Prevalence of diabetic retinopathy in patients with type 1 diabetes mellitus / Prevalência de retinopatia diabética em pacientes com diabetes mellitus tipo 1

OBJECTIVES: Diabetic retinopathy (DR) is the leading cause of legal blindness in young adults. Scarce data from Brazilian subjects with type 1 diabetes mellitus (DM) are available. Aims: The objectives of this study were to determine the prevalence of DR and its risk factors in type 1 diabetes mellitus (DM) outpatients from a general hospital. METHODS:A cross-sectional study of 437 type 1 DM (50.3 percent males, 82.4 percent whites) was conducted. DR was graded as absent, mild and moderate non-proliferative DR (mild/moderate NPDR) or severe non-proliferative and proliferative DR (advanced DR). Presence of clinically significant macular edema (CSME) was also recorded. RESULTS: Any DR was present in 44.4 percent of subjects. In multivariate analysis, DM duration, systolic blood pressure (SBP) and A1C test were associated with mild/moderate NPDR (P<0.005). Advanced DR, was associated with DM duration, SBP, smoking [odds ratio (OR) 2.75, 95 percentCI 1.15-6.60] and micro-or macroalbuminuria (OR 8.53, 95 percentCI 3.81-18.05). CSME was present in 21 (9.4 percent) patients and was associated with smoking (OR 3.19, 95 percentCI 1.24-8.2). Its frequency increased with the severity of DR (16.4 percent in advanced DR, 9.6 percent in mild/moderate NPDR, and 4.7 percent in the group without DR; P = 0.020). CONCLUSION: Patients with type 1 DM attending an endocrine out-patient clinic at a general hospital had a high prevalence of DR associated with traditional risk-factors and smoking.

OBJETIVOS: Determinar a prevalência de RD e seus fatores de risco em pacientes com DM tipo 1 atendidos em um hospital geral. MÉTODOS: Foi realizado um estudo transversal com 437 pacientes (50,3 por cento homens, 82,4 por cento brancos). RD foi agrupada em: 1) ausente; 2) não proliferativa leve e moderada (RDNP leve/moderada); 3) não prolifetiva grave e RD proliferativa (RD avançada). Edema de mácula clinicamente significativo (EMCS) também foi registrado. RESULTADOS: Qualquer grau de RD esteve presente em 44,4 por cento dos pacientes. Na análise multivariada, duração do DM, pressão arterial sistólica e teste A1C foram associados com a RD leve/moderada (P<0,005). RD avançada foi associada com duração do DM, pressão arterial sistólica (PAS), fumo [razão de chances (RC) 2,75, IC 95 por cento 1,15-6,60] e micro-ou macroalbuminúria (RC 8,53, CI 95 por cento 3,81-18,05). EMCS esteve presente em 21 (9,4 por cento) dos pacientes associado ao fumo, aumentando com a gravidade da RD (16,4 por cento RD avançada; 9,6 por cento RD leve/modera, e 4,7 por cento no grupo sem RD; P = 0,020). CONCLUSÃO: Pacientes com DM tipo 1 vistos em um hospital geral têm uma alta prevalência de RD, a qual foi associada aos fatores de risco tradicionais e fumo.

A role for lymphocytes and cytokines on the eosinophil migration induced by LPS

In the present work we review the existing evidence for a LPS-induced cytokine-mediated eosinophil accumulation in a model of acute inflammation. Intrathoracic administration of LPS into rodents (mice, rats and guinea pigs) induces a significant increase in the number of eosinophils recovered from the pleural fluid 24 hr later. This phenomenon is preceded by a neutrophil influx and accompanied by lymphocyte and monocyte accumulation. The eosinophil accumulation induced by LPS is not affected by inhibitors of cyclo or lipoxygenase nor by PAF antagonists but can be blocked by dexamethasone or the protein synthesis inhibitors cycloheximide. Transfer of cell-free pleural wash from LPS injected rats (LPS-PW) to naive recipient animals induces a selective eosinophil accumulation within 24 hr. The eosinophilotactic activity present on the LPS-PW has a molecular weight ranging between 10 and 50 kDa and its effect is abolished by trypsin digestion of the plural wash indicating the proteic nature of this activity. The production of the eosinophilotactic activity depends on the interaction between macrophages and T-lymphacytes and its effect can not be blocked by anti-IL-5 monoclonal antibodies. Accumulated evidence suggest that the eosinophil accumulation induced by LPS is a consequence of a eosinophilotactic cytokine produced through macrophage and T-cell interactions in the site of a LPS-induced inflammatory reaction.