Atenção domiciliar: caso clínico [anemia falciforme]

Vídeo produzido com o GoAnimate! em que Ivone solicita a visita da equipe de atenção domiciliar para consultarem sua filha, que apresenta febre, dores de barriga, palidez cutânea, entre outros sintomas. Diante do apresentado, o vídeo propõe a reflexão do manejo adequado para a situação.

Manifestações bucais da anemia falciforme: abordagem ao paciente pelo cirurgião-dentista

O presente estudo aborda a questão das manifestações bucais da anemia falciforme e o manejo do paciente pelo cirurgião-dentista na atenção básica. Tem como objetivo central o conhecimento das principais manifestações bucais da afecção e seu tratamento pela equipe de saúde bucal. Realizou-se pesquisa nos bancos de dados Lilacs, Scielo, Google, PubMed e o Portal Capes, onde foram selecionados apenas artigos que abordavam os temas saúde bucal e anemia falciforme. Foram selecionados os artigos compreendidos entre os anos de 2001 e 2011. Trata-se de uma revisão de literatura realizada após verificar-se que a anemia falciforme tem grande prevalência no Estado de Minas Gerais, principalmente na região norte. A anemia falciforme é uma doença genética autossômica hereditária que provoca afoiçamento dos eritrócitos o que ocasiona vasoclusão e infarto tecidual. As manifestações provocadas por essa vasoclusão acometem tecidos de todo o corpo, inclusive a mucosa bucal merecendo um cuidado especial pelo cirurgião-dentista. As alterações bucais mais comuns são encontradas nos ossos gnáticos (como a osteomielite) e mucosa bucal como o empalidecimento da mucosa podendo também acometer dentes e periodonto. O tratamento dos pacientes com anemia falciforme pelo cirurgião-dentista requer alguns cuidados como a prescrição antibiótica profilática em procedimentos invasivos e uma boa revisão da história clínica e estado atual do paciente para tratamento com menor chance de iatrogenias. Ainda são poucos os estudos a respeito do assunto sendo necessários estudos clínicos mais bem conduzidos para uma melhor análise dos pacientes acometidos pela doença.

Anemia ferropriva: importância de ações na atenção básica

A anemia ferropriva é a carência nutricional de maior magnitude no mundo, sendo considerada uma carência em expansão em todos os segmentos sociais, atingindo principalmente crianças menores de dois anos. Decorre principalmente da quantidade insuficiente de ferro na dieta para satisfazer as necessidades nutricionais individuais. Este estudo tem como objetivo analisar na literatura brasileira a produção científica relacionada à anemia ferropriva nas crianças e a importância de sua prevenção. Foi utilizado o estudo de revisão sistemática baseada em evidências e, como estratégia de busca para o levantamento dos artigos na literatura, a base de dados eletrônica SciELO com os seguintes descritores e suas combinações na língua portuguesa: criança, anemia ferropriva e suplementação alimentar. Como subsídios para a prática cotidiana no trabalho da equipe de saúde, cada unidade deverá adotar a sua estratégia para a identificação da população que será atendida e rotineiramente acompanhada, podendo ser por demanda espontânea, por busca ativa, em campanhas de vacinação e por meio da indicação de parceiros que atuam na prevenção e controle dos distúrbios nutricionais em nível local. Posteriormente, desenvolver habilidades para executar as ações básicas para prevenção da anemia ferropriva (suplementação medicamentosa, fortificação de alimentos com ferro, controle das infecções parasitárias e a educação associada às medidas de aumento do consumo de ferro, incluindo o incentivo ao aleitamento materno). Sendo assim, torna-se necessário que a equipe de saúde da família atue efetivamente na promoção destas ações e que os profissionais nela inseridos, possuam embasamento teórico-científico e prático para o desenvolvimento de estratégias, contribuindo na promoção da saúde e prevenção de doenças no âmbito da saúde pública, a fim de apresentar impacto nos indicadores de saúde e melhorias significativas na qualidade dos serviços de assistência prestada.

