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Some Comments on Its Pathogenesis and Course

William Dameshek, M.D.

Arch Intern Med. 1960;106(2):162-167.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Systemic lupus erythematosus (S.L.E.) has been a mysterious disease since it was first recognized as an entity years ago.¹ At first thought to be a "toxic" disturbance, later an infection closely related to tuberculosis, it was eventually placed in the category of the "collagen disorders." This was considered a group of disturbances characterized by a seeming lack of etiologic factors, a diversity of manifestations, and histologically, by a presumed generalized disturbance of collagen.³ To explain the latter finding, a rather vaguely defined hypersensitivity mechanism was invoked in some quarters.⁴ However, this was primarily the era of the histopathologist, and only in retrospect can one see now that the highly significant discovery of the L.E. phenomenon ⁵ represented a break from the morphologic approach to the predominantly immunologic.

The possibility that the L.E. factor in the serum could be immunologic in nature was rather slow in developing, but . . . [Full Text PDF of this Article]

Author Affiliations
Director, Blood Research Laboratory, New England Center Hospital, and Professor of Medicine, Tufts University School of Medicine, Boston

From the Blood Research Laboratory, a unit of the Ziskind Laboratories, New England Center Hospital, and the Department of Medicine, Tufts University School of Medicine.

Footnotes
Submitted for publication Dec. 22, 1959.

Aided by a grant from the U.S. Public Health Service, National Institutes of Health (Arthritis & Metabolic Diseases) No. A-2037 and a grant from the U.S. Public Health Service, National Institutes of Health (Heart) No. H-2021.

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