Rheumatologic Manifestations of Sarcoidosis

Nadera J. Sweiss, M.D.; Karen Patterson, M.D.; Ray Sawaqed, M.D.; Umair Jabbar; Peter Korsten, M.D.; Kyle Hogarth, M.D.; Robert Wollman, M.D.; Joe G.N. Garcia, M.D.; Timothy B. Niewold, M.D.; Robert P. Baughman, M.D.


Semin Respir Crit Care Med. 2010;31(4):463-473. 

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There is a need for well-designed clinical trials to further aid in the generation of a standardized approach to the treatment of all variations of rheumatic sarcoid. The optimal dose, type, and route of administration of corticosteroids are unknown. Typically the choice of medication use depends on what is required for other organ involvement in sarcoid, as well as on the treating physician's experience with corticosteroid-sparing agents. We support that the use of corticosteroid-sparing agents as well as biologics, while at times successful, should be considered investigational and should only be tried after thorough discussion with patients.

Additional future studies employing high throughput strategies such as genomewide expression studies and GWASs will likely push the field ahead and provide clinicians with a better understanding of the complex nature of this fascinating disease as well as identify novel targets for disease amelioration by targeted therapies. For example, given the role of TNF-α in sarcoidosis, use of TNF-α inhibitors is steadily increasing. Recently, these agents have been shown to improve index organ involvement in patients with refractory sarcoidosis.[17,66–69] However, drug-induced sarcoidosis in nonsarcoid patients treated with TNF-α inhibitors has been increasingly reported, and patients often relapse after discontinuation of therapy with these agents.[70–73] Although the potential mechanism for the induction of sarcoidosis by TNF-α inhibitors is not clear, there are interesting data supporting a cross-regulation of interferon (IFN-α) by TNF-α in humans,[74,75] including some studies in which TNF-α blockade results in increased IFN-α.[76] This is of interest because there are a number of cases of sarcoidosis and other autoimmune conditions induced by exogenous IFN-α given as a treatment.[77,78] It is possible that in some individuals, TNF-α blockade results in significant dysregulation of IFN-α and subsequent induction of sarcoidosis.

The use of B cell-depleting agents may also be of benefit in sarcoid arthritis. B cell-depleting agents are used with success in patients with rheumatoid arthritis who failed anti-TNF-α therapy. A recently published case report of a patient with sarcoidosis of the lungs and joints reported that the typical rheumatoid arthritis schedule of rituximab was effective in treating the sarcoidosis with no major side effects. However, the duration of symptom improvement was only 1 year.[79] Given the success of rituximab, other B cell therapies such as ocrelizumab, have also been evaluated in rheumatoid arthritis and have shown clinical efficacy and safety. More studies are warranted to further characterize the role of rituximab and ocrelizumab in rheumatoid arthritis and other autoimmune diseases, such as systemic sarcoidosis.[80] Other agents, abatacept and tocilizumab, have been successfully used in patients with rheumatoid arthritis. In the future, they could also potentially be used in patients with rheumatic manifestations of sarcoidosis.

Multidisciplinary approaches that incorporate translational research are required to address the many complex questions that remain in sarcoidosis research. Until better evidence is available from multicenter randomized trials, treating patients with rheumatic manifestations of sarcoidosis needs to be individualized and should take into consideration the multisystem nature of the disease and its comorbidities. A unified team approach is needed to serve our patients best.


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