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One hundred patients with facial seborrheic dermatitis and 42 control subjects were studied. The number of periodic acid-Schiff-positive Pityosporum ovale yeast cells in skin scrapings per high-power field were counted and designated 1 + to 4 +. Our data indicate a correlation between the density of P. ovale and the clinical severity of seborrheic dermatitis, both before and after therapy with a precipitated sulfur/salicyclic acid shampoo. The data support the concept that yeast contributes to the pathogenesis of seborrheic dermatitis.

Physiologically, the main function of alpha 2-macroglobulin is the binding of active endopeptidases rather than their inhibition. The interaction results in a conformational change in the alpha 2-macroglobulin that leads to its rapid elimination by the reticuloendothelial system. In this way, the reticuloendothelial system may help in the regulation of extracellular proteolytic activity resulting from the release of proteinases from injured pancreatic acinar cells in acute pancreatitis. To evaluate this concept, the effect of feeding a choline-deficient diet supplemented with 0.5% DL-ethionine was determined in 4 and 6-wk-old mice in which the reticuloendothelial system was normal, stimulated, or depressed. Stimulating the reticuloendothelial system in 4-wk-old mice significantly (a) decreased the mortality rate; (b) lessened the drop in the plasma content of both alpha 2-macroglobulin and alpha 1-antitrypsin; and (c) decreased the severity of pancreatitis noted microscopically. In contrast, reticuloendothelial suppression in this group of mice had no demonstrable effect. However, when similar studies were done in 6-wk-old mice, in which this diet induces a milder disease, reticuloendothelial suppression significantly increased the mortality rate as compared with normal mice, whereas reticuloendothelial stimulation significantly decreased it. The possible mechanism for the salutory effect of stimulating the reticuloendothelial system on the outcome of diet-induced pancreatitis in mice is discussed.

The presence of immunoglobulin and complement deposits in the skin of three patients with papular urticaria suggests that these lesions may be due to a cutaneous vasculitis. These deposits were most frequently found in biopsy specimens taken from lesions within 24 hours of their development. The presence of granular deposits of Clq, C3, and IgM in the walls of the superficial dermal blood vessels suggests that immune complexes (IgM aggregates) may be primarily involved in the pathogenesis of these lesions, with complement activation initiated by Clq through the classical pathway.