Presentation: Is Statin Use Protective Against Development of Systemic Sclerosis? A Retrospective Case Controlled Study (2007)

25 Is Statin Use Protective Against Development of Systemic Sclerosis? A Retrospective Case Controlled Study

PURPOSE: Systemic sclerosis is characterized by immunologic abnormalities, excessive fibrosis, and vasculopathy. Increasingly, endothelial abnormalities and defective angiogenesis and repair have been recognized as important contributors to pathogenesis in scleroderma, and possible targets of therapeutic intervention. Recently, statins have been recognized as potentially beneficial in scleroderma through their anti-inflammatory and pro-angiogenic effects. It has been suggested that they also increase circulating endothelial cell precursors, and thereby promote vascular repair. There are, however, few studies examining the use of statins as therapeutic agents in this disorder. In this case controlled study, we retrospectively compared prevalence of prior statin exposure between scleroderma patients and degenerative arthritis controls. We hypothesized that if statins indeed were protective against expression of the scleroderma phenotype, we would observe a lower prevalence of statin exposure in scleroderma patients than in matched degenerative arthritis controls.
METHODS: Patients with scleroderma who presented to an academically based rheumatology practice from 1992 through 2006 and had available information on statin exposure were identified. Control patients with degenerative arthritis were matched to each scleroderma patient based on age, gender, and date of initial presentation to the practice. Charts were retrospectively reviewed, and data was extracted regarding presence or absence of statin exposure at the time of initial presentation. Clinical and serologic data were also extracted and recorded. Prevalence of statin exposure was calculated for scleroderma patients and degenerative arthritis controls.
RESULTS: Seventy-one pairs of scleroderma patients and degenerative arthritis controls were identified. 68% of the scleroderma patients had limited disease, 30% had diffuse disease, and 2% had an unspecified disease pattern. The average age in the scleroderma group was 57.85 +/-11.05 (range 30-81) versus 57.23 +/-11.27 in the control group (range 29-81). Both groups were 82% female with a median year of initial visit of 2003 (range 1992-2006). 15/71 patients in the scleroderma group (21.1%) and 16/71 (22.5%) control patients had been treated with statins, which was not significantly different (P=0.8).
CONCLUSIONS: We did not observe a lower prevalence of statin exposure in scleroderma patients when compared with matched degenerative arthritis controls. Our findings do not support our hypothesis that statin exposure may be protective against scleroderma. Although this study has limitations owing to its retrospective design and small sample size, the findings argue against statins having a robust protective effect against the expression of the scleroderma clinical phenotype.

 R. Gross, None; M. Mehta, None; M. Peterson, None; H. Spiera, None; R.F. Spiera, None.