SCLERODERMA AND SILICONE GEL BREAST PROSTHESES - THE SYDNEY STUDY REVISITED

Background: Silicone augmentation mammoplasty has been postulated as a cause of environmentally-induced scleroderma. While representing a sm all proportion of all alleged causes of scleroderma, the issue has hug e social, ethical and medicolegal ramifications. The hypothesis, howev er, has been recently questioned in results of comparative studies. We have previously reported no association between augmentation mammopla sty and scleroderma. However, all information was self-reported includ ing augmentation mammoplasty status, and the prosthesis type was not i dentified. In addition, data were not available from untraceable cases . The current study addresses these issues. Aims: To validate self-rep orted augmentation mammoplasty status, re-analyse rates of exposure to silicone gel breast prostheses in 556 scleroderma patients and 289 ge neral practice controls and evaluate whether silicone gel breast prost heses are causally linked to scleroderma. Methods: Study design - popu lation-based case-control study; Cases - scleroderma patients resident in Sydney for at least six consecutive months between 1974-1988; Cont rols - patients from 29 randomly selected Sydney general practices, ag e- and gender-group-matched with cases. Validation of augmentation mam moplasty exposure was ascertained from the general medical practitione r of each interviewed case and control, or from the medical records of each deceased or untraceable case. Validation of the date of surgery and prosthesis type was from the relevant plastic surgeon. For each au gmentation mammoplasty-positive case, validation of both the date and nature of the scleroderma onset was from the patient's medical records . Controls were given a 'control date' for disease onset to adjust for duration of potential exposure. Results: Validation of augmentation m ammoplasty status was possible in 252 (87.2%) living controls, and 532 (95.7%) cases, of whom 287 were living. Self-reported augmentation ma mmoplasty status was highly reliable in living non-senile cases (kappa =1), and living validated controls (kappa=0.86). No association was id entified between silicone gel augmentation mammoplasty and scleroderma with unadjusted odds ratios of 1.33 (95% CI: 0.26-6.71), and 1.00 (95 % CI: 0.16-6.16) following adjustment for potential confounders of age , socioeconomic status and ethnicity. Conclusions: This validates the self-reported augmentation mammoplasty status previously reported and does not support the hypothesis that silicone gel augmentation mammopl asty is an environmental inducer of scleroderma in females.