A variety of medications and chemical compounds have been associated with the development of a spectrum of scleroderma-like conditions. Some compounds induce sclerotic skin changes along with Raynaud phenomenon, pulmonary fibrosis and other internal organ involvement, whereas others induce circumscribed morphea-like plaques.

Causative medications include chemotherapeutic agents, analgesics, neurological drugs, appetite suppressants and other agents, including penicillamine, tryptophan, cocaine, and phytonadione (vitamin K).

Certain chemical compounds, such as plastics, solvents (paint removers and thinners, trichloroethane, xylene, benzene), vinyl chloride, contaminated rapeseed oil, and minerals can cause scleroderma-like disease. Long-term silica exposure can induce scleroderma that is difficult to distinguish from idiopathic scleroderma. This association is more common in males due to occupational exposure.

Drug-induced scleroderma may be distinguished from idiopathic scleroderma by the lack of positive autoantibodies. Furthermore, if there is cessation or reversibility of disease process upon discontinuation of the drug, this supports a drug-induced process.

The pathogenesis of drug-induced scleroderma is incompletely understood and likely varies by drug. Timing of symptom onset varies by drug and ranges from 2 days to 11 years, with the majority of drugs inducing disease between 3 weeks and 9 months. The clinical course is similarly variable and ranges from slow evolution to rapidly progressive disease. Complete resolution after discontinuation of offending agent is usual but not absolute.

Related topics: Scleroderma, Scleroderma of childhood, Raynaud phenomenon, Morphea, Pulmonary fibrosis, Silicosis