Diffuse leprosy of Lucio and Latapí: a histologic study.

BACKGROUND AND PURPOSE Ladislao de la Pascua described the spotted or lazarine leprosy for first time in 1844. Later on, Lucio and Alvarado studied and published it with the same names in 1852. Latapí re-discovered it in 1938 and reported it as 'Spotted' leprosy of Lucio in 1948. Frenken named it diffuse leprosy of Lucio and Latapí in 1963. Latapí and Chévez-Zamora explained that the fundamental condition of this variety of leprosy was a diffuse generalised cutaneous infiltration, naming it pure and primitive diffuse lepromatosis, upon which necrotising lesions develop, calling these lesions Fenómeno de Lucio or erythema necrotisans. A great number of histopathological reports have addressed the study of Lucio's phenomenon, and few about the histologic changes that take place in the course of diffuse lepromatous leprosy. The purpose of this work is to report the histologic findings observed in the study of 170 cutaneous biopsies of diffuse leprosy of Lucio and Latapí and 30 of Lucio's phenomenon. METHODS This is a retrospective study, which included the examination of 200 biopsy skin specimens from 199 patients with diffuse leprosy at different course of the disease. These cases were diagnosed in Mexico from 1970 to 2004. RESULTS The histologic examination revealed a vascular pattern affecting all cutaneous vessels, characterised by five outstanding features: a) colonisation of endothelial cells by acid-fast bacilli, b) endothelial proliferation and marked thickening of vessel walls to the point of obliteration, c) angiogenesis, d) vascular ectasia, and e) thrombosis. Necrotising lesions seen in diffuse lepromatous leprosy displayed two histopathological patterns: one of them, non-inflammatory occlusive vasculopathy and, the other one, occlusive vasculopathy, leukocytoclastic vasculitis, large neutrophilic infiltrate and lobular panniculitis. The first appeared as a result of the course of the occlusive vasculopathy produced by the colonisation of endothelial cells by Mycobacterium leprae. The second, as a result of a previous occlusive vasculopathy plus a leprosy reaction which is considered here as variant of ENL. CONCLUSIONS Endothelial cell injury appears to be the main event in the pathogenesis of diffuse leprosy of Lucio and Latapí. Once M. leprae has entered the endothelial cell, the micro-organism damages the blood vessels, leading to the specific changes seen in this variety of lepromatous leprosy.