Primary lung cancer causing pulmonary artery microembolization and pulmonary hypertension

The authors present a rare cause of pulmonary hypertension, which occurred in a 57-year-old woman. Postmortem examination discovered an adenocarcinoma with bronchioloalveolar growth pattern as a cause of severe dyspnoea, extreme pulmonary hypertension, and chronic cor pulmonale. The tumour involved all lobes of the lung. In the hilar lymph node metastasis was detectable. Histology showed tumour cell emboli in branches of the pulmonary arteries, intimal fibrosis, which was associated with fibrin precipitation and involvement of lymphatic vessels showing lymphangiosis carcinomatosa. The intrapulmonary dissemination of the adenocarcinoma could be caused by the isolated haematogenous dissemination via the thoracic duct. The authors discuss the possible pathomechanism of pulmonary hypertension and the way of tumour cell dissemination in the lung. They highlight the histological changes, which accompany the syndrome of pulmonary tumour thrombotic microangiopathy. In this case, which can be regarded rarely published in the literature, they emphasise the differential diagnostic questions.     

复治涂阳肺结核与结核病耐药

结核病是严重危害人类健康的呼吸道传染病,是全球关注的公共卫生问题和社会问题.     

Hyperglycaemia and pulmonary infection

Pathophysiological stress from acute illness causes metabolic disturbance, including altered hepatic glucose metabolism, increased peripheral insulin resistance and hyperglycaemia. Acute hyperglycaemia is associated with increased morbidity and mortality in patients in intensive care units and patients with acute respiratory disease. The present review will consider mechanisms underlying this association. In normal lungs the glucose concentration of airway secretions is approximately 10-fold lower than that of plasma. Low airway glucose concentrations are maintained against a concentration gradient by active glucose transport. Airway glucose concentrations become elevated if normal homeostasis is disrupted by a rise in blood glucose concentrations or inflammation of the airway epithelium. Elevated airway glucose concentrations are associated with and precede increased isolation of respiratory pathogens, particularly methicillin-resistant Staphylococcus aureus, from bronchial aspirates of patients intubated on intensive care. Markers of elevated airway glucose are associated with similar patterns of respiratory infection in patients admitted with acute exacerbations of chronic obstructive pulmonary disease. Glucose at airway concentrations stimulates the growth of respiratory pathogens, over and above the effect of other nutrients. Elevated airway glucose concentrations may also worsen respiratory disease by promoting local inflammation. Hyperglycaemia may thus promote pulmonary infection, at least in part, by an effect on airway glucose concentrations. Therapeutic options, including systemic control of blood glucose and local manipulation of airway glucose homeostasis, will be considered.     

细胞自噬与肺纤维化疾病

肺纤维化是多种肺疾病常见的终末期病理学改变,其发生发展是由多种细胞、细胞因子、蛋白酶共同参与控制。研究表明,细胞自噬在肺部炎症和纤维化过程中发挥着重要作用,可以通过抑制炎性细胞因子和促纤维化因子的分泌、降解成纤维细胞中的胶原蛋白以及抑制上皮间质转化(epithelial-mesenchymal transition,EMT)过程,达到减轻肺纤维化的作用。本文就细胞自噬在特发性肺纤维化(IPF)、肺囊性纤维化(PCF)和矽肺所致肺纤维化(silicotic pulmonary fibrosis)中的作用及机制进行简要归纳,为今后工作提供参考。     

慢性阻塞性肺疾病合并吸入糖皮质激素相关肺结核三例

吸入糖皮质激素(ICS)广泛应用于慢性阻塞性肺疾病(COPD)患者的治疗,但长期使用ICS容易因局部免疫抑制并发各种感染。某院呼吸与危重症医学科分别于2015、2019、2021年各收治1例COPD合并肺结核患者,根据病史及相关检查考虑可能与ICS相关。本文拟分析该院收治的3例ICS相关肺结核病例的诊治经过,结合现有研究探讨COPD合并ICS相关肺结核患者的诊治策略。     

微小RNA与肺动脉高压

肺动脉高压(PAH)是一类以肺循环阻力增高为主要特征、最终导致右心功能不全、乃至死亡的慢性肺疾病,其病因复杂,预后差。微小RNA(miRNA)是一种内源性的非编码RNA,与PAH的发生、发展密切相关,可能是潜在的药物治疗靶点。本文主要对miRNA在PAH慢性缺氧、骨形成蛋白Ⅱ型受体(BMPR2)、apelin-APJ、以及右心功能不全等方面的研究进展进行综述,为探索PAH的发病机制、诊疗研究提供新的方向和思路。     

Fetal uropathies and pulmonary hypoplasia

The author discusses the role of fetal uropathies in the development of pulmonary hypoplasia. The predisposing abnormalities may occur at various locations, including the kidneys and the efferent urinary ducts (ureters, urocyst, urethra). Following a brief general overview of the normal development of the urinary system, the developmental abnormalities are discussed. These anomalies interfere with the secretion of urine or, alternatively, may hinder or obstruct its elimination through the urinary ducts, thus leading to oligohydramnios. Inadequate production of amniotic fluid hinders the respiratory movements and unfavourable affects or even arrests pulmonary development. The stage of lung maturity at the time of birth offers a key to the determination of the time of initial occurrence of pulmonary hypoplasia. Regretfully, the therapeutic options are rather limited, due to the substantial maternal and fetal risks of in utero fetal surgery. In case of valvula urethrae posterior, a vesico-amniotic shunt offers a realistic chance for success.     

Phthalate exposure and pulmonary function

Exposure to phthalates is widespread because of their use in plastics, cosmetics, and other consumer products. Phthalate exposure has been associated with adverse respiratory outcomes in children. With urinary phthalate measures, we assessed the association between phthalate exposure and four pulmonary function parameters [forced vital capacity (FVC), forced expiratory volume at 1 sec (FEV1), peak expiratory flow (PEF), and maximum mid-expiratory flow] among the 240 adult Third National Health and Nutrition Examination Survey (NHANES III) participants with urinary phthalate data. Linear regression models controlled for race, age, age squared, standing height, body mass index, cumulative smoking, and current smoking. Monobutyl phthalate (MBP) was significantly associated with decrements in three measures of pulmonary function (FVC, FEV1, PEF) in males but not in females. For a change from the 25th to the 75th percentile in MBP level among men, FEV1 decreased 112 mL (SE = 51, p = 0.03). Monoethyl phthalate (MEP) was associated with lower FVC and FEV1 values in men. Monoethylhexyl phthalate (MEHP), the metabolite of the plasticizer commonly used in medical tubing, was not adversely associated with any of the pulmonary function parameters evaluated. Our results suggest that MBP and MEP, but not MEHP, may influence pulmonary function among adult males.