结节病易误诊,据王洪武等~([1])收集国内18篇关于此病误诊的文献,误诊率高达63.2%,当然有误诊就会有误治,如孙永昌等~([2])报道26例结节病在影像学检查诊断的第一印象中拟诊结核5例,其中就有2例完成规范的抗结核治疗,为此应引起临床对本病诊治的重视。

Sarcoidosis

Asthma and chronic obstructive pulmonary disease (COPD) are both obstructive airway diseases that involve chronic inflammation of the respiratory tract, but the type of inflammation is markedly different between these diseases, with different patterns of inflammatory cells and mediators being involved As described in this Review, these inflammatory profiles are largely determined by the involvement of different immune cells, which orchestrate the recruitment and activation of inflammatory cells that drive the distinct patterns of structural changes in these diseases However, it is now becoming clear that the distinction between these diseases becomes blurred in patients with severe asthma, in asthmatic subjects who smoke and during acute exacerbations This has important implications for the development of new therapies

Immunology of asthma and chronic obstructive pulmonary disease

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Methods Of Enzymatic Analysis

Asthma and chronic obstructive pulmonary disease (COPD) are very common inflammatory diseases of the airways. They both cause airway narrowing and are increasing in incidence throughout the world, imposing enormous burdens on health care. Cytokines play a key role in orchestrating the chronic inflammation and structural changes of the respiratory tract in both asthma and COPD and have become important targets for the development of new therapeutic strategies in these diseases.

https://dm5migu4zj3pb.cloudfront.net/manuscripts/36000/36130/JCI0836130.v1.pdf

The cytokine network in asthma and chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation affecting predominantly the lung parenchyma and peripheral airways that results in largely irreversible and progressive airflow limitation. This inflammation is characterized by increased numbers of alveolar macrophages, neutrophils, T lymphocytes (predominantly TC1, TH1, and TH17 cells), and innate lymphoid cells recruited from the circulation. These cells and structural cells, including epithelial and endothelial cells and fibroblasts, secrete a variety of proinflammatory mediators, including cytokines, chemokines, growth factors, and lipid mediators. Although most patients with COPD have a predominantly neutrophilic inflammation, some have an increase in eosinophil counts, which might be orchestrated by TH2 cells and type 2 innate lymphoid cells though release of IL-33 from epithelial cells. These patients might be more responsive to corticosteroids and bronchodilators. Oxidative stress plays a key role in driving COPD-related inflammation, even in ex-smokers, and might result in activation of the proinflammatory transcription factor nuclear factor κB (NF-κB), impaired antiprotease defenses, DNA damage, cellular senescence, autoantibody generation, and corticosteroid resistance though inactivation of histone deacetylase 2. Systemic inflammation is also found in patients with COPD and can worsen comorbidities, such as cardiovascular diseases, diabetes, and osteoporosis. Accelerated aging in the lungs of patients with COPD can also generate inflammatory protein release from senescent cells in the lung. In the future, it will be important to recognize phenotypes of patients with optimal responses to more specific therapies, and development of biomarkers that identify the therapeutic phenotypes will be important.

Inflammatory mechanisms in patients with chronic obstructive pulmonary disease

Obesity is currently one of the major epidemics of this millennium and affects individuals throughout the world. It causes multiple systemic complications, some of which result in severe impairment of organs and tissues. These complications involve mechanical changes caused by the accumulation of adipose tissue and the numerous cytokines produced by adipocytes. Obesity also significantly interferes with respiratory function by decreasing lung volume, particularly the expiratory reserve volume and functional residual capacity. Because of the ineffectiveness of the respiratory muscles, strength and resistance may be reduced. All these factors lead to inspiratory overload, which increases respiratory effort, oxygen consumption, and respiratory energy expenditure. It is noteworthy that patterns of body fat distribution significantly influence the function of the respiratory system, likely via the direct mechanical effect of fat accumulation in the chest and abdominal regions. Weight loss caused by various types of treatment, including low-calorie diet, intragastric balloon, and bariatric surgery, significantly improves lung function and metabolic syndrome and reduces body mass index. Despite advances in the knowledge of pulmonary and systemic complications associated with obesity, longitudinal randomized studies are needed to assess the impact of weight loss on metabolic syndrome and lung function.

/pdf/obesity-systemic-and-pulmonary-complications-biochemical-2wxzbxuc3b.pdf

Obesity: systemic and pulmonary complications, biochemical abnormalities, and impairment of lung function.

