title: Seasonal influence on the onset of idiopathic inflammatory myopathies in serologically defined groups.
abstract: 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 using a Poisson model that assessed associations of ethnicity, sex, autoantibody presence, and month of onset of muscle weakness.
  
  
  RESULTS
  There were no significant seasonal patterns 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, myositis 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 autoantibodies 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).
  
  
  CONCLUSIONS
  These findings, in conjunction with other data, suggest that diverse environmental agents, acting upon different immunogenetic backgrounds, result in distinct immune responses and clinical syndromes in the idiopathic inflammatory myopathies. Our results emphasize the importance of considering more homogeneous disease groups, based on clinicopathologic features, immune responses, ethnicity, and sex, when attempting to decipher the pathogeneses of autoimmune disorders.
authors.affiliation: National Institute of Environmental Health Sciences, NIH, DHHS, Bethesda, MD 20892, USA. sarkark@mail.nih.gov
authors.forename: Kakali
authors.initials: K
authors.lastname: Sarkar
authors.forename: Clarice R
authors.initials: CR
authors.lastname: Weinberg
authors.forename: Chester V
authors.initials: CV
authors.lastname: Oddis
authors.forename: Thomas A
authors.initials: TA
authors.lastname: Medsger
authors.forename: Paul H
authors.initials: PH
authors.lastname: Plotz
authors.forename: John D
authors.initials: JD
authors.lastname: Reveille
authors.forename: Frank C
authors.initials: FC
authors.lastname: Arnett
authors.forename: Ira N
authors.initials: IN
authors.lastname: Targoff
authors.forename: Ekkehard
authors.initials: E
authors.lastname: Genth
authors.forename: Lori A
authors.initials: LA
authors.lastname: Love
authors.forename: Frederick W
authors.initials: FW
authors.lastname: Miller
mesh_terms: D001323:Autoantibodies / Q000097:blood*; D003430:Cross-Sectional Studies; D003882:Dermatomyositis / Q000209:etiology* / Q000276:immunology*; D005260:Female; D006801:Humans; D008025:Ligases / Q000276:immunology; D008297:Male; D017285:Polymyositis / Q000209:etiology* / Q000276:immunology*; D012189:Retrospective Studies; D012621:Seasons; D012737:Sex Factors; D018271:Signal Recognition Particle / Q000276:immunology
chemical_list: D001323:Autoantibodies; D018271:Signal Recognition Particle; D008025:Ligases