No clear cause for<unk>  and<unk>  sclerosis has been identified. Genetic predisposition appears to be limited, as genetic concordance is small; still, a familial predisposition for autoimmune disease is often seen. Polymorphisms in COL1A2 and TGF-β1 may influence severity and development of the disease. Evidence implicating cytomegalovirus (CMV) as the original epitope of the immune reaction is limited, as is parvovirus B19. Organic solvents and other chemical agents have been linked with<unk> . One of the suspected mechanisms behind the autoimmune phenomenon is the existence of microchimerism, i.e. fetal cells circulating in maternal blood, triggering an immune reaction to what is perceived as foreign material. A distinct form of<unk>  and<unk>  sclerosis may develop in patients with chronic kidney failure. This form, nephrogenic fibrosing dermopathy or nephrogenic<unk>  fibrosis, has been linked to exposure to gadolinium-containing radiocontrast. Bleomycin (a chemotherapeutic agent) and possibly taxane chemotherapy may cause<unk> , and occupational exposure to solvents has been linked to an increased risk of<unk>  sclerosis.
Systemic scleroderma
Scleroderma
Chilblain lupus erythematosus
Discoid lupus erythematosus
Tumid lupus erythematosus
Mixed connective tissue disease
Lupus erythematosus
Sjögren syndrome