Sarcoidosis around the world.

The 11th World Congress on Sarcoidosis and Other Granulomatous Disorders was held in the University of Milan in September 1987. It attracted 400 participants from 30 countries who enjoyed 96 communications and 148 poster presentations proof that research in these fascinating disorders is very much alive and kicking. The sarcoid granuloma is a battlefield between invading antigen and the cellular and humoral defences of the body. Such new techniques as immunofluorescence, histochemistry, monoclonal antibodies and ELISA have provided new insights in this immunologic battlefield for it is now possible to identify the uniforms of the participating warriors. The activated T helper lymphocyte releases interleukin-2 (IL-2) in abundance. The initiating signal for this exaggerated response has not yet been recognized but it seems that local stimuli in the battlefield maintain this exaggerated state of alert. The IL-2 gene is activated and soluble interleukin-2 receptors have elevated levels in serum and bronchoalveolar lavage fluid in active sarcoidosis.1 But if IL-2 is present in abundance, why is there no dramatic response to treatment with cyclosporin? In about 10% of sarcoidosis patients the granuloma persists with the development of extensive patchy fibrosis, mainly affecting the upper and middle lobes. What are the steps from granuloma to fibrosis? The alveolar macrophage hastens fibrogenesis via fibronectin and a progression growth factor, both of which influence fibroblasts to cause recruitment-attachment and to produce collagen type 1 fibrosis. Chemical mediators maintain a continuous cascade to fan on this process. The monocyte-macrophage lineage possesses calcitriol receptors, promoting the metamorphosis of macrophages into multinucleate giant cells and to granuloma formation.2 What are the best markers of this ongoing fibrosis? Is it electron microscopy, histochemistry, humoral mediators, monoclonal antibodies, magnetic resonance, or a combination of all of them and why the predominance of fibrosis in the lungs whereas it is inconspicuous and infrequent in the liver and other organs? Is it possible that a foreignbody giant cell reaction is the inciting nidus? Under certain circumstances this initial foreign body reaction progresses inexorably to granuloma formation and fibrosis but in the absence of co-factors fizzles out harmlessly. This theory is dictated by the like behaviour of the Kveim-Siltzbach test.3 The Kveim-Siltzbach skin test is no longer used