Coffee intake (Coffea arabica L. ) reduces advanced glycation end product (AGEs) formation and platelet aggregation in diabetic rats

Objectives: The study aimed to determine the effect of coffee intake on AGEs formation and platelet aggregation in diabetic Wistar rats. Methods: Coffee powder samples were used to prepare a 10% beverage. Diabetes mellitus was induced in the animals by administering 2% alloxan. All animal experiments were approved by the ethics committee for animal experiments under N°. 420/2012 and 536/2013. Diabetic and non-diabetic rats were divided into 6 groups treated and untreated with coffee (7.2 mL/Kg body weight) and aminoguanidine (AGE inhibiting agent) (100 mg/Kg body weight) for 50 days. After 50 days, the animals were fasted for 12 h and anesthetized (40 mg/Kg sodium pentobarbital) intraperitoneally. Blood samples were collected from the abdominal artery puncture. Hematological parameters (red cells, hemoglobin, hematocrit and leukocyte) and glycemic and HbA1c levels were measured. AGEs quantification (spectrofluorometric method) and the platelet aggregation test (aggregation of cuvettes in a four-channel platelet aggregometer) were also conducted. The rats' renal function was evaluated by measuring serum urea and creatinine. Results: Data showed that coffee intake had no effect on the hematological parameters. Fasting glucose and HbA1c dosage were significantly higher in diabetic animals compared to non-diabetic animals (confirmed the effectiveness of inducing and maintaining diabetic status). Results showed that coffee reduced AGE formation and platelet aggregation in our animal model, not altering the animals' renal function. Conclusions: These results suggest beneficial effects on vasculopathy, a common complication in diabetic patients.

Coffee beverage reduces ROS production and does not affect the organism's response against Candida albicans

Coffee is a mixture of substances with potential beneficial and adverse health effects. Several studies demonstrate the antioxidant effect of the phenolics compounds present in coffee. Neutrophils produce reactive oxygen species (ROS) by activating of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2), which plays a key role in organism defenseagainst microbial pathogens. Diabetes mellitus patients are more susceptible to bacterial and fungal infections. The present study evaluated the influence of coffee beverage on NOX2 activity and ROS generation and the impact of this effect on phagocytosis and killing of Candida albicansby neutrophils from diabetic and non-diabetic animals. Diabetes mellitus was induced in male Wistar rats using 2% alloxan. Diabetic and non-diabetic animals were divided into groups treated and untreated with coffee drink (7.2 mL/kg/day) or apocyanine (16 mg/kg/day) for 50 days. After 50 days, the animals' glycemic profile was measured by blood glucose and glycated hemoglobin (HbA1c) tests. The generation of ROS in neutrophilic cells was measured by chemiluminescence and cytochrome C reduction assays. C. albicans phagocytosis and death were evaluated by optical microscopy using the May-Grunwald-Giemsa staining method. The coffee drink has not altered the glycemic profile and NOX2 activity of the animals. However, coffee reduced the ROS pool in non-diabetic and diabetic animals, but this activity did not harm the phagocytosis or killing of neutrophils. Treatment with apocyanin decreased ROS production and killing capacity of neutrophils from non-diabetic animals against C. albicans. We suggest that the coffee drink intake prevents oxidative damage and does not impair response of the organism against opportunistic microorganism.