CXCR3 and CCR5 chemokines in induced sputum from patients with COPD

INTRODUCTION: The Sleep Apnea Clinical Score (SACS) and the Berlin Questionnaire (BQ) are used to predict the likelihood of obstructive sleep apnea (OSA). The Epworth Sleepiness Scale (ESS) is used to assess daytime sleepiness, a common OSA symptom. These clinical tools help prioritize individuals with the most severe illness regarding on whom polysomnography (PSG) should be performed. It is necessary to check the applicability of these tools in patients with chronic obstructive pulmonary disease (COPD). The aim of this study is to compare SACS, BQ, and ESS performance in patients with COPD. METHODS: The SACS, BQ, and ESS were applied to 91 patients with COPD. From this group, 24 underwent PSG. In this transversal study, these three tests were compared regarding their likelihood to predict OSA in patients with COPD using receiver-operating characteristic curve statistics. RESULTS: In this sample, 58 (63.7%) patients were men, and their mean age was 69.4±9.6 years. Fourteen patients (15.4%) had a high probability of OSA by SACS, 32 (32.5%) had a high probability by BQ, and 37 (40.7%) had excessive diurnal somnolence according to the ESS. From the 24 patients who underwent PSG, OSA diagnosis was confirmed in five (20.8%), according to the American Academy of Sleep Medicine criteria. BQ and ESS did not accurately predict OSA in this group of patients with COPD, with a receiver-operating characteristic curve area under the curves of 0.54 (95% CI: 0.329-0.745, P=0.75) and 0.69 (95% CI: 0.47-0.860, P=0.10), respectively. SACS performance was significantly better, with an area under the curve of 0.82 (95% CI: 0.606-0.943, P=0.02). CONCLUSION: SACS was better than BQ and ESS in predicting OSA in this group of patients with COPD.

/pdf/sleep-apnea-clinical-score-berlin-questionnaire-or-epworth-2qihx4m48g.pdf

Sleep Apnea Clinical Score, Berlin Questionnaire, or Epworth Sleepiness Scale: which is the best obstructive sleep apnea predictor in patients with COPD?

Idiopathic pulmonary fibrosis is a type of chronic fibrosing interstitial pneumonia, of unknown etiology, which is associated with a progressive decrease in pulmonary function and with high mortality rates. Interest in and knowledge of this disorder have grown substantially in recent years. In this review article, we broadly discuss distinct aspects related to the diagnosis and treatment of idiopathic pulmonary fibrosis. We list the current diagnostic criteria and describe the therapeutic approaches currently available, symptomatic treatments, the action of new drugs that are effective in slowing the decline in pulmonary function, and indications for lung transplantation.

/pdf/update-on-diagnosis-and-treatment-of-idiopathic-pulmonary-ht59z7lrlx.pdf

Update on diagnosis and treatment of idiopathic pulmonary fibrosis

The relationship between asthma and obesity is well established, although the pathophysiological mechanisms linking both diseases remain unknown Adiponectin is a hormone secreted by adipose cells, plays a role in the modulation of inflammation and may be the key linking these two types of inflammation We conducted a cross-sectional study with asthma with different body mass indices (BMI); the patients were classified as eutrophic, overweight, or obese We assessed disease control using the GINA consensus, and the levels of adiponectin, C-reactive protein (CRP) and interleukin 33 (IL-33) in each of the patients We evaluated 75 of the 96 patients eligible for the study, including 25 in each BMI group The CRP levels were significantly higher in the obese patients compared with both the eutrophic (p = 001) and the overweight (p = 003) patients The mean adiponectin level was 2182 ± 993 mg/L for the eutrophic asthmatics, which is a level that was significantly higher than in the overweight (1531 ± 627 mg/L, p = 00140) and the obese (1669 ± 1145 mg/L, p = 00287) patients The patients with higher adiponectin levels exhibited smaller FEV1 (p = 002) and lower FVC (p = 0003) The IL-33 levels were not different between the groups Adiponectin does not protect against the development of inflammation in the setting of asthma and may in fact exacerbate the disease via its anti-TH1 inflammatory effects, allowing for increased TH2 differentiation and a more severe allergic response

Rogério Rufino

Papers

Obesity: systemic and pulmonary complications, biochemical abnormalities, and impairment of lung function.

CXCR3 and CCR5 chemokines in induced sputum from patients with COPD

Sleep Apnea Clinical Score, Berlin Questionnaire, or Epworth Sleepiness Scale: which is the best obstructive sleep apnea predictor in patients with COPD?

Update on diagnosis and treatment of idiopathic pulmonary fibrosis

Adiponectin in Asthma and Obesity: Protective Agent or Risk Factor for More Severe Disease?