Pityriasis rosea--an autoaggressive disease? Statistical studies in relation to aethiology and pathogenesis.

Abstract

SUMMARY.— Distributions of the age of onset of pityriasis rosea, in 8 clinical series, are shown to be closely comparable. They fit a simple biological model which also accounts for the sex- and age-distributions of many other age-dependent diseases. The crude sex-ratio (M/F) in the Leeds series (241/246) is close to unity. Month-to-month fluctuations in the presentation of new cases exceed those expected on a random basis: the monthly pattern in the Leeds series broadly resembles those reported previously in an Essex, and a Swedish series. The causes of these temporal fluctuations are unknown. The anatomical distribution of the site of the primary plaque in the Leeds series resembles that found in other series, from other countries. From the statistical evidence, and the clinical course of pityriasis rosea, it is concluded that the aetiology is probably autoaggressive. Autoaggressive diseases are believed to arise in genetically predisposed people as the result of somatic gene mutations in stem cells of the central system that regulates growth. The mutant stem cell propagates a “forbidden clone” of descendant cells, and the products of this clone attack target cells bearing complementary recognition structures or “tissue coding factors”. After a latent period, symptoms and signs of the disease appear. The mutant cells of the forbidden-clone evoke an endogenous defence which is probably mediated through immunoglobulins. Extrinsic factors can sometimes disturb the balance between defence and attack to precipitate the onset of autoaggressive disease. The short clinical course of pityriasis rosea, and the rarity of second and third episodes, can probably be attributed to the relatively high efficiency of the endogenous defence mechanism.