Livedoid vasculopathy is a skin disease that occludes the blood vessels of the dermis. It has a pauciinflammatory or non-inflammatory nature. It is characterized by the presence of macular or papular, erythematous-purpuric lesions affecting the legs, especially the ankles and feet, and producing intensely painful ulcerations, which cause white atrophic scars called "atrophie blanche". This review includes studies and case reports found in the medical literature regarding the etiopathogenic associations of the disease, particularly those related to thrombophilia, their histopathological findings and the therapeutic approaches used in the difficult clinical management of these cases. Keywords: Leg ulcer; Livedo reticularis; Thrombophilia; Thrombosis; Venous thrombosis Resumo: A vasculopatia livedoide é uma afecção cutânea oclusiva dos vasos sanguíneos da derme, de caráter pauci-inflamatório ou não-inflamatório. Caracteriza-se pela presença de lesões maculosas ou papulosas, eritêmato-purpúricas, nas pernas, especialmente nos tornozelos e pés, as quais produzem ulcerações intensamente dolorosas, que originam cicatrizes atróficas esbranquiçadas, denominadas "atrofia branca". Nesta revisão, abordamos os estudos e relatos de caso da literatura médica referentes às associações etiopatogênicas da doença, particularmente as que se referem aos estados de trombofilia, seus achados histopatológicos e abordagens terapêuticas empregadas na difícil condução clínica destes casos.

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This study presents a single center experience with livedoid vasculopathy (LV). A rare disease that can lead to severe quality of life impairment. Characterize clinical data of LV patients at the Dermatology Division at the University of São Paulo. A retrospective and transversal study was conducted, from 1 January 2005 to 31 December 2019. About 75 patients diagnosed as LV and confirmed by skin biopsy were included. Epidemiology, clinical appearance, histopathology data, and treatment history were observed. There were 78.66% Caucasian women, with a mean age of 39.9 years. Frequent cutaneous manifestations were ulcers, atrophic blanche-like scars, hyperpigmentation, purpuras, telangiectasias, and livedo racemosa. Pain, pruritus, and hypoesthesia were the main symptoms. After treatment, almost 40% of

Tecidual reaction at the inoculation site of L. (L.)chagasi promastigotes in hamsters depleted and non-depleted of complement was studied within 2, 6, 12, 24, 48 and 72 hours of infection. The inflammatory reaction was characterized by early predominance of polymorphonuclear cells (PMN) at 2, 6 and 12 hours of infection, mixed infiltrate of PMN and mononuclear cells (MN) at 24 hours, followed by predominance of MN at 48 and 72 hours after infection. The group depleted of complement showed a higher number of PMN at 2 hours and lower numbers of MN at 72 hours after infection (P < 0.0001). In the depleted group the phagocytosis by PMN was lower at 2 and 24 hours and by MN was lower at 24, 48 and 72 hours after infection. Electron microscopy showed extracellular intact and degenerated parasites, and lysed intracellular parasites, in PMN; and, rarely, preserved intracellular parasites in MN at 2, 6 and 12 hours after infection. The groups examined at 24, 48 and 72 hours of infection showed only cellular and parasite debris in mononuclear inflammatory cells. C3b deposits were detected by immunofluorescence in the interstitium and in the cytoplasm of inflammatory cells in non-depleted group at 2, 6 and 12 hours of infection. No immunoglobulin was detected in either group. Visceralization was detected 240 days after infection. The complement system has an important role in the inflammatory reaction and phagocytosis. The ultrastructural findings showed that the escape of the parasite probably occurs soon after inoculation.