databases (1996 to September 2007) searching the index terms "infliximab," "etanercept," "adalimumab," "tumor necrosis factor alpha inhibitor," and "TNF inhibitor," combined with the terms "psoriasis," "pustular," "skin," "rash," and "palmoplantar." All relevant articles in English were reviewed. Pertinent secondary references were also analyzed. Results. According to the literature, new-onset psoriasis may occur any time after initiation of TNF antagonist therapy, is often of an uncommon morphology, may respond to psoriasis treatments, and usually resolves with TNF discontinuation. The pathogenesis of this response appears to involve a disruption in cytokine balance following TNF inhibition, resulting in the up-regulation of plasmacytoid dendritic cells and the subsequent production of unopposed interferon-␣, following a triggering event in predisposed individuals. Conclusion. TNF antagonist-induced psoriasis is a newly recognized adverse effect of these medications that typically does not require therapy cessation. We recommend aggressive treatment of the skin disease and consideration of a change in the TNF antagonist if the lesions are unresponsive to conventional psoriasis treatment.

Objective. To describe the character and composition of the 2015 US adult rheumatology workforce, evaluate workforce trends, and project supply and demand for clinical rheumatology care for 2015-2030. Methods. The 2015 Workforce Study of Rheumatology Specialists in the US used primary and secondary data sources to estimate the baseline adult rheumatology workforce and determine demographic and geographic factors relevant to workforce modeling. Supply and demand was projected through 2030, utilizing data-driven estimations regarding the proportion and clinical full-time equivalent (FTE) of academic versus nonacademic practitioners. Results. The 2015 adult workforce (physicians, nurse practitioners, and physician assistants) was estimated to be 6,013 providers (5,415 clinical FTE). At baseline, the estimated demand exceeded the supply of clinical FTE by 700 (12.9%). By 2030, the supply of rheumatology clinical providers is projected to fall to 4,882 providers, or 4,051 clinical FTE (a 25.2% decrease in supply from 2015 baseline levels). Demand in 2030 is projected to exceed supply by 4,133 clinical FTE (102%). Conclusion. The adult rheumatology workforce projections reflect a major demographic and geographic shift that will significantly impact the supply of the future workforce by 2030. These shifts include baby-boomer retirements, a millennial predominance, and an increase of female and part-time providers, in parallel with an increased demand for adult rheumatology care due to the growing and aging US population. Regional and innovative strategies will be necessary to manage access to care and reduce barriers to care for rheumatology patients.

Objective. To delineate daily and cumulative glucocorticoid dose thresholds associated with increased mortality rates in rheumatoid arthritis (RA).Methods. We studied RA patients recruited from rheumatology clinics. Annually, we assessed the glucocorticoid dose, demographic, socioeconomic, clinical, and laboratory features of RA, cardiovascular (CV) risk factors, and vital status. We used Cox proportional hazards regression to assess associations between the daily or cumulative glucocorticoid dose and death, adjusting for potential confounders and for the propensity to receive glucocorticoids. We tested strata of the glucocorticoid dose to delineate the threshold associated with death.Results. We studied 779 RA patients with a total of 7,203 person-years of observation, during which 237 of them died, yielding a mortality rate of 3.2 per 100 person-years (95% confidence interval [95% CI] 2.8-3.7). One hundred twenty of the deaths were due to CV causes, yielding a CV mortality rate of 1.8 (95% CI 1.5-2.1). Exposure to glucocorticoids was associated with a dose-dependent increase in death from all causes, with a ratio (HR) of 1.07 per mg of prednisone per day (95% CI 1.05-1.08). Compared to patients who were not receiving corticosteroids, the minimum daily prednisone dose threshold associated with an increase in all-cause mortality was 8-15 mg, with an adjusted HR of 1.78 (95% CI 1.22-2.60). For the cumulative dose of glucocorticoids, the minimum dosage associated with allcause mortality was 40 gm (HR 1.74 [95% CI 1.25- 2.44]).Conclusion. Glucocorticoid use in RA is associated with a dose-dependent increase in mortality rates, with a daily threshold dose of 8 mg, at which the number of deaths increased in a dose-dependent manner. These findings may assist clinicians in selecting the appropriate glucocorticoid dosage for RA patients who require these agents.