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Previous Volume 350:1044-1046 March 4, 2004 Number 10 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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From a historical perspective, there are few diseases for which the cause, natural history, and response to treatment have been as complex or difficult to define as those of systemic lupus erythematosus (SLE). In large part, this is because SLE represents a clinical syndrome rather than a unique disease entity. The apparent diversity of pathogenic mechanisms operating in individual patients, which parallels the diversity observed in various animal models of SLE, underscores the fact that the disease phenotype arises from a variable mixture of environmental factors, the hormonal milieu, genes that contribute to an autoimmune diathesis, and other causes of . . . [Full Text of this Article]

Source Information

From the Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Md.

Related Letters:

Sequential Therapies for Proliferative Lupus Nephritis
Yee C.-S., Gordon C., Gelber A. C., Christopher-Stine L., Fine D. M., Farhey Y., Hess E., Contreras G., Lenz O., Roth D.
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N Engl J Med 2004; 350:2518-2520, Jun 10, 2004. Correspondence

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