Proposta de implantação de um protocolo profilático da anemia em crianças no PSF do centro de Ponte Nova

A anemia é uma endemia mundial, sendo mais prevalente em países emergentes. Atinge principalmente crianças menores de 2 anos, especialmente no 2º semestre de vida quando inicia-se a alimentação suplementar. Pode ocasionar inúmeras consequências, não somente na infância, mas também na vida adulta. A anemia é de fácil prevenção e esse projeto tem como objetivo implantar um protocolo de profilaxia da anemia no PSF do Centro de Ponte Nova. Esse projeto se justifica pela alta prevalência de anemia no Brasil, nessa faixa etária, por suas consequências e facilidade de prevenção. O objetivo deste estudo é propor um protocolo de profilaxia da anemia em crianças no PSF do Centro de Ponte Nova. Para tanto, realizou-se busca ativa dessas crianças a fim de que fossem avaliadas em consulta médica quanto à necessidade da suplementação. Finalmente, a responsabilidade da prescrição da suplementação pertence ao médico, com a participação da equipe interdisciplinar e da família

Pyrimidine-5'-nucleotidase Campinas, A New Mutation (p.r56g) In The Nt5c3 Gene Associated With Pyrimidine-5'-nucleotidase Type I Deficiency And Influence Of Gilbert's Syndrome On Clinical Expression.

Pyrimidine-5'-nucleotidase type I (P5'NI) deficiency is an autosomal recessive condition that causes nonspherocytic hemolytic anemia, characterized by marked basophilic stippling and pyrimidine nucleotide accumulation in erythrocytes. We herein present two African descendant patients, father and daughter, with P5'N deficiency, both born from first cousins. Investigation of the promoter polymorphism of the uridine diphospho glucuronosyl transferase 1A (UGT1A) gene revealed that the father was homozygous for the allele (TA7) and the daughter heterozygous (TA6/TA7). P5'NI gene (NT5C3) gene sequencing revealed a further change in homozygosity at amino acid position 56 (p.R56G), located in a highly conserved region. Both patients developed gallstones; however the father, who had undergone surgery for the removal of stones, had extremely severe intrahepatic cholestasis and, liver biopsy revealed fibrosis and siderosis grade III, leading us to believe that the homozygosity of the UGT1A polymorphism was responsible for the more severe clinical features in the father. Moreover, our results show how the clinical expression of hemolytic anemia is influenced by epistatic factors and we describe a new mutation in the P5'N gene associated with enzyme deficiency, iron overload, and severe gallstone formation. To our knowledge, this is the first description of P5'N deficiency in South Americans.

Reduced Plasma Angiotensin Ii Levels Are Reversed By Hydroxyurea Treatment In Mice With Sickle Cell Disease.

Sickle cell disease (SCD) pathogenesis leads to recurrent vaso-occlusive and hemolytic processes, causing numerous clinical complications including renal damage. As vasoconstrictive mechanisms may be enhanced in SCD, due to endothelial dysfunction and vasoactive protein production, we aimed to determine whether the expression of proteins of the renin-angiotensin system (RAS) may be altered in an animal model of SCD. Plasma angiotensin II (Ang II) was measured in C57BL/6 (WT) mice and mice with SCD by ELISA, while quantitative PCR was used to compare the expressions of the genes encoding the angiotensin-II-receptors 1 and 2 (AT1R and AT2R) and the angiotensin-converting enzymes (ACE1 and ACE2) in the kidneys, hearts, livers and brains of mice. The effects of hydroxyurea (HU; 50-75mg/kg/day, 4weeks) treatment on these parameters were also determined. Plasma Ang II was significantly diminished in SCD mice, compared with WT mice, in association with decreased AT1R and ACE1 expressions in SCD mice kidneys. Treatment of SCD mice with HU reduced leukocyte and platelet counts and increased plasma Ang II to levels similar to those of WT mice. HU also increased AT1R and ACE2 gene expression in the kidney and heart. Results indicate an imbalanced RAS in an SCD mouse model; HU therapy may be able to restore some RAS parameters in these mice. Further investigations regarding Ang II production and the RAS in human SCD may be warranted, as such changes may reflect or contribute to renal damage and alterations in blood pressure.

