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Increased Dermal Mast Cell Populations in Progressive Systemic Sclerosis: A Link in Chronic Fibrosis?

ROBERT A. HAWKINS, M.D.; HENRY N. CLAMAN, M.D.; RICHARD A. F. CLARK, M.D.; and JAMES C. STEIGERWALD, M.D.
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Grant support: in part by a General Clinical Research Center Grant (#RR 00051-22) from the National Institutes of Health.

Presented in part on 9 February 1984 at the meeting of the western section of the American Federation for Clinical Research, Carmel, California.

▸Requests for reprints should be addressed to James C. Steigerwald, M.D.; Division of Rheumatology, Box B-115, University of Colorado Health Sciences Center, 4200 East 9th Avenue; Denver, CO 80262.


Denver, Colorado


© 1985 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1985;102(2):182-186. doi:10.7326/0003-4819-102-2-182
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Dermal collagen deposition is the hallmark of the early indurative phase of progressive systemic sclerosis (scleroderma). This process, however, tends to remit in late stages of the disease. Because mast cells are believed to participate in the development of fibrotic processes, we measured the density of the cutaneous mast cell population in clinically involved and uninvolved skin of a group of patients with scleroderma. Mast cell counts in clinically involved skin of patients with early stages of scleroderma (111 ±28 [SD] cells/mm2) were significantly greater than those in clinically uninvolved skin of the same patients (58 ±26 cells/mm2) and also greater than those of normal controls (50 ±14 cells/ mm2). Mast cell counts in clinically involved and uninvolved skin of patients with late scleroderma were normal. When mast cell density was analyzed by depth of dermis, an 85% increase was noted in involved papillary dermis and a 152% increase in involved reticular dermis in patients with early scleroderma when compared with densities in controls. These results suggest that mast cells may be important in the pathogenesis of the early cutaneous lesions of progressive systemic sclerosis, perhaps by promoting fibrosis.

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