Objective To quantify vehicle control as a metric of automobile driving performance in patients with rheumatoid arthritis (RA). Methods Naturalistic driving assessments were completed in patients with active RA and controls without disease. Data were collected using in‐car, sensor‐based instrumentation installed in the participants’ own vehicles to observe typical driving habits. RA disease status, disease activity, and functional status were associated with vehicle control (lateral [steering] and longitudinal [braking/accelerating] acceleration variability) using mixed‐effect linear regression models stratified by road type (defined by roadway speed limit). Results Across 1,292 driving hours, RA drivers (n = 33) demonstrated differences in vehicle control compared to controls (n = 23), with evidence of significant statistical interaction between disease status and road type ( P < 0.001). On residential roads, participants with RA demonstrated overall lower braking/accelerating variability than controls ( P ≤ 0.004) and, when disease activity was low, lower steering variability ( P = 0.03). On interstates/highways, RA was associated with increased steering variability among those with moderate/high Clinical Disease Activity Index scores ( P = 0.04). In models limited to RA, increases in disease activity and physical disability over 12 weeks of observation were associated with a significant increase in braking/accelerating variability on interstate/highways (both P < 0.05). Conclusion Using novel naturalistic assessments, we linked RA and worsening RA disease severity with aberrant vehicle control. These findings support the need for further research to map these observed patterns in vehicle control to metrics of driver risk and, in turn, to link patterns of real‐world driving behavior to diagnosis and disease activity.

Refractory gout can be treated with infusions of pegloticase, which metabolizes uric acid into a product readily excreted in urine. Antidrug antibodies often develop, leading to reduced efficacy and potential infusion reactions. The concomitant administration of immunosuppressive agents has been suggested as a means of mitigating the effects of drug-related immunogenicity, rendering treatment more tolerable, and resulting in better outcomes. This report presents cases of 2 patients with tophaceous gout, each having previously undergone a solid-organ transplant, each taking immunosuppressants to prevent organ rejection, and each successfully treated with pegloticase. Although data from randomized controlled studies are needed, these cases suggest that it may be beneficial to coadminister an immunosuppressive medication to extend drug persistence with pegloticase in the management of refractory gout. This approach could allow patients to receive long-term treatment, resulting in improved patient outcomes.

IIMs are autoimmune disorders that can affect all ages and are characterized by a spectrum of clinical manifestations, the most common of which is skeletal muscle weakness. Several MSAs have been identified and may help to inform treatment and direct the evaluation for extramuscular features. As a multisystemic disorder, a thoughtful approach taking into consideration clinical, serologic, and histologic data is required to develop a patient-specific management strategy. Treatment remains suboptimal in many cases and, owing to the rarity of these disorders, is based primarily on small series because there a few randomized controlled trials to inform management of IIMs.

The introduction of tumor necrosis factor (TNF) inhibitors in the late 1990s - significantly changed the therapeutic approach for rheumatoid arthritis (RA). With the approval of subsequent TNF inhibitors as well as other biologic agents effective in the management of RA, the treatment paradigm has become increasingly complex. This review examines the current literature regarding the efficacy and toxicity of these and other new anti- rheumatic therapies and discusses effective therapeutic strategies for their use.

Purpose of review The present review will focus on the role of conventional disease-modifying antirheumatic drugs (DMARDs) in the current management of rheumatoid arthritis (RA). Recent findings Over the past several decades, the treatment of RA has been revolutionized, not only by the development of highly effective biologic agents but also through a better understanding of the critical importance of early DMARD treatment with a goal of remission or low disease activity and of how to effectively and safely use conventional DMARDs, either as monotherapy or in combinations. Summary Conventional DMARDs have proven efficacy in the management of RA and remain a valid treatment option, either in monotherapy or as a component of combination regimens. Although conventional DMARDs have associated toxicities, these are distinct from those of the biologic DMARDs. In addition, conventional DMARDs are much less expensive than biologic DMARDs, and in many cases can be successful in achieving similar control of disease activity. The goal for all patients should be achieving remission, or at least low disease activity, with the most cost-effective therapy possible.

Background: Rheumatoid arthritis (RA) is a chronic, systemic inflammatory disorder primarily targeting the synovium. Unchecked disease activity is associated with significant morbidity and an increased mortality. Recent advances in the understanding of the pathogenesis of RA and the capability of biologically engineered treatments for RA have expanded the armamentarium of antirheumatic agents. Methods: A systematic literature review was conducted through PubMed. Results/conclusions: At present, a common strategy for the treatment of RA uses methotrexate either as monotherapy or in combination with a variety of conventional and/or biologic disease-modifying antirheumatic drugs (DMARDs), with the goal of inducing remission of active disease. The choice of which agent(s) to use is based upon patient-specific criteria (activity of disease, comorbidities, patient preferences, costs etc.). Emerging therapies that target specific cytokines and growth factors in the inflammatory cascade of RA offer a potent new means of modifying disease activity, but many questions regarding their use remain unanswered.

Osteochondroma most frequently arises sporadically and as a solitary lesion, but may also arise as multiple lesions characterizing the autosomal dominant disorder hereditary multiple exostoses (HME) and the contiguous gene-deletion syndrome, Langer-Giedion syndrome (LGS). Various germline mutations of two putative tumor suppressor genes, EXT1 localized to 8q24.1 and EXT2 localized to 11p11∼p12, have been demonstrated in HME families. Constitutional chromosomal deletions or structural rearrangements of 8q24.1 are seen in LGS. Cytogenetic reports of sporadic and hereditary osteochondromas are few, but have revealed loss or structural rearrangements of 8q24.1 in a small number of tumors. In the current study, karyotypic evaluation of 37 osteochondroma specimens (both sporadic and hereditary lesions) revealed chromosomal anomalies of 8q24.1 in 10 specimens (27%). In an effort to determine the presence and frequency of submicroscopic deletions, molecular cytogenetic studies were performed on this same set of tumors utilizing a chromosome 8 specific centromeric probe and an 8q24.1 cosmid probe (locus D8S51, within the minimal LGS deletion region). Loss of the 8q24.1 locus was detected by fluorescence in situ hybridization in 27 of 34 (79%) osteochondroma specimens analyzed including all 10 specimens exhibiting chromosome 8 abnormalities cytogenetically. These findings indicate that a significant subset of osteochondromas harbor genetic aberrations at the EXT1 locus and suggest that loss or mutation of EXT1 plays an important role in the pathogenesis of sporadic as well as hereditary osteochondromas.

Elastofibroma, an unusual pseudotumor composed of excessive collagen and abnormal elastic fibers, has rarely been subjected to cytogenetic analysis. Only two cases have been previously defined, both of which demonstrated nonclonal abnormalities. In the present study, three cases of elastofibroma were cytogenetically analyzed. Abnormalities of the short arm of chromosome 1 were seen in all three cases (either clonally or as the most frequently involved region among nonclonal aberrations). In addition, a translocation involving chromosomes 8 and 12 was detected as a clonal rearrangement in one of the three cases. The observation of clonal abnormalities in elastofibroma suggests that this lesion may represent a neoplastic rather than a reactive process.

Cytogenetic studies of epithelioid sarcoma, a rare malignant soft tissue neoplasm of adolescents and young adults, are few. A characteristic anomaly has not yet been identified for this sarcoma. In this study, cytogenetic studies of a primary epithelioid sarcoma of a 15-year-old male revealed the following abnormalities: t(6;8)(p25;q11.2) and add(7)(p15).