Understanding Red Blood Cell Parameters In The Context Of The Frailty Phenotype: Interpretations Of The Fibra (frailty In Brazilian Seniors) Study.

Frailty and anemia in the elderly appear to share a common pathophysiology associated with chronic inflammatory processes. This study uses an analytical, cross-sectional, population-based methodology to investigate the probable relationships between frailty, red blood cell parameters and inflammatory markers in 255 community-dwelling elders aged 65 years or older. The frailty phenotype was assessed by non-intentional weight loss, fatigue, low grip strength, low energy expenditure and reduced gait speed. Blood sample analyses were performed to determine hemoglobin level, hematocrit and reticulocyte count, as well as the inflammatory variables IL-6, IL-1ra and hsCRP. In the first multivariate analysis (model I), considering only the erythroid parameters, Hb concentration was a significant variable for both general frailty status and weight loss: a 1.0g/dL drop in serum Hb concentration represented a 2.02-fold increase (CI 1.12-3.63) in an individual's chance of being frail. In the second analysis (model II), which also included inflammatory cytokine levels, hsCRP was independently selected as a significant variable. Each additional year of age represented a 1.21-fold increase in the chance of being frail, and each 1-unit increase in serum hsCRP represented a 3.64-fold increase in the chance of having the frailty phenotype. In model II reticulocyte counts were associated with weight loss and reduced metabolic expenditure criteria. Our findings suggest that reduced Hb concentration, reduced RetAbs count and elevated serum hsCRP levels should be considered components of frailty, which in turn is correlated with sarcopenia, as evidenced by weight loss.

Unusual Erythrocyte Split Chimerism In Pregnancy After Allogeneic Stem Cell Transplantation.

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Elevated Hypercoagulability Markers In Hemoglobin Sc Disease.

Hemoglobin SC disease is a very prevalent hemoglobinopathy, however very little is known specifically about this condition. There appears to be an increased risk of thromboembolic events in hemoglobin SC disease, but studies evaluating the hemostatic alterations are lacking. We describe a cross-sectional observational study evaluating coagulation activation markers in adult hemoglobin SC patients, in comparison with sickle cell anemia patients and healthy controls. A total of 56 hemoglobin SC and 39 sickle cell anemia patients were included in the study, all in steady state, and 27 healthy controls. None of the patients were in use of hydroxyurea. Hemoglobin SC patients presented a significantly up-regulated relative expression of tissue factor, as well as elevations in thrombin-antithrombin complex and D-dimer, in comparison to controls (p<0.01). Hemoglobin SC patients presented lower tissue factor expression, and thrombin-antithrombin complex and D-dimer levels when compared to sickle cell anemia patients (p<0.05). Endothelial activation (soluble thrombomodulin and soluble vascular cell adhesion molecule-1), and inflammation (tumor necrosis factor-alpha) markers were both significantly elevated in hemoglobin SC patients when compared to controls, being as high as the levels seen in sickle cell anemia. Overall, in hemoglobin SC patients, higher hemolytic activity and inflammation were associated with a more intense activation of coagulation, and hemostatic activation was associated with two very prevalent chronic complications seen in hemoglobin SC disease: retinopathy and osteonecrosis. In summary, our results demonstrate that hemoglobin SC patients present a hypercoagulable state, although this manifestation was not as intense as that seen in sickle cell anemia.

Key Endothelial Cell Angiogenic Mechanisms Are Stimulated By The Circulating Milieu In Sickle Cell Disease And Attenuated By Hydroxyurea.

