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E. William Rosenberg, MD; Patricia W. Belew, PhD
Memphis

Arch Dermatol. 1982;118(3):143-144.

	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.—

Recent reports have suggested a role for the alternative complement pathway in psoriasis.^1-6 A search for endotoxemia in psoriasis and its possible pharmacologic modification followed. The results reported by Belew et al⁷ and Skinner et al⁸ now afford us enough support to propose the following hypothesis. Psoriasis results from the interaction of a more or less vulnerable alternative complement pathway with varying amounts of yeast, Gram-negative, and streptococcal organisms.

This hypothesis accounts for the following features of psoriasis:

1. Seborrheic localization. The presence of a large quantity of Malassezia ovalis in so-called seborrheic locations would be adequate to provoke a psoriatic reaction in susceptible persons.
   
2. Predilection of psoriasis to localize at sites of old trauma and scars, and its frequent symmetry. While the presence of abnormal numbers of activating surface micro-flora might account for psoriasis in body folds, hairy areas, and (its favorite
   

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