Advances in understanding of the pathophysiology of rheumatoid arthritis with concurrent advances in protein engineering led to the development of biological disease-modifying antirheumatic drugs which have dramatically revolutionized the treatment of this condition. This review article focuses on the role of biological agents currently employed in the treatment of rheumatoid arthritis, as well as novel biological agents in development.

Objective While salivary gland ultrasound (SGU) has gained prominence for evaluating Sjögren's syndrome, little information exists on SGU appearance of sarcoidosis and amyloidosis, potential mimics of Sjögren's syndrome. Our goal in this study was to estimate the diagnostic accuracy of major SGU features in differentiating Sjögren's syndrome from sarcoidosis, amyloidosis, and controls. Methods We enrolled consecutive adult ambulatory patients with a clinical diagnosis of Sjögren's syndrome fulfilling the 2016 American College of Rheumatology (ACR) classification criteria; we also enrolled patients with a clinical diagnosis of sarcoidosis or systemic immunoglobulin light chain (AL) amyloidosis, with histologic confirmation from any tissue, and rheumatology outpatients without diagnoses affecting salivary glands. Subjects underwent major SGU using the Hočevar protocol, with resulting video clips reviewed blind to clinical diagnosis. Results Sjögren's syndrome SGU scores were greater than in patients from the other groups, but there were no distinguishing salivary gland features from AL amyloidosis or sarcoidosis. None of the patients in the control group scored higher than 17, a cutoff previously suggested for Sjögren's syndrome, but 27% of patients with AL amyloidosis and 19% with sarcoidosis scored higher than 17. Adding Hočevar SGU scores of ≥17 to the 2016 ACR/European League Against Rheumatism criteria in a parallel scheme increased the sensitivity for Sjögren's syndrome from 87% to 98%, while combining the 2 criteria in series increased specificity from 81% to 98%. Conclusion Sjögren's syndrome, sarcoidosis, and AL amyloidosis share common SGU features that can help distinguish these conditions from patients without systemic rheumatologic disease. Clinicians should carefully consider these potential mimics when interpreting salivary gland US results.

ORIGINAL RESEARCH ARTICLE cations adversely affect the quality of life of patients and, in the extreme, can affect the integrity and viability of any digit. The pathophysiology of scleroderma spectrum digital vasculopathy (including RP) is poorly understood, but is likely multifactorial. However, studies have suggested that an overproduction of the vasoconstrictor endothelin-1 (1), and/or an underproduction of the vasodilators nitric oxide and prostacyclin by endothelial cells of peripheral blood vessels are important contributing factors (2). Management options for scleroderma spectrum digital vasculopathy include first-line therapy such as dihydropyridine-type calcium channel receptor antagonists. For severe or refractory cases of SSc-related vasculopathy, phosphodiesterase-5 inhibitors (PDE-5i), nitroglycerin ointment, and other vasodilators have been used. In cases where digits are at imminent risk of necrosis, prostanoids have been utilized (3-14). For example, a multicenter, placebo-controlled, double-blind study of iloprost observed a mean reduction in weekly RP attacks of 39% (compared with 22% in the placebo arm, p = 0.005) (12). There were also statistically significant improvements in RP clinical scores and degree of digital ulcer healing. Although much of the healing of pre-existing ulcers occurred in the first few weeks of the study, the effect of the iloprost