an association of autoantibodies and silicone breast implants (except anti-ssDNA). The study examined antibodies in a large, random cohort with identified techniques, blinded laboratory personnel and four appropriate concurrent control groups (Karlson et al., 1999). In general, the reports discussed earlier of ANAs in women with implants describe ANAs that are not reactive to defined autoantigens, and specific antinuclear autoantibodies when evaluated are not found.
As noted at the outset, studies of ANAs in women with silicone breast implants are subject to a number of weaknesses. Results reported have varied from positive to negative in a number of experimental groups, including women with saline or gel implants and those with connective tissue disease, an array of symptoms and disabilities, fibromyalgia, or no symptoms. No differences between saline and gel implants emerge from these studies, but results are not always reported by type of implant. A number of different control groups have been reported including historical, concurrent, asymptomatic or healthy, with fibromyalgia, with soft tissue rheumatism, with connective tissue disease, and with diabetes, and they have been assessed using different ANA technologies and criteria for positivity. Studies with no controls at all are essentially case reports. Even though some may report large numbers of women, they offer only weak evidence. Different results of testing for defined antinuclear autoantibodies have also been reported. Even theoretically well designed, prospective studies (Miller et al., 1998) have problems, such as short follow-up, failure to include significant portions of the potential experimental group, and no description of the testing technology. The fact that a positive ANA test is not a disease diagnosis should also be kept firmly in mind.
The cohort studies, however, add strength to the evidence against an association between silicone breast implants and ANAs or other autoantibodies. The committee concludes that the data in support of a finding of increased prevalence, higher titers, or different profiles of antinuclear antibodies in women with gel- or saline-filled silicone breast implants compared to control women without breast implants are insufficient or flawed. The weight of the better-quality evidence suggests the lack of an association between silicone breast implants and positive ANAs. Although there are fewer data on specific autoantibodies, they also suggest no association and are insufficient to support a finding of increased prevalence or different profiles of specific autoantibodies in women with silicone breast implants.