RESUMEN
Asthma and chronic obstructive pulmonary disease (COPD) are highly prevalent chronic obstructive lung diseases with an associated high burden of disease. Asthma, which is often allergic in origin, frequently begins in infancy or childhood with variable airflow obstruction and intermittent wheezing, cough, and dyspnea. Patients with COPD, in contrast, are usually current or former smokers who present after the age of 40 years with symptoms (often persistent) including dyspnea and a productive cough. On the basis of age and smoking history, it is often easy to distinguish between asthma and COPD. However, some patients have features compatible with both diseases. Because clinical studies typically exclude these patients, their underlying disease mechanisms and appropriate treatment remain largely uncertain. To explore the status of and opportunities for research in this area, the NHLBI, in partnership with the American Thoracic Society, convened a workshop of investigators in San Francisco, California on May 14, 2016. At the workshop, current understanding of asthma-COPD overlap was discussed among clinicians, pathologists, radiologists, epidemiologists, and investigators with expertise in asthma and COPD. They considered knowledge gaps in our understanding of asthma-COPD overlap and identified strategies and research priorities that will advance its understanding. This report summarizes those discussions.
Asunto(s)
Asma/fisiopatología , Asma/terapia , Enfermedad Pulmonar Obstructiva Crónica/fisiopatología , Enfermedad Pulmonar Obstructiva Crónica/terapia , Asma/diagnóstico , Diagnóstico por Imagen , Pulmón/fisiopatología , National Heart, Lung, and Blood Institute (U.S.) , Enfermedad Pulmonar Obstructiva Crónica/diagnóstico , Sociedades Médicas , Estados UnidosRESUMEN
Asthma is a common chronic disease without cure. Our understanding of asthma onset, pathobiology, classification, and management has evolved substantially over the past decade; however, significant asthma-related morbidity and excess healthcare use and costs persist. To address this important clinical condition, the NHLBI convened a group of extramural investigators for an Asthma Research Strategic Planning workshop on September 18-19, 2014, to accelerate discoveries and their translation to patients. The workshop focused on (1) in utero and early-life origins of asthma, (2) the use of phenotypes and endotypes to classify disease, (3) defining disease modification, (4) disease management, and (5) implementation research. This report summarizes the workshop and produces recommendations to guide future research in asthma.
Asunto(s)
Asma/terapia , National Heart, Lung, and Blood Institute (U.S.) , Investigación , Asma/fisiopatología , Educación , Humanos , Estados UnidosRESUMEN
The National Heart, Lung, and Blood Institute (NHLBI) provides global leadership for a research, training, and education program to promote the prevention and treatment of heart, lung, and blood diseases and enhance the health of all individuals so that they can live longer and more fulfilling lives. Inherent in this mission is the commitment to advance health equity research as an avenue for enhancing the health of all individuals. Additionally, the four goals and eight research objectives of the NHLBI Strategic Vision directly support the commitment to health equity. In this article, we present selected examples of the NHLBI Strategic Vision implementation approaches for advancing health equity research in our mission areas of heart, lung, and blood diseases. Examples of diseases for which the burden of health inequities and our strategic vision implementation approaches are discussed include hypertension, heart failure, vascular dementia, asthma, and sickle cell disease. Examples are provided of new avenues of Institute-solicited research to stimulate and address compelling scientific questions and critical challenges to advance health equity. We also highlight the emerging fields of implementation science and predictive analytics as important opportunities to accelerate the translation of discovery science into health impact for all and to advance health equity.
Asunto(s)
Equidad en Salud , National Heart, Lung, and Blood Institute (U.S.) , Investigación , Asma , Cardiopatías , Enfermedades Hematológicas , Humanos , Enfermedades Pulmonares , Modelos Teóricos , Estados UnidosRESUMEN
High resolution CT (HRCT) scanning has contributed significantly to the evaluation of patients with interstitial lung disease and is particularly useful in the diagnosis of idiopathic pulmonary fibrosis (IPF). The characteristic radiographic features of the idiopathic interstitial pneumonias on HRCT scans have been increasingly analysed and are now fairly well described. Based on current data, HRCT scanning can provide a confident, highly specific diagnosis of IPF in many patients with diffuse lung disease. This article reviews an organised approach to HRCT scanning and identifies the features that allow an accurate diagnosis of the idiopathic interstitial pneumonias to be made. The role of surgical lung biopsy is discussed in the diagnosis of cases when a definite HRCT diagnosis cannot be made.
Asunto(s)
Enfermedades Pulmonares Intersticiales/diagnóstico por imagen , Pulmón/patología , Fibrosis Pulmonar/diagnóstico por imagen , Tomografía Computarizada por Rayos X/métodos , Enfermedad Aguda , Biopsia/métodos , Humanos , Pronóstico , Sensibilidad y Especificidad , Tomografía Computarizada por Rayos X/normasRESUMEN
OBJECTIVE: To define the contribution of polymorphisms in genes encoding tumor necrosis factor (TNF), mannose-binding lectin (MBL), and Fcgamma receptor IIa (FCGR2A) as well as clinical factors, to the development of pneumonia in patients with systemic lupus erythematosus (SLE). METHODS: We studied 282 SLE patients from a multiethnic cohort. Pneumonia events and clinical risk factors for pneumonia were identified through medical record review. Genotyping was performed for MBL (+223, +230, and +239), TNF (-308, -238, and +488), and FCGR2A (-131H/R) polymorphisms. Univariate analyses were performed to identify clinical and genetic risk factors for pneumonia. Covariates for multivariate analysis included sex, ethnicity, treatment with immunomodulators, and leukopenia. RESULTS: Forty-two patients (15%) had at least 1 episode of pneumonia. Polymorphism of the TNF gene, particularly the -238A allele and a related haplotype, revealed the most striking and consistent association with pneumonia in univariate analyses. Results of multivariate analyses indicated an odds ratio (OR) for the TNF -238A allele of 3.5 (P = 0.007) and an OR for the related haplotype of 5.4 (P = 0.001). Male sex, treatment with immunomodulators, and leukopenia also influenced the risk of pneumonia. CONCLUSION: These findings suggest that specific TNF variants may identify SLE patients who are at particularly high risk of developing pneumonia. Given the prevalence and excessive morbidity associated with pneumonia in SLE, these findings have clinical relevance and provide insight into the pathogenesis.