Asma quase fatal em pediatria / Near-fatal asthma in Pediatrics

Este estudo tem como objetivo revisar a literatura a respeito da asma fatal e asma quase fatal. A associação de diversos parâmetros clínicos, fisiopatológicos e radiológicos é fundamental para a compreensão do quadro clínico, prognóstico e dos fatores de risco para que se desenvolva asma fatal ou quase fatal. A identificação desses pacientes comalto risco de desenvolverem essa forma às vezes fatal de asma e a adesão a consensos de tratamento visando à prevenção de novas crises e exacerbações mostraram-se extremamente eficazes no controle desses pacientes, reduzindo de forma significativa a morbimortalidade. A revisão da bibliografia foi realizada nas bases de dados Medline, Literatura Latino-Americana e do Caribe em Ciências da Saúde e HighWire, nos últimos 30 anos, empregando-se os descritores asthma, near fatal asthma, epidemiology, diagnosis e treatment. Foram selecionados 13 artigos paracompor as referências desta revisão.

This study aims to review the literature about fatal asthma and near-fatal asthma. The association of various clinical, physiopathological, and radiological parameters is essential for understanding the clinical condition, prognosis, and risk factors for the development of fatal or near-fatal asthma. The identification of patients at high risk of developing this form of asthma, sometimes fatal, and their adherence to consensus treatmentaimed at preventing new crises and exacerbations have been proved extremely effective in the control of these patients, significantly reducing morbidity and mortality. The bibliographical review was performed accessing the Medline, Latin American and Caribbean Literature in Health Sciences, and HighWire databases, and the search of articles published in the past 30 years, and using the following descriptors: asthma, near fatal asthma, epidemiology, diagnosis, and treatment. Thirteen articles were selected to compose the references in this review.

HIV-1 induced activation of CD4+ T cells creates new targets for HIV-1 infection in human lymphoid tissue ex vivo.

We demonstrate mechanisms by which HIV-1 appears to facilitate its own infection in ex vivo-infected human lymphoid tissue. In this system, HIV-1 readily infects various CD4+ T cells, but productive viral infection was supported predominantly by activated T cells expressing either CD25 or HLA-DR or both (CD25/HLA-DR) but not other activation markers: There was a strong positive correlation (r=0.64, P=.001) between virus production and the number of CD25+/HLA-DR+ T cells. HIV-1 infection of lymphoid tissue was associated with activation of both HIV-1-infected and uninfected (bystanders) T cells. In these tissues, apoptosis was selectively increased in T cells expressing CD25/HLA-DR and p24gag but not in cells expressing either of these markers alone. In the course of HIV-1 infection, there was a significant increase in the number of activated (CD25+/HLA-DR+) T cells both infected and uninfected (bystander). By inducing T cells to express particular markers of activation that create new targets for infection, HIV-1 generates in ex vivo lymphoid tissues a vicious destructive circle of activation and infection. In vivo, such self-perpetuating cycle could contribute to HIV-1 disease.

Atenuação do vírus vacinal do sarampo: infecção sub-ótima do tecido linfático e alteração do tropismo / Measles vaccine virus attenuation: suboptimal lymphatic tissue infection and tropism alteration

Os mecanismos de atenuação do vírus vacinal do sarampo ainda não foram suficientemente caracterizados. Uma vez que a linhagem vacinal consegue penetrar as células através do receptor CD46 além do receptor primário do vírus do sarampo CD150 / SLAM (molécula de ativação e de sinalização linfocitária) nós nos perguntamos se (e como) o seu tropismo está alterado. Em tecido amigdaliano humano, a linhagem vacinal infecta linfócitos T virgens (CD45RA+ CD62L+), que expressam SLAM em pequena quantidade, com muito mais eficiência que as linhagens selvagens. Por outro lado, a linhagem vacinal infecta significativamente menos linfócitos B, macrófagos e células NK que as linhagens selvagens. Os níveis de infecção das linhagens selvagens se correlacionam com a freqüência de expressão da SLAM, sendo mais elevados nos linfócitos B, que apresentam níveis de infecção entre 40-55%. As células T que expressam SLAM são mais facilmente infectáveis que as células B que expressam essa molécula. Desta forma, a atenuação da linhagem vacinal parece ser causada por uma alteração no seu tropismo, juntamente com uma replicação menos eficiente.

