Pathogenesis of sarcoidosis: an hypothetical model

Abstract

An hypothetical model for the pathogenesis of sarcoidosis is presented which is compatible with its generalized nature, lack of an apparent etiologic agent and biochemical difference from other granulomas, including marked elevation of angiotensin converting enzyme. Widespread genetic alteration of epithelioid cell precursors by a virus or early precursor mutation is hypothesized to trigger transformation to epithelioid cells and the synthesis of certain proteins which may differ qualitatively from those of non-sarcoid epithelioid cells. At some point in the transformation the epithelioid cells develop an affinity for each other by altered surface properties, resulting in the widespread formation of granulomas.