Inflammatory Myopathy with ILD is Seasonal!

A growing area of research in autoimmune diseases in general is identification of disease triggers. Triggers in general that have been proposed include infections and environmental triggers. Certainly, for dermatomyositis (DM) and polymyositis (PM), the concept of environmental triggers involved in the onset of disease has been explored.

A group from Japan sought to examine this further, by analyzing the influence of seasonal and residential environment on the development of PM and DM associated interstitial lung disease (ILD), and their relationship with myositis-specific autoantibodies (MSAs). Their work was featured at this year's ACR as part of the myositis poster session on Tuesday, November 15 (Abstract #2307). This was an analysis of a multicentre retrospective cohort of Japanese patients with ILD, and they also tested patients for the presence of melanoma differentiation- associated gene 5 (MDA-5) and RNA immunoprecipitation for anti-synthetase autoantibodies.

MDA-5 associated inflammatory myopathy has a distinct phenotype associated with features of ILD as well as clinically amyopathic DM. In this patient cohort, seasonality of onset was determined, as well as evaluation of whether the patients' place of residence at disease onset was close to major freshwater sites (i.e. environmental triggers). Almost 500 patients were enrolled; 42% were positive for MDA-5 and 33% positive for the anti-synthetase antibodies. Seasonality of disease onset was found in MDA-5 patients, with more patients developing the disease in autumn/winter vs spring/summer, but clinical features were comparable for all seasons. In addition, patients who resided in the freshwater waterfront environments were significantly more positive for MDA-5 autoantibodies.

In conclusion, the onset of MDA-5 associated inflammatory myopathy with ILD seemed to be associated with presentation in autumn/winter vs spring/summer, and cases clustered around freshwater areas. This does suggest the role of environmental triggers in the onset of disease. It will be interesting to see if such patterns can be identified for other autoantibodies as well as clinical phenotypes in subsets of inflammatory myopathy. It would be interesting to determine if such factors are seen in association with inflammatory myopathy in other regions of the world.

More reports from ACR 2016