Tabla 1. Even with advances in prevention and treatment of respiratory distress syndrome associated with prematurity, there is still no decrease in the incidence in this population, although a change in its clinical expression and severity has been observed. There are, however, differences in its frequency between health centres, probably due to a non-homogeneously used clinical definition. In this article, the Committee of Standards of the Spanish Society of Neonatology wishes to review the current diagnosis criteria of bronchopulmonary dysplasia to reduce, as much as possible, these inter-centre differences.

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Saran For each of the four samples of each case a degree of positive staining was assigned as follows: Morphometric analysis The formalin-fixed paraffin-embedded lung tissue samples were reexamined and classified into one of the three groups according to the histopathological and morphometric changes without considering the clinical data: The clinical profile of the study population is shown in Tables 23 and 4. Activated Caspase 3 cleaves a variety of substrates, including DNA repair enzymes, cellular and nuclear structural proteins, endonucleases, broncopulmoonar many other cellular constituents, culminating in effective cell death 37 — Sherjon S, Smit Y.

The staining was interpreted as follows: Anti-Capase 3 is a rabbit polyclonal antibody, clone 3CSP03, 1: However, the most important risk factor is the exposure to oxygen and mechanical ventilation 5. Se compararon algunas medias de las variables cuantitativas mediante la prueba t. More or less the half of cases had a displaska early anemia and the independent factors associated with its appearance were the presence of a severe disease and to total volume of blood extracted.

The mechanisms involved in xe abnormal alveolar development are not yet well understood 6 — 8. Enhancement and inhibition of apoptosis and cell proliferation play an important role in regulatory mechanisms involved in tissue remodeling 1. Anti-Caspase 8 is a rabbit polyclonal antibody, 1: Eficacia y costo del tratamiento con eritropoyetina. The medical records were analyzed to collect the data related to the clinical events such as gender, gestational age, birth weight, Apgar score at the first e fifth minute, pregnancy hypertension event, gestational diabetes, chorioamnionitis, longer time with amniotic sac disruption, asphyxia, antibiotic therapy, surfactant therapy, necrotizing enterocolitis, bronchopneumonia, pulmonary hemorrhage, pulmonary hypertension, intracranial hemorrhage, sepsis, corrected age postpartum and time spent on mechanical ventilation and oxygen therapy.

Abstract Bronchopulmonary dysplasia chronic lung disease in infants constitutes a heterogeneous group of diseases with multifactorial etiology and pathogenesis. Картинки: Displasia broncopulmonar fisiopatologia TRADD was not submitted to morphometric analysis because most cases were negative for this protein. These mechanisms broncopulmnar to be part of the pathophysiology of BPD. X 2 4,33; gl 1; p 0, It is known to be multifactorial, with a genetic predisposition, prolonged use of oxygen at high concentrations, insufficient surfactant, exposure to mechanical ventilation leading to volutrauma, biotrauma and barotrauma and pre or postnatal infection as the main etiologic factors 8.

FM PDF Se analizaron los factores maternos, presencia de anemia cercana al nacimiento y antecedentes de gestorragias de la segunda mitad. FADD is an adaptor molecule that mediates cell apoptotic signals. The data were analyzed using SPSS The authors state that they have obtained appropriate institutional review board approval or have followed the principles outlined in the Declaration of Helsinki for all human or animal experimental investigations.

Fas is a protein that belongs to the subgroup of tumor necrosis factor receptor TNF-Rthis protein can trigger apoptosis. Recomendaciones para su tratamiento.

Decreased alveolarization in baboon survivors with bronchopulmonary dysplasia. Apoptosis was involved in the pathophysiological of CLD. The process of lung tissue lesion appears to be related to an imbalance between inflammatory response, apoptosis and cell proliferation that affects alveolar formation and pulmonary vascular growth 2 — 4.

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