914 resultados para Diabetes Mellitus Type 1


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Diabetes Mellitus (DM) é uma doença crônica que acomete 7,6% da população entre 30 e 69 anos de idade e se não controlada pode ter conseqüências desfavoráveis para a saúde do portador interferindo drasticamente em sua qualidade de vida, além de aumentar os custos para saúde pública, tornando-se um desafio constante para os profissionais de saúde. Uma das principais causas de mau controle da doença é a não adesão ao tratamento farmacológico e não farmacológico por parte do paciente. A partir da observação de diversos casos de abandono ao tratamento e níveis metabólicos alterados na Unidade de Saúde da Família (UBS) de Marilândia – ES, área de atuação da autora, surgiu a necessidade da criação de um plano de intervenção direcionado aos diabéticos pertencentes a esta UBS com o objetivo de identificar e corrigir as causas de adesão incorreta ao tratamento e assim obter bom controle metabólico e diminuição das taxas de complicações.

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O presente estudo é parte integrante do Trabalho de Conclusão do Curso de Especialização em Saúde da Família oferecido pela Universidade Aberta do SUS (UNASUS) em parceria com a Universidade do Estado do Rio de Janeiro (UERJ), preconiza a elaboração de uma intervenção para os pacientes atendidos na Unidade Básica de Saúde (UBS) de Chaves, do município de Santa Leopoldina. A intervenção irá abranger uma ação educativa contemplando o controle nutricional no tratamento coadjuvante da HAS e do DM da população UBS de Chaves, no período de janeiro a junho de 2016, por considerar que a implementação dessa ação seja capaz de contribuir com eficácia, para melhoria de vida para os pacientes hipertensos e diabéticos atendidos e tratados na UBS em estudo. Espera-se que a execução da ação educativa na UBS de Chaves, alcance o objetivo que é informar a respeito de práticas inerentes a assistência quanto ao controle nutricional no tratamento coadjuvante da HAS e do DM. Com isso, espera-se que o hábito alimentar dos pacientes atendidos na unidade de saúde em estudo, passe a fazer parte de um novo cenário, enfatizado no idealismo de uma alimentação saudável.

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O diabetes mellitus tipo 1 (DM 1) é definido como uma doença crônica que acomete principalmente crianças e adolescentes. Tal patologia é caracterizada pela destruição das células beta, levando ao estágio de deficiência absoluta de insulina, sendo necessário a administração de insulina para prevenir cetoacidose, coma e morte. A presença de uma doença crônica, como o diabetes, na adolescência caracteriza uma crise existencial, representada pela enfermidade incurável e respectiva necessidade de tratamento continuado. Foi abordada a importância do médico da família na comunidade, na realização do diagnóstico e na abordagem de doenças crônicas nas Unidades de Saúde, através de um estudo de um paciente, 13 anos, sexo masculino, com Diabetes Mellitus tipo 1 sem tratamento adequado. A doença implicou em mudanças no contexto familiar, social, psicológico e biológico, mudanças estas de difícil enfrentamento para este adolescente. Esse fato implica na necessidade de se prestar um atendimento multiprofissional e interdisciplinar, interferindo positivamente no processo saúde-doença daquela e de outras famílias. A pesquisa foi de natureza descritiva, exploratória e de abordagem qualitativa uma vez que esta possibilita maior aproximação com o cotidiano e as experiências.

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A hipertensão arterial sistêmica e o diabetes mellitus são doenças altamente prevalentes na população adscrita pela Estratégia de Saúde da Familia (ESF) de São Sebastião na cidade de Campos dos Goytacazes. A partir desta constatação foi proposta a criação de um grupo Hiperdia (grupo de hipertensos e diabéticos) com reunião quinzenal às quintas-feiras pela manhã. Este grupo foi proposto com o objetivo de aumentar o conhecimento sobre as doenças, melhorar a aderência destes pacientes, ressaltando a importância do tratamento não farmacológico, além de compartilhar experiências e estabelecer um diálogo entre a equipe de saúde e a população hipertensa e diabética local. Conclui-se necessário a abordagem de prevenção e promoção em saúde para o esclarecimento sobre as doenças (HAS e DM) e melhora na adesão terapêutica.

