Amputação de membros inferiores em pacientes diabéticos ­ qual é o controle dos fatores de risco? / Lower extremity amputation in diabetic patients: what is the control of risk factors?

Introdução: Define-se pé diabético como "infecção, ulceração e ou destruição dos tecidos profundos, associados a anormalidades neurológicas e vários graus de doença vascular periférica nos membros inferiores", que é a principal causa de amputações não traumá- ticas. Este estudo objetiva identificar fatores de risco para amputação de pé diabético dos portadores de diabetes. Métodos: Trata-se de um estudo do tipo caso-controle, transversal, observacional e prospectivo, realizado através da coleta de dados por aplicação de questionário e pesquisa de outras informações no sistema de registro eletrônico de prontuários do Hospital Santa Isabel (HSI) e do Núcleo de Atenção ao Diabético (NAD) em Blumenau/SC. As variáveis analisadas nos prontuários foram: complicações microvasculares e macrovasculares, valor de HbA1c, perfil lipídico, cálculo de IMC (índice de massa corporal), realização prévia de arteriografia, presença de pulsos arteriais e classificação de Wagner. Resultados: Verificou-se que o tempo de diagnóstico da doença foi fator de risco e o HDL-C foi considerado fator protetor para o desfecho. Entre as demais variáveis, não possuir amputações prévias, neuropatia, doença vascular periférica e complicações cardiovasculares, não se consultar no NAD, não realizar arteriografia e ausência de pulsos distais bilaterais foram considerados significativos (p<0.05). Apesar da variável HbA1c não ter apresentado valor significativo, é de suma importância o seu controle. Conclusões: Através do estudo, conclui-se que os pacientes amputados apresentam maior proporção de fatores de risco não controlados. Estudos, com delineamento longitudinal e amostras maiores, são necessários para se estabelecer as correlações significativas entre essas variáveis e os desfechos de amputação de membros inferiores nos pacientes diabéticos(AU)

Introduction: Diabetic foot is defined as "infection, ulceration and/or destruction of deep tissues associated with neurological abnormalities and various degrees of peripheral vascular disease of the lower limbs", which is the leading cause of nontraumatic amputations. This study aims to identify risk factors for diabetic foot amputation in patients with diabetes. Methods: This is a case-control, cross-sectional, observational and prospective study conducted by collecting data through questionnaire administration and research on other information in the electronic registration system of medical records of Hospital Santa Isabel (HSI) and the Diabetic Care Center (NAD) in Blumenau, SC. The variables analyzed in the medical records were microvascular and macrovascular complications, HbA1c value, lipid profile, BMI (body mass index) calculation, previous performance of arteriography, presence of arterial pulses, and Wagner's classification. Results: The time of disease diagnosis was found to be a risk factor, and HDL-C was considered as a protective factor for the outcome. Among the other variables, not having previous amputations, neuropathy, peripheral vascular disease and cardiovascular complications, not consulting the NAD, not performing arteriography, and absence of bilateral distal pulses were considered as significant (p<0.05). Although the HbA1c variable did not present significant value, its control is extremely important. Conclusions: Amputee patients have a higher proportion of uncontrolled risk factors. Studies with a longitudinal design and larger samples are needed to establish significant correlations between these variables and the outcomes of lower limb amputation in diabetic patients(AU)

Acute Administration of Diazepam Provokes Redox Homeostasis Imbalance in the Rat Brain: Prevention by Simvastatin.

We investigated the effects of acute diazepam (DZP) administration on thiobarbituric acid-reactive substance (TBARS) levels, protein carbonyl content, and on the activities of the antioxidant enzymes catalase, glutathione peroxidase, and superoxide dismutase in the brain of rats. Additionally, we investigated the antioxidant role of chronic pretreatment with simvastatin on the effects provoked by DZP. Simvastatin was administered (1 or 10 mg/kg by oral gavage) for 30 days. On the 30th day of treatment, groups were randomized and DZP was administered (0.5 or 1.0 mg/kg by intraperitoneal injection). Control groups received saline. Results showed that DZP enhanced TBARS levels and protein carbonyl content and altered enzymatic activity in the brain of rats. Simvastatin prevented most of the alterations caused by DZP on the oxidative stress parameters. Data indicate that DZP administration causes an oxidative imbalance in the brain areas studied; however, in the presence of simvastatin, some of these alterations in oxidative stress were prevented.

Guanidinoacetate alters antioxidant defenses and butyrylcholinesterase activity in the blood of rats

Deficiency of guanidinoacetate methyltransferase, the first described creatine biosynthesis defect, leads to depletion of creatine and phosphocreatine, and accumulation of guanidinoacetate (GAA) in brain and body fluids. The present study aimed to investigate the influence of GAA on the activities of antioxidant enzymes, as well as on thiobarbituric acid-reactive substances (TBARS) and butyrylcholinesterase (BuChE) activity in the blood of rats. We also evaluated the effect of trolox (6-hydr oxy-2,5,7,8-tetramethylchroman-2-carboxylic acid), GSH (glutathione) and L-NAME (NG-nitro-L-arginine methyl ester) on the alterations elicited by GAA. Methods: The rats were randomly divided into 8 groups: (1) control; (2) GAA (10, 30, 50, 100 mM/kg); (3) trolox (1 mM/kg) + control; (4) trolox (1 mM/kg) + GAA (100 mM/kg); (5) GSH (1 mM/kg) + control; (6) GSH (1 mM/kg) + GAA (100 mM/kg); (7) L-NAME (1 mM/kg) + control; (8) L-NAME + GAA (100 mM/kg). After the addition of compounds, erythrocytes and plasma were pre-incubated at 37°C for 1h and tested immediately. Results: GAA enhanced the activities of catalase (CAT) and glutathione peroxidase (GSH-Px) in the erythrocytes and BuChE activity. In addition, GAA enhanced TBARS levels in the plasma. Trolox, GSH and L-NAME addition prevented the majority of alterations in oxidative stress parameters and the increase of BuChE activity that were caused by GAA. Data suggest that GAA alters antioxidant defenses and induces lipid peroxidation in the blood, as well altering BuChE activity. However, in the presence of trolox, GSH and L-NAME some of these alterations in oxidative stress and BuChE activity were prevented. Conclusions: Our findings lend support to a potential therapeutic strategy for this condition, which may include the use of appropriate antioxidants for ameliorating the damage caused by GAA...