ARTHRITIS & RHEUMATISM Vol. 52, No. 8, August 2005, pp 2433–2438 DOI 10.1002/art.21198 © 2005, American College of Rheumatology Seasonal Influence on the Onset of Idiopathic Inflammatory Myopathies in Serologically Defined Groups Kakali Sarkar, 1 Clarice R. Weinberg, 1 Chester V. Oddis, 2 Thomas A. Medsger, Jr., 2 Paul H. Plotz, 3 John D. Reveille, 4 Frank C. Arnett, 4 Ira N. Targoff, 5 Ekkehard Genth, 6 Lori A. Love, 1 and Frederick W. Miller 1 Objective. To assess possible seasonal patterns in the onset of polymyositis (PM) and dermatomyositis (DM). Methods. The study group comprised 503 patients who met the criteria for probable or definite PM or DM and for whom detailed data on the time of myositis onset were available. Statistical analyses were performed us- ing a Poisson model that assessed associations of ethni- city, sex, autoantibody presence, and month of onset of muscle weakness. Results. There were no significant seasonal pat- terns of disease onset in myositis patients as a whole or in the total PM or DM populations. Significant seasonal associations were present, however, in the serologically defined groups. In the 131 patients with antisynthetase autoantibodies who were categorized as non-black, my- ositis onset peaked in March–April (P  0.03). Among the antisynthetase-positive patients, the association was predominantly in those with PM (n  85; P  0.05) and in men (n  51; P  0.042). Patients with anti–signal recognition particle autoantibodies, however, did not have a significant seasonal onset, which is in contrast to previous findings. Patients without myositis-specific au- toantibodies showed a significant peak in summer, with myositis onset in June–July (n  252; P  0.03); this seasonal association was significant in women (n  182; P  0.005), whereas there was no seasonal pattern in men (P  0.9). Conclusion. These findings, in conjunction with other data, suggest that diverse environmental agents, acting upon different immunogenetic backgrounds, re- sult in distinct immune responses and clinical syn- dromes in the idiopathic inflammatory myopathies. Our results emphasize the importance of considering more homogeneous disease groups, based on clinicopatho- logic features, immune responses, ethnicity, and sex, when attempting to decipher the pathogeneses of auto- immune disorders. Idiopathic inflammatory myopathy (IIM) consti- tutes a diverse group of syndromes that share the characteristic of weakness due to chronic inflammation in the muscle as their common feature (1). The most frequent forms, polymyositis (PM) and dermatomyositis (DM), are traditionally diagnosed by the presence of proximal muscle weakness, elevations in the serum levels of muscle-associated enzymes, characteristic rashes in the case of DM, typical myopathic changes on electro- myography, and chronic mononuclear cell infiltration with evidence of degeneration and regeneration of myo- cytes on muscle biopsy (2). Although the causes of these disorders remain unknown, many lines of evidence sug- gest that they are the result of environmental exposures that induce immune activation in genetically susceptible individuals, resulting in chronic tissue inflammation (1). Case reports, case series, and epidemiologic in- vestigations have suggested that either infectious or 1 Kakali Sarkar, PhD, Clarice R. Weinberg, PhD, Lori A. Love, MD, PhD, Frederick W. Miller, MD, PhD: National Institute of Environmental Health Sciences, NIH, DHHS, Bethesda, Maryland; 2 Chester V. Oddis, MD, Thomas A. Medsger, Jr., MD: University of Pittsburgh, Pittsburgh, Pennsylvania; 3 Paul H. Plotz, MD: National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, DHHS, Bethesda, Maryland; 4 John D. Reveille, MD, Frank C. Arnett, MD: University of Texas, Houston; 5 Ira N. Targoff, MD: University of Oklahoma Health Sciences Center, Veterans Administration Medical Center, and OMRF, Oklahoma City; 6 Ekkehard Genth, MD: Clinic and Research Institute for Rheumatic Diseases, Aachen, Germany. Address correspondence and reprint requests to Kakali Sarkar, PhD, Environmental Autoimmunity Group, NIEHS/NIH, 9000 Rockville Pike, Building 9, Room 1W107, MSC 0958, Bethesda, MD 20892. E-mail: sarkark@mail.nih.gov. Submitted for publication December 17, 2004; accepted in revised form April 20, 2005. 2433