RESUMO
We report four cases of necrotizing reactions of the Lucio's phenomenon type, an entity rarely observed in Brazil despite the high prevalence of leprosy. Clinical, histopathological and therapeutic aspects are described and compared to those reported in the literature for cases classified as diffuse, non-nodular lepromatous leprosy with Lucio's phenomenon.
Assuntos
Anti-Inflamatórios/uso terapêutico , Hansenostáticos/uso terapêutico , Hanseníase Virchowiana/patologia , Mycobacterium leprae , Pentoxifilina/uso terapêutico , Inibidores da Agregação Plaquetária/uso terapêutico , Prednisona/uso terapêutico , Idoso , Anti-Inflamatórios/administração & dosagem , Brasil , Progressão da Doença , Endotélio Vascular/microbiologia , Evolução Fatal , Feminino , Humanos , Hansenostáticos/administração & dosagem , Hanseníase Virchowiana/tratamento farmacológico , Hanseníase Virchowiana/microbiologia , Masculino , Pessoa de Meia-Idade , Mycobacterium leprae/isolamento & purificação , Necrose , Prednisona/administração & dosagem , Úlcera Cutânea/microbiologia , Úlcera Cutânea/patologia , Trombose/patologia , Vasculite/patologiaRESUMO
Immunohistochemical studies were performed to determine the presence and distribution of polypeptide transforming growth factor (TGF)-beta 1, a cytokine with macrophage-suppressing activity, in skin biopsies from 41 patients with different clinical forms of leprosy. We used an anti-TGF-beta 1 polyclonal antibody and the avidinbiotin-peroxidase (ABC complex) method. The results demonstrated that the lesions of the lepromatous and borderline lepromatous forms presented intense cytoplasm staining for TGF-beta 1 in the cells of the dermal infiltrate. A reaction of moderate intensity was observed in the cells of granulomas from borderline borderline cases, whereas no detectable immunoreaction was observed in granuloma cells from the tuberculoid and borderline tuberculoid forms. Considering that in the lepromatous leprosy form Mycobacterium leprae multiplies in the cytoplasm of macrophages and the lesions are diffuse and consist of poorly differentiated young macrophages, we believe that these alternations may be explained at least in part by the presence of TGF-beta 1 in the dermal infiltrate. Production of the cytokine may be induced by the presence of the bacillus itself and of its constituents, causing a mechanism of parasite evasion. Similarly, the absence of TGF-beta 1 in tuberculoid leprosy, which progresses with a specific immune response to M. leprae, may explain the intense differentiation of macrophage cells with the formation of well defined epithelioid granulomas capable of eliminating most of the bacilli.