Autoimmunity as a secondary phenomenon in scleroderma (and so-called human adjuvant disease).

ABSTRACT

Autoantibodies form under diverse circumstances. Some autoantibodies are clearly secondary phenomena in response to tissue injury. When there is defective microdebridement, tissue antigens will persist and will produce even more autoantibody. Scleroderma is classified as an autoimmune disease but autoantibodies are not always present. There is extensive literature on the early role of vascular changes and the presence of connective tissue active substances. There are clinical cases of scleroderma following implants of silicone, paraffin injections, and occupational silica or polyvinyl chloride exposure. It would be hard to describe a worse group of nondegradable substances capable of overloading the debridement system. It has been demonstrated that macrophages that ingest silica release factors that increase biosynthesis by fibroblasts. There may be many methods of arriving at the clinical pattern of scleroderma. Elimination of autoantibodies as a primary etiologic consideration will allow concentration on the other known physiologic factors. There is, in some cases, a secondary injury of the kidney from immune complexes. Autoimmunity, when it occurs, is a secondary phenomenon in scleroderma, or so-called 'human adjuvant disease'.