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Editorial: The Sound and the Fury: Musculoskeletal Ultrasound in the Diagnosis of Gout

Gout is the most common form of inflammatory arthritis and currently affects ;8 million people in the United States (1). Gout is painful, disabling in the short and often long term, and a cause of work lost and dollars spent (2,3). Gout patients also have comorbidities such as renal and cardiovascular disease (4), and recent studies suggest that gout treatment may help reduce the incidence and/or severity of several of those comorbidities (5,6). For most patients, gout should be highly responsive to therapy. Unfortunately, gout frequently goes undertreated, or even untreated altogether. The reasons for inadequate treatment of gout are complex, and relate to patient and physician knowledge and expectations (including physician underestimation of the adverse impact of gout), the necessity of recognizing gout as a problem that requires ongoing management, and other factors (7). One such factor is the fact that gout in the population is both misdiagnosed and underdiagnosed (1,8,9). Again, physician and patient knowledge appear to play major roles, along with an underutilization of joint aspiration as the gold standard for diagnosis. Unfortunately, it is unlikely that the use of joint aspiration will increase significantly; although not a difficult procedure, it requires training, practice, and operator comfort, and most primary care and many emergency room doctors eschew joint aspiration in favor of clinical judgment. However, clinical judgment is not always correct, and the ability to use alternative approaches to achieve an accurate gout diagnosis will be critical to improving the health of our patients. One of the most exciting advances in the past decade of gout study has been the use of musculoskeletal ultrasound (MSUS) to characterize the extent and nature of urate deposition (10). In this issue of Arthritis & Rheumatology, Ogdie et al (11) report the results of the largest and best-controlled study to date, providing evidence that MSUS can play an important role in the clinical diagnosis of gout. Like every good study, this one both answers, and raises, some important questions. These questions largely fall into two categories. The first is technical: what are the standards by which we judge MSUS in gout, and how is it best used? The second is nosologic: what, exactly, do we mean, when we make a clinical diagnosis of gout? Diagnosing gout by MSUS depends on finding key imaging features typical of the condition. The two validated features are the double contour sign and the soft tissue tophus. The Outcome Measures in Rheumatology group has characterized these two findings (10). Double contour is defined as “hyperechoic irregular enhancement of the chondrosynovial margin of the cartilage that is independent of the insonation angle of the US beam.” US tophus is defined as “heterogeneous hyperechoic (relative to subdermal fat) aggregates with poorly defined margins with or without areas with acoustic shadowing.” The “snowstorm” appearance has not been validated, but has been described as hyperechoic dots swirling in the synovial fluid when the joint is agitated (Figures 1a–d). The degree to which these findings can distinguish gout from other forms of arthritis—particularly calcium pyrophosphate deposition disease (CPDD)—is a subject of debate. Specifically, some experts have expressed concern that the deposition of monosodium urate monohydrate on the surface of cartilage (double contour sign), and calcium pyrophosphate within the matrix of the cartilage (interface sign), may be difficult to distinguish in clinical practice (Figures 1a and b). To a significant extent, Ogdie et al assuage these concerns, reporting excellent specificity for all 3 of the above findings for gout (including distinguishing gout from CPDD), with sensitivities that ranged from a high of 60% for double Dr. Pillinger’s work is supported by the NIH (NYU Clinical and Translational Science Award 1UL1-TR-001445 from the National Center for Advancing Translational Sciences). Eugene Y. Kissin, MD: Boston University School of Medicine, Boston, Massachusetts; Michael H. Pillinger, MD: New York University School of Medicine, New York, New York. Dr. Pillinger has received consulting fees from AstraZeneca and Crealta/Horizon (more than $10,000 each) and Sobi (less than $10,000). Dr. Pillinger has served as an uncompensated investigator for a sponsored trial by Takeda. Address correspondence to Eugene Y. Kissin, MD, Boston University School of Medicine, 72 East Concord Street, E-506, Boston, MA 02118. E-mail: eugene.kissin@bmc.org. Submitted for publication September 7, 2016; accepted in revised form October 11, 2016.