Síndrome de Wilson: relato de caso / Wilson´s Disease: a case repor

Objetivos: Este relato descreve um distúrbio genético raro, denominado de Síndrome de Wilson, herdado em caráter autossômico recessivo, com sintomas muito facilmente confundidos com outras doenças. A causa básica responsável pelas manifestações clínicas é o acúmulo de cobre em diversos compartimentos do organismo humano, especialmente em locais como fígado, cérebro, rins e córneas, devido a mutações no gene ATP7B que codifica a Cu+2 ATPase, uma proteína transportadora de cobre que está localizada no complexo de Golgi dos hepatócitos. As alterações hepáticas podem se apresentar como hepatite crônica, cirrose e, mais raramente, hepatite fulminante. As alterações neurológicas são variáveis, predominando os sintomas extrapiramidais, tremores, distonia, disartria, alterações de humor, sintomas psiquiátricos e, se não tratada, diminuição progressiva da capacidade intelectual. Uma das características mais extraordinárias dessa síndrome é a grande variabilidade de manifestações fenotípicas em pacientes que possuem a mesma mutação. No diagnóstico da doença de Wilson são analisados diversos parâmetros bioquímicos, sendo eles: ceruloplasmina sérica, cobre sérico, excreção urinária de cobre e concentração hepática de cobre. Além disso, realiza-se exame oftalmológico com a observação de anéis de Kayser ­ Fleischer. A fim de complementar e facilitar o diagnóstico podem ser realizados estudos genéticos, visto que muitas vezes os sintomas e alterações laboratoriais podem estar associados a outras doenças. O tratamento baseia-se no uso de drogas quelantes do cobre. A Dpenicilamina é a droga de escolha, apesar do risco de piora neurológica em até 50% dos pacientes e dos diversos efeitos colaterais associados ao seu uso. Trientina e tetratiomolibdato são drogas alternativas, sendo a última escolhida para indivíduos com sintomas neurológicos. O zinco tem indicação em assintomáticos ou em terapia de manutenção. O tratamento precoce evita graves complicações. Relato de caso: Paciente de 14 anos de idade, natural de Poço Fundo-MG, procurou atendimento médico por apresentar episódios frequentes de paralisia facial, principalmente na região mandibular, que levava à disfagia e disfonia, além de irritabilidade e anormalidades na marcha. Foi submetida ao exame de ressonância magnética que mostrou "alteração de sinal simétrica nos corpos estriados bilateralmente, com sinais de edema dos putâmens e núcleos caudados, e atrofia dos globos pálidos. Diante do histórico familiar para a síndrome de Wilson, foi realizado o diagnóstico diferencial, por meio da concentração de sérica de ceruloplasmina e cobre sérico e urinário, que mostraram alterações típicas da síndrome de Wilson e a biomicroscopia ocular que constatou a presença do anel de Kayser-Fleischer. Conclusões: Ainda há um longo caminho a ser seguido no que se diz respeito ao diagnóstico precoce da Síndrome de Wilson. Nesse caso, a paciente não apresentou hepatopatia pregressa. Isso mostra que a doença nem sempre se apresenta da forma esperada, e reflete a dificuldade de estabelecer um diagnóstico precoce que possa impedir o surgimento dos primeiros sintomas. Todos os portadores da síndrome de Wilson necessitam de atendimento multidisciplinar, (AU)

Objectives: This report describes a rare genetic disorder, called Wilson's Disease, inherited in an autosomal recessive form, with symptoms very easily confused with other diseases. The underlying cause of the clinical manifestations is the accumulation of copper in various compartments of the human body, especially in places such as liver, brain, kidneys and corneas, due to mutations in the ATP7B gene encoding Cu + 2 ATPase, a copper carrier protein which is located in the Golgi complex of hepatocytes. Liver changes may present as chronic hepatitis, cirrhosis and, more rarely, fulminant hepatitis. Neurological changes are variable, predominantly extrapyramidal symptoms, tremors, dystonia, dysarthria, mood changes, and psychiatric symptoms, if not treated, progressive decrease in intellectual capacity. One of the most extraordinary characteristics of this syndrome is the great variability of phenotypic manifestations in patients who have the same mutation. In the diagnosis of Wilson's disease, several biochemical parameters are analyzed: serum ceruloplasmin, serum copper, urinary excretion of copper and hepatic copper concentration. In addition, an ophthalmologic examination is performed with Kayser-Fleischer rings observation. In order to complement and facilitate the diagnosis, genetic studies can be performed, since the symptoms and laboratory abnormalities can often be associated with other diseases. Treatment is based on the use of copper chelating drugs. D-penicillamine is the drug of choice, despite the risk of neurological worsening in up to 50% of patients and the various side effects associated with its use. Trientin and tetrathiomolybdate are alternative drugs, the latter being chosen for individuals with neurological symptoms. Zinc is indicated for asymptomatic or maintenance therapy. Early treatment prevents serious complications. Case report: A 14-year-old patient from Poço Fundo-MG sought medical attention because of frequent episodes of facial paralysis, especially in the mandibular region, leading to dysphagia and dysphonia, as well as irritability and gait abnormalities. She underwent magnetic resonance imaging (MRI), which showed "symmetrical signal changes in the bilaterally striatum, with signs of edema of the caudate nuclei and caudate nuclei, and atrophy of the pale globes." In view of the family history of Wilson's syndrome, a differential diagnosis was performed, by serum concentration of ceruloplasmin and serum and urinary copper, which showed typical changes in Wilson's syndrome and ocular biomicroscopy, which verified the presence of the Kayser-Fleischer ring. The patient did not present previous liver disease, showing that the disease does not always present as expected, and reflects the difficulty in establishing an early diagnosis that may prevent the emergence of the first symptoms. All patients with Wilson's syndrome require multidisciplinary care since it is a disease that can significantly affect various organs and systems (AU)