Seasonal influence on the onset of idiopathic inflammatory myopathies in serologically defined groups.
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.
Sarkar
Kakali
K
National Institute of Environmental Health Sciences, NIH, DHHS, Bethesda, MD 20892, USA. sarkark@mail.nih.gov
Weinberg
Clarice R
CR
Oddis
Chester V
CV
Medsger
Thomas A
TA
Plotz
Paul H
PH
Reveille
John D
JD
Arnett
Frank C
FC
Targoff
Ira N
IN
Genth
Ekkehard
E
Love
Lori A
LA
Miller
Frederick W
FW
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
D001323:Autoantibodies; D018271:Signal Recognition Particle; D008025:Ligases