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Denny L. Tuffanelli, MD
San Francisco

Arch Dermatol. 1977;113(3):374-375.

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

To the Editor.—

There are a number of reports in the literature of patients who, in association with connective tissue disease, have deficiencies of one or another component of the complement system. Recently Kohler et al¹ reported identical male twins with longstanding discoid lupus erythematosus (LE) and hereditary angioedema with Cl inhibitor (C1 INH) deficiency and a marked secondary decrease in C4.

Two genetic forms of hereditary angioedema have been described, the common and variant forms.² About 85% of patients have the common form. Immunochemical and functional concentrations of C1 INH in these patients range from undetectable to about 50% of normal. The remaining 15% of patients have the variant form of the disease; that is, normal or increased levels of an antigenically identical, but functionally deficient protein.³ We recently have had the opportunity to study a patient with classical discoid LE and the variant form of . . . [Full Text PDF of this Article]

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