Asthma

McFadden, E.R.; Gilbert, Ileen

doi:10.1056/nejm199212313272708

Cited by 257 publications

(140 citation statements)

References 129 publications

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“…8 Apesar dos avanços na compreensão da sua fisiopatologia e da crescente oferta de medicações, diversos estudos vêm demonstrando aumento da prevalência, da morbidade e da mortalidade por asma em vários países. 2,3 A falta de manejo adequado tem sido descrita como uma das principais causas da demanda em salas de emergência por crianças asmáticas.…”

Section: Introductionunclassified

Fatores de risco para consultas em pronto-socorro por crianças asmáticas no Sul do Brasil

et al. 2000

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OBJETIVOS: Traçar um perfil das crianças asmáticas do município de Pelotas, RS, conhecer o manejo da doença e os fatores de risco associados a consultas em pronto-socorro, motivadas por asma. MÉTODOS: Estudo transversal aninhado a um estudo de coorte, realizado na área urbana de Pelotas, cidade de médio porte do Sul do Brasil. Participaram 981 crianças de 4-5 anos, pertencentes à coorte de 1993. RESULTADOS: A prevalência de asma encontrada na amostra estudada foi de 25,4%. A morbidade por asma foi elevada: 31% das crianças asmáticas haviam procurado o pronto-socorro no último ano, 57% tinham consultado médico e 26%, de 1 a 4 anos, foram internadas por asma. Na análise geral, escolaridade e renda familiar baixas associaram-se com consultas em pronto-socorro (RO=4,1 para 0 a 4 anos de escolaridade e RO=6,5 para menos de 1 salário-mínimo). Dormir em quartos com 3 ou mais pessoas também mostrou-se associado (RO=2,2), bem como severidade das crises (RO=2,7), uso de medicamentos para asma no último ano (RO=1,9) e internações por asma (RO=3,0). CONCLUSÕES: A prevalência de asma entre crianças pré-escolares em Pelotas é alta, levando a grande morbidade. Encontraram-se como fatores preditores de consultas em pronto-socorro por asma, após análise multivariada, a baixa escolaridade das mães, severidade das crises e internação por asma.

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Section: Introductionunclassified

Fatores de risco para consultas em pronto-socorro por crianças asmáticas no Sul do Brasil

et al. 2000

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“…Asthma is characterized by episodic airway obstruction, increased bronchial responsiveness to the inhalation of non-specific irritants and airway inflammation (McFadden & Gilbert 1992). The link between abnormal airway physiology and airway inflammation was initially suggested by the results of post-mortem studies of asthmatic lungs which documented the presence of an inflammatory infiltrate (Dunnill 1960).…”

Section: Asthma and Allergic Inflammationmentioning

confidence: 99%

IL-5 and IL-5 receptor in asthma

Kotsimbos

Hamid

1997

Mem. Inst. Oswaldo Cruz

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and a soluble isoform (αIL-5Rs). Cytokines such as IL-5 produce specific and non-specific cellular responses through specific cell membrane receptor mediated activation of intracellular signal transduction pathways which, to a large part, regulate gene expression. The major intracellular signal transduction mechanism is activation of non-receptor associated tyrosine kinases including JAK and MAP kinases which can then transduce signals via a novel family of transcriptional factors named signal transducers and activators of transcription (STATS). JAK2, STAT1 and STAT 5 appear to be particularly important in IL-5 mediated eosinophil responses. Asthma is characterized by episodic airways obstruction, increased bronchial responsiveness, and airway inflammation. Several studies have shown an association between the number of activated T cells and eosinophils in the airways and abnormalities in FEV1, airway reactivity and clinical severity in asthma. It has now been well documented that IL-5 is highly expressed in the bronchial mucosa of atopic and intrinsic asthmatics and that the increased IL-5 mRNA present in airway tissues is predominantly T cell derived. Immunocytochemical staining of bronchial biopsy sections has confirmed that IL-5 mRNA transcripts are translated into protein in asthmatic subjects. Furthermore, the number of activated CD 4 + T cells and IL-5 mRNA positive cells are increased in asthmatic airways following antigen challenge and studies that have examined IL-5 expression in asthmatic subjects before and after steroids have shown significantly decreased expression following oral corticosteroid treatment in steroid-sensitive asthma but not in steroid resistant and chronic severe steroid dependent asthma. The link between T cell derived IL-5 and eosinophil activation in asthmatic airways is further strengthened by the demonstration that there is an increased number of αIL-5R mRNA positive cells in the bronchial biopsies of atopic and non-atopic asthmatic subjects and that the eosinophil is the predominant site of this increased

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“…1,2 This inflammation involves epithelial damage, deposition of collagen beneath the basement membrane, eosinophilic and lymphocytic infiltration, and hypertrophy and hyperplasia of goblet cells, submucosal glands, and airway smooth muscle. 3,4 Ample evidence suggests that a combination of genetic and environmental factors causes asthma.…”

Section: Introductionmentioning

confidence: 99%

Association of the hCLCA1 gene with childhood and adult asthma

et al. 2004

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Asthma is caused by bronchial inflammation. This inflammation involves mucus overproduction and hypersecretion. Recently, a mouse model of asthma showed that gob-5 is involved in the pathogenesis of asthma. The gob-5 gene is involved in mucus secretion and its expression is upregulated upon antigen attack in sensitized mice. The observation suggests that human homologue of gob-5, hCLCA1 (human calcium-dependent chloride channel-1), may be involved in human disease. We screened for single-nucleotide polymorphisms (SNPs) in hCLCA1 in the Japanese population. We identified eight SNPs, and performed association studies using 384 child patients with asthma, 480 adult patients with asthma, and 672 controls. In haplotype analysis, we found a different haplotype distribution pattern between controls and childhood asthma (Po0.0001) and between controls and adult asthma (P ¼ 0.0031). We identified a high-risk haplotype (CATCAAGT haplotype; P ¼ 0.0014) and a low-risk haplotype (TGCCAAGT haplotype; P ¼ 0.00010) in cases of childhood asthma. In diplotype analysis, patients who had the CATCAAGT haplotype showed a higher risk for childhood asthma than those who did not (P ¼ 0.0011). Individuals who had the TGCCAAGT haplotype showed a lower risk for childhood asthma than those who did not (Po0.0001). Our data suggested that variation of the hCLCA1 gene affects patients' susceptibility for asthma.

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Asthma

Cited by 257 publications

References 129 publications

Fatores de risco para consultas em pronto-socorro por crianças asmáticas no Sul do Brasil

Fatores de risco para consultas em pronto-socorro por crianças asmáticas no Sul do Brasil

IL-5 and IL-5 receptor in asthma

Association of the hCLCA1 gene with childhood and adult asthma

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