The mechanisms of measles virus (MV) vaccine attenuation are insufficiently characterized. Because the vaccine strain can enter cells through CD46 in addition to the primary MV receptor signaling lymphocyte activation molecule (SLAM, CD150), we asked whether and how its tropism is altered. In human tonsillar tissue, this vaccine strain infects naive (CD45RA+ CD62L+) T lymphocytes, which express SLAM very infrequently, with much higher efficiency than do wild-type strains. By contrast, it infects B-lymphocytes, macrophages, and NK cells with significantly lower efficiencies than those of wild-type strains. Infection levels by wild-type strains correlate with the frequency of SLAM expression, and are highest in B-cells, which are 40-55% infected. SLAM-expressing Tcells are more readily infected by all MV strains than are SLAM-expressing B-cells. Thus, vaccine attenuation may be caused by tropism alteration in combination with suboptimal replication.

Measles virus vaccine attenuation: suboptimal infection of lymphatic tissue and tropism alteration.

The mechanisms of measles virus (MV) vaccine attenuation are insufficiently characterized. Because the Edmonston vaccine strain can enter cells through CD46 in addition to the primary MV receptor signaling lymphocyte activation molecule (SLAM or CD150), we asked whether and how its tropism is altered. In human tonsillar tissue, this vaccine strain infects naive (CD45RA(+)CD62L(+)) T lymphocytes, which express SLAM very infrequently, with much higher efficiency than do wild-type strains. By contrast, it infects B lymphocytes, macrophages, and NK cells with significantly lower efficiencies than those of wild-type strains. Infection levels by wild-type strains correlate with the frequency of SLAM expression and are highest in B cells, which are 40%-55% infected. SLAM-expressing T cells are more readily infected by all MV strains than are SLAM-expressing B cells. Thus, vaccine attenuation may be caused by tropism alteration in combination with suboptimal replication.

HIV-1 pathogenesis differs in rectosigmoid and tonsillar tissues infected ex vivo with CCR5- and CXCR4-tropic HIV-1.

Gut-associated lymphoid tissue (GALT) has been identified as the primary target of HIV-1 infection. To investigate why GALT is especially vulnerable to HIV-1, and to determine whether the selective transmission of CCR5-using viral variants (R5) in vivo is the result of a greater susceptibility of GALT to this viral variant, we performed comparative studies of CXCR4-using (X4) and R5 HIV-1 infections of human lymphoid (tonsillar) and rectosigmoid tissues ex vivo under controlled laboratory conditions. We found that the relative level of R5 replication in rectosigmoid tissue is much greater than in tonsillar tissue. This difference is associated with the expression of the CCR5 co-receptor on approximately 70% of CD4 T cells in rectosigmoid tissue, whereas in tonsillar tissue it is expressed on fewer than 15% of CD4 T cells. Furthermore, tonsillar tissue responds to X4 HIV-1 infection by upregulating the secretion of CC-chemokines, providing a potential CCR5 blockade and further resistance to R5 infection, whereas gut tissue failed to increase such innate immune responses. Our results show that rectosigmoid tissue is more prone than tonsillar lymphoid tissue to R5 HIV-1 infection, primarily because of the high prevalence and availability of R5 cell targets and reduced chemokine blockade. The majority of CD4 T cells express CXCR4, however, and X4 HIV-1 readily replicates in both tissues, suggesting that although the differential expression of co-receptors contributes to the GALT vulnerability to R5 HIV-1, it alone cannot account for the selective R5 infection of the rectal mucosa in vivo.

A propósito de um paciente com leucemia mielóide crônica evoluindo com tromboembolismo pulmonar de repetiçäo simulando choque séptico / A case of recurrent pulmonary thromboembolism in patient with chronic myeloid leukemia like septic shock

Trata-se de paciente no limiar da idade senil, com diagnóstico recente de Leucemia Mielóide Crônica e instabilidade hemodinâmica de difícil tratamento. Embora tivesse outras doenças que pudessem explicar estas manifestaçSes, como miocardiopatia chagásica e insuficiência cardíaca congestiva, foi necessário buscar novas possibilidades diagnósticas. O objetivo do tratamento é evidenciar a importância de buscar novas hipóteses, baseando-se na lógica e raciocínio clínico. Usar com discernimento a propedêutica complementar. Estar pronto para reconhecer erros e mudar condutas. Tudo isso para proporcionar o melhor atendimento, evitando agressSes e riscos desnecessários ao paciente.