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Linear Scleroderma: Clinical Spectrum, Prognosis, and Laboratory Abnormalities

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▸Requests for reprints should be addressed to Vincent Falanga, M.D.; Department of Dermatology, University of Pittsburgh, 3601 Fifth Avenue; Pittsburgh, PA 15213.

▸From the Department of Dermatology and the Division of Rheumatology and Clinical Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; and the Arthritis and Immunology Laboratory, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma.†Dr. Gerald Rodnan is deceased.

Pittsburgh, Pennsylvania; and Oklahoma City, Oklahoma

© 1986 American College of PhysiciansAmerican College of Physicians

Ann Intern Med. 1986;104(6):849-857. doi:10.7326/0003-4819-104-6-849
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The clinical features and natural history of linear scleroderma in 53 patients and the laboratory tests helpful in the management of this disease are described. No patient had Raynaud's phenomenon or signs of systemic connective tissue disease in a mean follow-up of 10 years. Blood eosinophilia (> 300 cells/mm3) was present in half the patients, usually those with clinically active disease rather than inactive disease (p < 0.02). An elevated serum IgG level correlated with the presence of joint contractures (p < 0.02). Antinuclear antibodies, commoner in patients with extensive and prolonged disease, were present in 31% and 46% of patients whose sera were tested on mouse kidney and HEp-2 cells, respectively. Antibodies to single-stranded DNA, present in 50% of patients, were associated with extensive disease, joint contractures (p < 0.001), and active disease of greater than 2 years' duration (p < 0.001). Discordance in immune reactivity indicates that at least three serum autoantibodies exist in these patients: antibodies to single-stranded DNA and antinuclear antibodies with homogeneous and nucleolar immunofluorescence patterns.





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