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To the Editor:

Gerli et al proposed an interesting idea that SS and SLE may share some similar immunologic features associated with atherosclerosis progression. This hypothesis is raised because of previous reports indicating that leukopenia is associated with atherosclerosis in SS (1) and that lymphopenia is associated with atherosclerosis in SLE (2). Their study also reveals that anti-SSA antibodies are a risk factor for the progression of atherosclerosis, and data from SLE studies showed that lymphopenia is highly associated with the presence of anti-SSA antibodies (3). Gerli and colleagues therefore inferred that anti-SSA antibodies may also be associated with atherosclerosis in patients with SLE.

The data concerning anti-SSA antibodies in our SLE patients are easily accessible from our previously established database (Huang L, et al: unpublished observations). We performed an analysis to examine the correlations between anti-SSA antibodies, lymphopenia, and carotid IMT in our study subjects. The presence of anti-SSA antibodies was not associated with lymphopenia in our cohort of patients with juvenile-onset SLE. The proportions of patients with lymphopenia were not different in the groups with and without (67% versus 68%; P = 0.93). The presence of anti-SSA antibodies did not influence either the baseline (first measurement) carotid IMT or the longitudinal change in the carotid IMT. There were no differences in the baseline carotid IMT between patients with and those without (mean ± SD 0.62 ± 0.07 versus 0.64 ± 0.09; P = 0.26). Furthermore, we used the generalized estimating equation (GEE) method to analyze the correlation between the anti-SSA antibody data and the progression of atherosclerosis (2). Progression of IMT was not associated with the presence of anti-SSA antibodies (P = 0.93) in univariate analysis. In multivariate analysis, lymphopenia at baseline and lymphopenia at diagnosis were still significantly related to carotid IMT progression (P = 0.012 and P = 0.045, respectively) when anti-SSA antibodies were concurrently entered into the multivariate GEE models.

Gerli and colleagues proposed an intriguing hypothesis to link the similar findings in SS and SLE, and that is through the association of low leukocyte counts and anti-SSA autoantibodies. However, from our additional analysis of anti-SSA antibodies, this idea cannot be proven in the cohort of patients with juvenile-onset SLE in our study.

  • 1
    Vaudo G, Bocci EB, Shoenfeld Y, Schillaci G, Wu R, del Papa N, et al. Precocious intima-media thickening in patients with primary Sjögren's syndrome. Arthritis Rheum 2005; 52: 38907.
  • 2
    Huang YL, Chung HT, Chang CJ, Yeh KW, Chen LC, Huang JL. Lymphopenia is a risk factor in the progression of carotid intima-media thickness in juvenile-onset systemic lupus erythematosus. Arthritis Rheum 2009; 60: 376675.
  • 3
    Vila LM, Alarcon GS, McGwin G Jr, Bastian HM, Fessler BJ, Reveille JD for the LUMINA Study Group. Systemic lupus erythematosus in a multiethnic US cohort. XXXVII. Association of lymphopenia with clinical manifestations, serologic abnormalities, disease activity, and damage accrual. Arthritis Rheum 2006; 55: 799806.

Yu-Lin Huang MD*, Hung-Tao Chung MD*, Jing-Long Huang MD*, * Chang Gung Memorial Hospital, and Chang Gung University, Taoyuan, Taiwan.