Objetivos Avaliar a mobilidade funcional e sua relação com a capacidade cognitiva em pacientes com diabetes tipo 2 (DM2) entre 50 e 65 anos de idade, e com menos de 10 anos de diagnóstico. Materiais e métodos Estudo observacional, analítico e transversal envolvendo indivíduos não diabéticos e pacientes com DM2 com controle glicêmico inadequado, selecionados por amostra de conveniência. Em ambos os grupos, foram aplicados questionário estruturado, avaliação cognitiva com Miniexame do Estado Mental (MEEM) e teste do relógio (TDR), além da avaliação de mobilidade funcional pelo teste Timed Up & GO (TUG). Resultados No TUG os pacientes com DM2 apresentaram tempo médio de 11,27 segundos versus 9,52 segundos nos controles (p = 0,013). A associação entre declínio cognitivo e dismobilidade foi positiva nos indivíduos com DM2 (p = 0,037). No subgrupo que apresentou dismobilidade e declínio cognitivo associados, 18% eram portadores de DM2 e 1,6% era do grupo sem DM2 (p < 0,01). Conclusões Pacientes com DM2 apresentaram pior mobilidade funcional e desempenho cognitivo, favorecendo a hipótese de que o DM2 influencia a mobilidade funcional e capacidade cognitiva antes do aparecimento de complicações vasculares ou neuropáticas. Esses dados sugerem que a hiperglicemia é um fator agravante no desempenho de atividades que exijam funções mentais como atenção, orientação e memória de trabalho. Arq Bras Endocrinol Metab. 2014;58(9):946-52

Objectives The aim of the present study was to evaluate the functional mobility and its relationship to cognitive ability in patients with type 2 diabetes (T2DM), age between 50 and 65 years and under 10 years of diagnosis. Materials and methods An observational, analytical and cross-sectional study, involving no diabetic and type 2 diabetic individuals with inadequate glycemic control, selected by convenience sampling. In both groups, were administered structured questionnaire and cognitive assessment with Mini-Mental State Examination (MMSE) and the clock drawing test (CDT), besides assessment of functional mobility by the Timed Up & Go (TUG). Results In TUG, DM2 patients presented a mean time of 11.27 seconds versus 9.52 seconds (p = 0.013). The association between cognitive decline and decrease of mobility was positive in individuals with T2DM (p = 0.037). In the subgroup that showed decrease of mobility and associated cognitive decline, 18% were patients with DM2 and 1.6% were individuals without T2DM (p < 0.01). Conclusions Patients with T2DM presented worse functional mobility and cognitive performance, supporting the hypothesis that DM2 influence functional mobility and cognitive ability, regardless of neuropathic or vascular complications. These data suggest that hyperglycemia is an aggravating factor in the performance of activities requiring mental functions such as attention, working memory and orientation. Arq Bras Endocrinol Metab. 2014;58(9):946-52

OBJECTIVE: To compare the effects of glimepiride and metformin on vascular reactivity, hemostatic factors and glucose and lipid profiles in patients with type 2 diabetes. METHODS: A prospective study was performed in 16 uncontrolled patients with diabetes previously treated with dietary intervention. The participants were randomized into metformin or glimepiride therapy groups. After four months, the patients were crossed over with no washout period to the alternative treatment for an additional four-month period on similar dosage schedules. The following variables were assessed before and after four months of each treatment: 1) fasting glycemia, insulin, catecholamines, lipid profiles and HbA1 levels; 2) t-PA and PAI-1 (antigen and activity), platelet aggregation and fibrinogen and plasminogen levels; and 3) the flow indices of the carotid and brachial arteries. In addition, at the end of each period, a 12-hour metabolic profile was obtained after fasting and every 2 hours thereafter. RESULTS: Both therapies resulted in similar decreases in fasting glucose, triglyceride and norepinephrine levels, and they increased the fibrinolytic factor plasminogen but decreased t-PA activity. Metformin caused lower insulin and pro-insulin levels and higher glucagon levels and increased systolic carotid diameter and blood flow. Neither metformin nor glimepiride affected endothelial-dependent or endothelial-independent vasodilation of the brachial artery. CONCLUSIONS: Glimepiride and metformin were effective in improving glucose and lipid profiles and norepinephrine levels. Metformin afforded more protection against macrovascular diabetes complications, increased systolic carotid artery diameter and total and systolic blood flow, and decreased insulin levels. As both therapies increased plasminogen levels but reduced t-PA activity, a coagulation process was likely still ongoing.

A retinopatia é das complicações mais comuns e está presente tanto no diabetes tipo 1 quanto no tipo 2, especialmente em pacientes com longo tempo de doença e mau controle glicêmico. Quando culmina em perda visual é considerada trágica e constitui fator importante de morbidade de elevado impacto econômico, uma vez que a retinopatia diabética é a causa mais freqüente de cegueira adquirida. A fisiopatologia das alterações microvasculares do tecido retiniano está relacionada à hiperglicemia crônica, que leva a alterações circulatórias como a perda do tônus vascular, alteração do fluxo sangüíneo, aumento da permeabilidade vascular e conseqüentemente extravasamentos e edemas e, por fim, obstrução vascular que leva à neovascularização, com vasos frágeis que se rompem, levando a hemorragias e descolamento da retina. O controle metabólico e pressórico estritos podem retardar a progressão da retinopatia. Até o momento, nenhum agente farmacológico se mostrou eficaz em prevenir, retardar ou reverter a retinopatia diabética.O tratamento disponível no momento é a fotocoagulação a laser de argônio e, em alguns casos, a vitrectomia. O sucesso do tratamento depende da detecção precoce das lesões. Muitos estudos têm revelado mecanismos, assim como antagonistas importantes na evolução da retinopatia.

Diabetic retinopathy is a frequently observed complication in both type 1 and type 2 diabetes, specially in patients with long term disease and poor glicemic control. Irreversible visual loss appears at the final stages of diabetic retinopathy and it is considered one of the most tragic of diabetic complications. It is also considered an important factor of morbidity and has a high economical impact once it is the leading cause of blindness. The pathophysiology of the retinal microvascular alterations is related to the chronic hyperglycemia that leads to the following circulatory disturbances: loss of vascular tonus, increase in vascular permeability, edema and exudation, with vascular obstruction and ischemia that stimulates neovascularization, which may lead to fibrous retraction and vitreous hemorrhages with retinal detachment. Recent studies have indicated that the strict glicemic and blood pressure controls are effective in reducing or blocking the progression of retinopathy. Up to now no pharmacological agents have shown to be effective in preventing or reducing neovascularization and visual loss. Presently, the most effective available treatment for proliferative retinopathy is laser photocoagulation. Further studies are needed to obtain new products and technologies that could effectively prevent or block retinopathy progression.