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The complement system is an important humoral defense mechanism that plays a relevant role against microbial agents, inflammatory response control, and immunocomplex clearance. Classical complement pathway activation is antibody-dependent. The C4 component participates in the initial step of activation, and C4 expression is determined by 2 pairs of allotypes: C4A and C4B. Deficiencies in C4 allotypes have been associated with several diseases. The aim of the present review is evaluate the reported data in the literature regarding specific C4A and C4B deficiencies and characterize their clinical relevance. We searched the MEDLINE and LILACS databases. Papers referring to total C4 deficiency without allotype evaluation and case reports of primary C4 deficiency were not included. Deficiencies in C4 allotypes have been associated with Mycobacterium leprae infection, erythema nodosum, systemic sclerosis with anti-topoisomerase I antibodies, intermediate congenital adrenal hyperplasia with DR5 genotype, diabetes mellitus type 1 with DR3,4 genotype, and diabetes mellitus with antibodies against islet cells. C4 allotype deficiency is also related to C4B deficiency and autoimmune-associated diseases, such as systemic lupus erythematosus, or diseases with an autoimmune component, such as autism. Some reports associate C4A with thyroiditis after delivery as well as limited and systemic sclerosis without anti-topoisomerase I antibodies. However, the studies with C4A and C4B have been concentrated in isolated populations, and some of the studies could not be reproduced by other authors.

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OBJECTIVE-We studied whether manganese-enhanced high-field magnetic resonance (MR) imaging (MEHFMRI) could quantitatively detect individual islets in situ and in vivo and evaluate changes in a model of experimental diabetes.RESEARCH DESIGN AND METHODS-Whole pancreata from untreated (n = 3), MnCl(2) and glucose-injected mice (n = 6), and mice injected with either streptozotocin (STZ; n = 4) or citrate buffer (n = 4) were imaged ex vivo for unambiguous evaluation of islets. Exteriorized pancreata of MnCl(2) and glucose-injected mice (n = 6) were imaged in vivo to directly visualize the gland and minimize movements. In all cases, MR images were acquired in a 14.1 Testa scanner and correlated with the corresponding (immuno)histological sections.RESULTS-In ex vivo experiments, MEHFMRI distinguished different pancreatic tissues and evaluated the relative abundance of islets in the pancreata of normoglycemic mice. MEHFMRI also detected a significant decrease in the numerical and volume density of islets in STZ-injected mice. However, in the latter measurements the loss of beta-cells was undervalued under the conditions tested. The experiments on the externalized pancreata confirmed that MEHFMRI could visualize native individual islets in living, anesthetized mice.CONCLUSIONS-Data show that MEHFMRI quantitatively visualizes individual islets in the intact mouse pancreas, both ex vivo and in vivo. Diabetes 60:2853-2860, 2011

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Transplantation of insulin secreting cells is regarded as a possible treatment for type 1 diabetes. One major difficulty in this approach is, however, that the transplanted cells are exposed to the patient's inflammatory and autoimmune environment, which originally destroyed their own beta-cells. Therefore, even if a good source of insulin-secreting cells can be identified for transplantation therapy, these cells need to be protected against these destructive influences. The aim of this project was to evaluate, using a clonal mouse beta-cell line, whether genetic engineering of protective genes could be a viable option to allow these cells to survive when transplanted into autoimmune diabetic mice. We demonstrated that transfer of the Bcl-2 anti-apoptotic gene and of several genes specifically interfering with cytokines intracellular signalling pathways, greatly improved resistance of the cells to inflammatory stresses in vitro. We further showed that these modifications did not interfere with the capacity of these cells to correct hyperglycaemia for several months in syngeneic or allogeneic streptozocin-diabetic mice. However, these cells were not protected against autoimmune destruction when transplanted into type 1 diabetic NOD mice. This suggests that in addition to inflammatory attacks by cytokines, autoimmunity very efficiently kills the transplanted cells, indicating that multiple protective mechanisms are required for efficient transplantation of insulin-secreting cells to treat type 1 diabetes.

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In type I diabetes mellitus, islet transplantation provides a moment-to-moment fine regulation of insulin. Success rates vary widely, however, necessitating suitable methods to monitor islet delivery, engraftment and survival. Here magnetic resonance-trackable magnetocapsules have been used simultaneously to immunoprotect pancreatic beta-cells and to monitor, non-invasively in real-time, hepatic delivery and engraftment by magnetic resonance imaging (MRI). Magnetocapsules were detected as single capsules with an altered magnetic resonance appearance on capsule rupture. Magnetocapsules were functional in vivo because mouse beta-cells restored normal glycemia in streptozotocin-induced diabetic mice and human islets induced sustained C-peptide levels in swine. In this large-animal model, magnetocapsules could be precisely targeted for infusion by using magnetic resonance fluoroscopy, whereas MRI facilitated monitoring of liver engraftment over time. These findings are directly applicable to ongoing improvements in islet cell transplantation for human diabetes, particularly because our magnetocapsules comprise clinically applicable materials.

