Pathogenesis of lesions in leprosy.

Leprosy patients, including those with various clinical forms, present widely disseminated lesions in tissues and organs, of diverse histopathology. These lesions are present in skin and mucosa, peripheral nerves, organs, vessels, muscles, bones, etc. According to the clinical form, lesions vary-in characteristic, borderline, tuberculoid and lepromatous-and, in general, are inflmmatory or degenerative. Nonspecific infective processess can be seen ; also a major incidence of cancer and of secondary lesions to physical causes such as compression. In this work we shall study inflammatory and degenerative lesions such as erythemas (simple, polimorphous, necrotizing), pigmentary disorders, oedemas, non-specific infiltrates and of granulomatous type, amyloidosis, hydropic and fatty degeneration, atrophy, fibrosis, sclerosis, bone resorption, etc ; histopathologic disorders that can give place to dermatitis, liver disorders, splenitis, orchitis, adenitis, arthritis, chondritis, myositis, vasculitis, etc. The mechanisms that explain these histopathologic lesions in tissues and organs-in each clinical form-are of primary and secondary causes. Primary causes are : a) Lesions due to non-specific diffuse infiltrates and granulomatous infiltrates : tuberculoid or lepromatous. b) Lesions due to antigens and/or "toxines" (?) of viable M. leprae and/or detritus of non-viable M. leprae origin. c) Lesions due to circulating or fixed immune-complex. Secondary causes are : a) Neurotrophic lesions as a consequence of peripheral nerve destruction because of infiltrates, fibrosis, such as atrophy, ulcers, etc. b) Lesions as a consequence of compression, retraction, etc. of mechanic cause, with cicatricial and retractive sequels. c) Non-specific infections secondary to trauma, burns, etc. d) Lesions which are a consequence of the interaction of various pathogenic mechanisms already mentioned. The above stated, according to orthodox leprosy, is incomplete. In fact, the primary and essential cause of these histopathologic lesions, which is not mentioned, is the highly reactive metabolite toxic inflammative activity, that appears as a consequence of lipid auto-oxidation disorder, known as "auto-oxidative disease" (Bergel). These abnormal metabolites, hydroperoxide generally, and a product of lipid cell auto-oxidation, are highly reactive, through chain reaction, generate free radicals which damage, among others, lisosomic membranes, allowing hydrolytic enzyme get out, etc. Poli-unsaturated fatty acid auto-oxidation is in relation with the synthesis and/or inactivation of prostaglandines, essential factors in the genesis of the inflammatory process. Leprosy reaction in the form of erythema nodosum leprosum with erythema, arthralgias, adenopathy, myalgias, serum globulinic disorders, etc. configurate a situation seen in leprosy