COMMENTARY

10 Rheumatology Advances From 2016

Kevin D. Deane, MD, PhD

Disclosures

December 19, 2016

7: Hepatitis C Now Has a Cure (Mostly)

Rheumatologists typically encounter hepatitis C virus (HCV) because of cryoglobulinemia, or while evaluating a patient for the safety of DMARD therapy or for rheumatoid factor positivity. Over the past several years, many interferon-free/direct-acting HCV treatments have been introduced; these agents are expensive, but they are demonstrating high cure rates that are revolutionizing HCV care.[10,11] Although substantial literature has not yet been published regarding the role of the newer regimens, there is hope that they will have a twofold benefit in rheumatology: (1) improving (or preventing) cryoglobulinemia, and (2) potentially making the use of DMARD therapy in the setting of HCV safer.[12] This will be something to watch in the near future.

8: Therapies for Rheumatologic Lung Diseases

The Scleroderma Lung Study II was a comparison of mycophenolate mofetil (MMF) and cyclophosphamide in scleroderma lung disease. Although the primary endpoint that MMF would be superior to cyclophosphamide was not met, post hoc analyses demonstrated that a 1-year course of therapy with MMF or cyclophosphamide resulted in significant improvements in lung function over 2 years; MMF was better tolerated and had less toxicity.[13] However, the overall benefits were small, and the rheumatology community still lacks effective therapies for most rheumatic disease-related lung diseases.

Two antifibrotic agents, pirfenidone and nintedanib, have been shown to offer modest benefit in terms of reduced rates of decline in lung function in idiopathic pulmonary fibrosis, and both of these agents are now approved by the FDA for use in this condition.[14] Several trials of these agents in rheumatic lung disease (including scleroderma) are under way. In a recently published, 16-week, small, open-label study of pirfenidone, there was no clear lung benefit in patients with scleroderma, but this trial was probably of too short a duration to make any firm conclusions.[15] Furthermore, there are concerns that such agents will not be effective in certain diseases, such as cellular nonspecific interstitial pneumonia, or other rheumatic lung diseases where inflammation rather than fibrosis is the predominant component.[16]

Despite these issues, the hope is that antifibrotic agents will be helpful in some rheumatologic lung diseases and that other treatments will be available soon for these devastating manifestations of rheumatic disease.

9: More Effective Treatment for IgG4 Disease?

Immunoglobulin G4 (IgG4)-related disease is a condition that can affect multiple tissues, most commonly the pancreas, biliary tract, salivary glands, retroperitoneum, and lymph nodes. Because the manifestations of IgG4-related disease are similar to those of other rheumatic diseases (eg, salivary gland involvement mimicking Sjögren syndrome) and because of the agents used to treat it (steroids, other immunomodulation, and B-cell depletion[17]), rheumatologists are often asked to manage this disease and are thus becoming increasingly aware of it.

IgG4-related disease can be characterized by elevated circulating levels of IgG4 and low complement levels; however, in one series, approximately 50% of patients with biopsy-proven disease had normal serum IgG4 values.[18] As such, the hallmark of disease is dense lymphoplasmacytic tissue infiltrates with IgG4 cells, storiform fibrosis (ie, having a cartwheel pattern, with spokes), and obliterative phlebitis being highly suggestive of disease.[19]

B-cell depletion is emerging as an effective treatment for IgG4-related disease,[20] and studies on the etiology and optimal treatment regimens are ongoing. Rheumatologists should watch for advances in these areas in 2017.

10: Management of Gout, and Hyperuricemia and Systemic Disease

In 2016, the American College of Physicians (ACP) published a clinical practice guideline for the management of acute and recurrent gout.[21] Given the large burden that hyperuricemia and gout have on health, and the effective lifestyle and pharmacologic therapies that exist, the increasing attention being given to management of this disease is welcome.

These guidelines, based on best evidence, are complex and somewhat controversial. In particular, one of the most interesting points for rheumatologists was that treatment should be given to avoid symptoms, not necessarily to treat to a target uric acid goal. For many rheumatologists, that target value is at least < 6.8 mg/dL, and typically <6 mg/dL; the latter level is especially important if one is following the 2012 ACR gout guidelines,[22] as well as the 2016 EULAR guidelines.[23] To quote the outstanding editorial that accompanied the ACP guidelines, "...we await clarity on these important clinical issues."[24]

In addition, several studies published in 2016 suggested that hyperuricemia is related to nonarticular disease, including as an independent risk factor for hypertension, atrial fibrillation, atherosclerotic disease, and progression of renal disease.[25,26,27] Several small studies reviewed in Mallat and colleagues' study[25] also suggest that lowering uric acid can improve blood pressure or progression of renal disease.

More research is needed, but we may be moving to a point where hyperuricemia is managed even in the absence of articular disease. Given the projected workforce shortfalls in rheumatology, if indeed this becomes the case, hopefully a variety of healthcare providers will be able to provide care in this area.

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