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We aimed to compare physical activity level and cardiorespiratory fitness in children with different chronic diseases, such as type 1 diabetes mellitus (T1DM), obesity (OB) and juvenile idiopathic arthritis (JIA), with healthy controls (HC). We performed a cross-sectional study including 209 children: OB: n = 45, T1DM: n = 48, JIA: n = 31, and HC: n = 85. Physical activity level was assessed by accelerometer and cardiorespiratory fitness by a treadmill test. ANOVA, linear regressions and Pearson correlations were used. Children with chronic diseases had reduced total daily physical activity counts (T1DM 497 +/- 54 cpm, p = 0.003; JIA 518 +/- 28, p < 0.001, OB 590 +/- 25, p = 0.003) and cardiorespiratory fitness (JIA 39.3 +/- 1.7, p = 0.001, OB 41.7 +/- 1.2, p = 0.020) compared to HC (668 +/- 35 cpm; 45.3 +/- 0.9 ml kg(-1) min(-1), respectively). Only 60.4% of HC, 51.6% of OB, 38.1% of JIA and 38.5% of T1DM children met the recommended daily 60 min of moderate-to-vigorous physical activity. Low cardiorespiratory fitness was associated with female gender and low daily PA. Children with chronic diseases had reduced physical activity and cardiorespiratory fitness. As the benefits of PA on health have been well demonstrated during growth, it should be encouraged in those children to prevent a reduction of cardiorespiratory fitness and the development of comorbidities.

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BACKGROUND: Rhino-orbito-cerebral mucormycosis is an opportunistic rapidly progressive infection affecting almost exclusively diabetic or immunocompromised patients. CASE REPORTS: Three cases are reported. For one patient mucormycosis was the first manifestation of juvenile diabetes and the evolution was favorable. In the second case the infection affected a known diabetic patient and the clinical course was fatal. The third patient was immunocompromised, showed mild clinical features and a rapidly fatal evolution, the diagnosis being made only postmortem. CONCLUSION: These three cases illustrate the wide clinical spectrum of rhino-orbito-cerebral mucormycosis, its serious nature and difficult diagnosis.

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During the initial phases of type 1 diabetes, pancreatic islets are invaded by immune cells, exposing β-cells to proinflammatory cytokines. This unfavorable environment results in gene expression modifications leading to loss of β-cell functions. To study the contribution of microRNAs (miRNAs) in this process, we used microarray analysis to search for changes in miRNA expression in prediabetic NOD mice islets. We found that the levels of miR-29a/b/c increased in islets of NOD mice during the phases preceding diabetes manifestation and in isolated mouse and human islets exposed to proinflammatory cytokines. Overexpression of miR-29a/b/c in MIN6 and dissociated islet cells led to impairment in glucose-induced insulin secretion. Defective insulin release was associated with diminished expression of the transcription factor Onecut2, and a consequent rise of granuphilin, an inhibitor of β-cell exocytosis. Overexpression of miR-29a/b/c also promoted apoptosis by decreasing the level of the antiapoptotic protein Mcl1. Indeed, a decoy molecule selectively masking the miR-29 binding site on Mcl1 mRNA protected insulin-secreting cells from apoptosis triggered by miR-29 or cytokines. Taken together, our findings suggest that changes in the level of miR-29 family members contribute to cytokine-mediated β-cell dysfunction occurring during the initial phases of type 1 diabetes.

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The non-obese diabetic (NOD) mouse is a model for the study of insulin-dependent diabetes mellitus (IDDM). Recently transgenic NOD mice have been derived (NOD-E) that express the major histocompatibility complex (MHC) class II I-E molecule. NOD-E do not become diabetic and show negligible pancreatic insulitis. The possibility pertained that NOD-E mice are protected from disease by a process of T-cell deletion or anergy. This paper describes our attempts to discover whether this was so, by comparing NOD and NOD-E mouse T-cell receptor V beta usage. Splenocytes and lymph node cells were therefore tested for their ability to proliferate in response to monoclonal anti-V beta antibodies. We were unable to show any consistent differences between NOD and NOD-E responses to the panel of antibodies used. Previously proposed V beta were shown to be unlikely candidates for deletion or anergy. T cells present at low frequency (V beta 5+) in both NOD and NOD-E mice were shown to be as capable of expansion in response to antigenic stimulation as were more frequently expressed V beta. Our data therefore do not support deletion or anergy as mechanisms which could account for the observed disease protection in NOD-E mice.

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37 insulin-dependent and non-insulin-dependent diabetics answered a multiple-choice questionnaire during inpatient educational sessions. 12 dietetic and 12 pathophysiologic questions had to be answered. Statistical analysis of factors influencing the number of errors can be summed up as follows: there is a direct correlation between age of the patient and number of errors; the older the patient, the greater the number of errors. However, insulin-dependent diabetics committed fewer errors than non-insulin-dependent subjects of the same age, which suggests greater motivation in the first group due to their treatment. The test likewise affords the patients an opportunity of reviewing unclear topics and enables the educational team to adapt their teaching to the patients.