As hypoxia-induced inflammatory angiogenesis may contribute to sickle cell disease manifestations, we compared the angiogenic molecular profiles of plasma from sickle cell disease individuals and correlated these with in vitro endothelial cell-mediated angiogenesis-stimulating activity and in vivo neovascularization. Bioplex demonstrated that plasma from steady-state sickle cell anemia patients presented elevated concentrations of pro-angiogenic factors (Angiopoietin-1, basic fibroblast growth factor, vascular endothelial growth factor, vascular endothelial growth factor-D and placental growth factor) and displayed potent pro-angiogenic activity, significantly augmenting endothelial cell proliferation, migration and capillary-like structure formation. In vivo neovascularization of Matrigel plugs was significantly greater in sickle cell disease mice, compared with non-sickle cell disease mice, consistent with an upregulation of angiogenesis in the disease. In plasma from patients with hemoglobin SC disease without proliferative retinopathy, anti-angiogenic endostatin and thrombospondin-2 were significantly elevated. In contrast, plasma from hemoglobin SC individuals with proliferative retinopathy displayed a pro-angiogenic profile and had more significant effects on endothelial cell proliferation and capillary formation than plasma of patients without retinopathy. Hydroxyurea therapy was associated with significant reductions in plasma angiogenic factor profile, in association with an inhibition of endothelial cell-mediated angiogenic mechanisms and neovascularization. Thus, sickle cell anemia and retinopathic hemoglobin SC individuals present a highly angiogenic circulating milieu, capable of stimulating key endothelial cell-mediated angiogenic mechanisms. Combination anti-angiogenic therapy for preventing progression of unregulated neovascularization and associated manifestations in sickle cell disease, such as pulmonary hypertension, may be indicated; furthermore, the benefits and drawbacks of the potent anti-angiogenic effects of hydroxyurea should be clarified.

In vitro Microfluidic Model For The Study Of Vaso-occlusive Processes.

Vaso-occlusion, responsible for much of the morbidity of sickle-cell disease, is a complex multicellular process, apparently triggered by leukocyte adhesion to the vessel wall. The microcirculation represents a major site of leukocyte-endothelial interactions and vaso-occlusive processes. We have developed a biochip with subdividing interconnecting microchannels that decrease in size (40 μm to 10 μm in width), for use in conjunction with a precise microfluidic device, to mimic cell flow and adhesion through channels of sizes that approach those of the microcirculation. The biochips were utilized to observe the dynamics of the passage of neutrophils and red blood cells, isolated from healthy and sickle-cell anemia (SCA) individuals, through laminin or endothelial adhesion molecule-coated microchannels at physiologically relevant rates of flow and shear stress. Obstruction of E-selectin/intercellular adhesion molecule 1-coated biochip microchannels by SCA neutrophils was significantly greater than that observed for healthy neutrophils, particularly in the microchannels of 40-15 μm in width. Whereas SCA red blood cells alone did not significantly adhere to, or obstruct, microchannels, mixed suspensions of SCA neutrophils and red blood cells significantly adhered to and obstructed laminin-coated channels. Results from this in vitro microfluidic model support a primary role for leukocytes in the initiation of SCA occlusive processes in the microcirculation. This assay represents an easy-to-use and reproducible in vitro technique for understanding molecular mechanisms and cellular interactions occurring in subdividing microchannels of widths approaching those observed in the microvasculature. The assay could hold potential for testing drugs developed to inhibit occlusive mechanisms such as those observed in SCA and thrombotic diseases.

Identidade social e auto conceito do dançarino em cadeira de rodas

Universidade Estadual de Campinas . Faculdade de Educação Física

Validação de uma bateria de testes de habilidades motoras para atletas de handebol em cadeira de rodas

Universidade Estadual de Campinas . Faculdade de Educação Física

Adaptação do handebol para a prática em cadeira de rodas

Universidade Estadual de Campinas . Faculdade de Educação Física

Esgrima em cadeira de rodas : pedagogia de ensino a partir das dimensões e contexto da modalidade

Universidade Estadual de Campinas . Faculdade de Educação Física