Abstract
LUPUS erythematosus has been tentatively classified as one of the so-called collagen, or mesenchymal, diseases, not only as a result of the pathological work which has demonstrated fibrinoid degeneration 1 possibly due to precipitation of mucopolysaccharides from collagen ground substance 2 but also on the basis of the clinical response of the acute forms of the disease to adrenal cortical substitution or stimulation. 3 Recent extensive histological studies of the skin lesions by the Mayo group 4 stress vascular involvement in all stages of the disease and support the report that there is demonstrable interference with fluid exchange between vessels and tissue spaces. 5 The characteristic lesions of the skin are apparently not the primary manifestation of lupus erythematosus in that they do not account for the systemic pathology. Beyond the demonstration of the L. E. cell in acute forms of the disease 6 there are several other suggestive systemic
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