CD8-CLA(+) T cells are reduced in peripheral blood of patients with non-segmental vitiligo. This finding may be related to the previously reported increase of CD8(+) cells in both lesions and perilesional skin of these patients.

Background: The evidence that vitiligo is an autoimmune disease is supported by its association with autoimmune conditions, the presence of activated cytotoxic T lymphocytes in the lesions and melanocyte-specific circulating auto-antibodies. Some studies have indicated the normal-appearing skin being immune-targeted for latent melanocyte disappearance. Method: We aimed to characterize immunohistologically the cellular infiltrate and to identify the distribution pattern of T and Langerhans cells (LCs) in the active border of depigmenting lesions and clinically normal skin of 22 patients with progressive non-segmental vitiligo, besides the cellular expression for the cutaneous lymphocyte-associated antigen (CLA), comparing to 10 controls. Results: Immunohistochemical analyses showed an overall reduction of the number of CD1a+ cells, dermal increase of CD8+ T cells, and increase of the epidermal CD3+ T cells number in the active border of lesions. Surprisingly, those cellular changes were also observed in clinically pigmented skin. However, a significant intra-epidermal infiltration of CD8+ T cells was evident only within active border biopsies. The CLA+ cells were not significantly increased in the patients' skin. Conclusions: The findings of this study suggest an extensively immune-committed skin in active vitiligo, mainly characterized by overall scarcity of CD1a+ cells and dermal increase of CD8+ cells even in apparently normal skin, in addition to the epidermal infiltrate of CD8+ T cells in the depigmenting areas. This report further supports that some CD8+ T and LCs cells play a pivotal role in the process of melanocyte loss, and strengthens an auto-immune hypothesis for vitiligo.

ComunicaçãoResumo: Na patogênese do vitiligo tem-se enfatizado o papel das células T citotóxicas. Identificadas pelo antígeno linfocitário cutâneo (CLA), essas células já foram descritas no sangue de pacientes com outras dermatoses e podem ser depletadas pela fototerapia concomitantemente à melhora clínica. Descreve-se caso de vitiligo generalizado com melhora clínica expressiva após Puva, no qual houve redução de 25% dos linfócitos T CD8 + -CLA + circulantes. Palavras-chave: Imunofenotipagem; Terapia Puva; Vitiligo Abstract: The role of cytotoxic T cells (CD8+) has been emphasized in the pathogenesis

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Objectives:To determine the more frequently seen clinical and immunologic manifestations in the antiphospholipid syndrome (APS) in patients of 2 referral centers. Methods: We studied 50 patients with the diagnosis of primary or secondary APS, 49 females and 1 male, with ages ranging between 15 and 65-year-old, using a predetermined protocol in which we measured the immunologic and clinical spectrum, including the determination of anticardiolipin antibodies (ACA) and lupus anticoagulant (LA); in some cases we also measured anti-␤ 2-glycoprotein I. Results: The most frequent clinical manifestations were thromboses in several sites detected in 88% of cases; the most common location was the lower extremities (40%) and as pulmonary emboli was detected in 20%. Arthritis was found in 70% of the cases, livedo reticularis in 52%, Raynaud phenomena in 50%, migraine in 40%, hemolytic anemia in 30%, major depressive disorder in 22% and recurrent miscarriage in 18%. Immunologic studies showed antinuclear antibodies (ANA) in 80%, ACA of IgM and IgG isotypes were found in 56% and 44% respectively, LA in 34% and anti-DNA antibodies in 40%. Conclusions:The main clinical manifestations in patients with APS are: lower extremities thromboses, pulmonary emboli, cutaneous, articular and neurologic involvements, with the presence of ACA (isotype IgM). Introduction:The catastrophic antiphospholipid syndrome (CAPS) is characterized by a rapid-progressive thrombosis of small vessels, multiple organ failure in the presence of antiphospholipid antibodies, might be fatal in more than 50% of cases. The risk-factors identified in the develop of CAPS are, bacterial and/or viral infections, surgery, inadequate treatment of systemic lupus erythematosus (SLE), inadequate treatment of antiphospholipid syndrome (APS), or use of estrogens. Objectives: To identify methods to prevent the progression to CAPS in patients with primary and secondary antiphospholipid syndrome (APS). Patients: Patient 1: 28-year-old female with SLE without treatment, with a previous history of 2 fetal losses and 2 normal vaginal deliveries. During the 3rd trimester of her 5th pregnancy the patient presented with fever, hypertension, renal involvement, deep vein thrombosis, cerebral organic syndrome, convulsions and coma. Patient 2: 22-year-old female with SLE, lupus nephropathy classified as WHO class IV, secondary APS and cutaneous vasculitis. Exacerbation of the SLE was secondary to sun exposure and insufficient corticosteroids doses. Methods:The risk-factors were identified and the patients were treated with: 1. High corticosteroid doses. 2. Full anticoagulation with low molecular weight heparin. 3. Aggressive broad-spectrum antibiotic treatment. 4. Intravenous immunoglobulins infusions at the doses of 1g/kg/d for 2 subsequent days. 5. Control of the hematological disorder in the intensive care unit (ICU). Results: The outcomes of both patients were successful as demonstrated by controlling the events and not developing CAPS. Conclusions: Our experience suggests that ever...