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.

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.

Atopic dermatitis (AD) is a chronic inflammatory immune-mediated skin disease characterized by skin colonization by Staphylococcus aureus. Interleukin (IL)-22, in cooperation with IL-17, triggers antimicrobial peptide elaboration and enhances certain immunological responses. In AD, IL-22 is related to epidermal hyperplasia, keratinocyte apoptosis, and inhibition of antimicrobial peptide (AMP) production. We aimed to evaluate the impact of staphylococcal enterotoxins on the Tc22/Th22 induction in the peripheral blood of AD patients and on CD4+/CD8+ T cells expressing IL-22 in AD skin. Our study showed inhibition of the staphylococcal enterotoxins A and B (SEA and SEB) response by Th22 (CD4+IL-22+IL-17A−IFN-γ−) cells in AD patients. In contrast, Tc22 (CD8+IL-22+IL-17A−IFN-γ−) cells were less susceptible to the inhibitory effects of staphylococcal enterotoxins and exhibited an enhanced response to the bacterial stimuli. In AD skin, we detected increased IL-22 transcript expression and T lymphocytes expressing IL-22. Together, our results provide two major findings in response to staphylococcal enterotoxins in adults with AD: dysfunctional CD4+ IL-22 secreting T cells and increased Tc22 cells. Our hypothesis reinforces the relevance of CD8 T cells modulated by staphylococcal enterotoxins as a potential source of IL-22 in adults with AD, which is relevant for the maintenance of immunological imbalance.

BackgroundSince macrophages are one of the major cell types involved in the Mycobacterium leprae immune response, roles of the M1 and M2 macrophage subpopulations have been well defined. However, the role of M4 macrophages in leprosy or other infectious diseases caused by mycobacteria has not yet been clearly characterized. This study aimed to investigate the presence and potential role of M4 macrophages in the immunopathology of leprosy.MethodsWe analyzed the presence of M4 macrophage markers (CD68, MRP8, MMP7, IL-6, and TNF-α) in 33 leprosy skin lesion samples from 18 patients with tuberculoid leprosy and 15 with lepromatous leprosy by immunohistochemistry.ResultsThe M4 phenotype was more strongly expressed in patients with the lepromatous form of the disease, indicating that this subpopulation is less effective in the elimination of the bacillus and consequently is associated with the evolution to one of the multibacillary clinical forms of infection.ConclusionM4 macrophages are one of the cell types involved in the microbial response to M. leprae and probably are less effective in controlling bacillus replication, contributing to the evolution to the lepromatous form of the disease.

Vasculite é a inflamação da parede dos vasos. Pode variar em gravidade desde doença autolimitada de um único órgão até doença grave com risco de morte por falência de múltiplos órgãos. Existem várias causas, embora só se apresente por poucos padrões histológicos de inflamação vascular. Vasos de qualquer tipo e em qualquer órgão podem ser afetados, resultando em ampla variedade de sinais e sintomas. Diferentes vasculites com apresentações clínicas indistinguíveis têm evolução e tratamento muito diferentes. Essa condição representa desafio para o médico, incluindo classificação, diagnóstico, exames laboratoriais pertinentes, tratamento e seguimento adequado. Neste artigo são revistos a classificação, a etiologia, a patogênese e os critérios diagnósticos das vasculites cutâneas.

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First described in 1985, intermediate cell histiocytosis is a rare disorder of the cutaneous dendritic cell group with a varied clinical presentation and evolution. The pathologic substrate is constituted by the proliferation of indeterminate cells (ICs) that are immunophenotypically characterized by the positivity of CD1a, CD68, and faint/focal S100, plus the negativity for CD207 (langerin). The authors present the case of a healthy elderly woman who presented generalized dome-shaped reddish cutaneous nodules over her trunk, neck, face, and extremities over a period of 18 months. A laboratory and imaging work-up ruled out internal involvement. The skin biopsy was consistent with IC histiocytosis. The patient was treated with narrowband ultraviolet B phototherapy, which resulted in an excellent short-term outcome.