支气管哮喘患者血清TNC、POSTN水平及意义探讨

目的探讨支气管哮喘患者血清肌腱蛋白(TNC)、骨膜蛋白(POSTN)水平及意义。方法选取2016年6月至2018年5月我院收治的122例支气管哮喘患者为研究对象。同时选取60例体检健康者作为对照组。采用酶联法检测受试者血清TNS及POSTN水平,分析血清TNC、POSTN与EOS计数、IgE、FeNO、FEV_1及FVC的相关性。并分析TNC、POSTN及联合检测诊断重度哮喘的效能。结果支气管哮喘组患者血清TNC水平明显高于对照组,而血清POSTN水平明显低于对照组(均P0.05)。重度组哮喘患者血清TNC水平明显高于轻/中度组,而血清POSTN水平明显低于轻/中度组(均P0.05)。重度组哮喘患者EOS计数、IgE、FEV_1及FVC明显低于轻/中度组患者(P0.05)。多元线性回归分析显示血清TNC与EOS计数、IgE及FEV_1、FVC呈负相关(P0.05),而POSTN与EOS计数、IgE、FeNO及FEV_1、FVC均呈正相关(P0.05)。ROC曲线分析显示,单独指标检测时,TNC诊断重度哮喘的效能高于POSTN,两者联合检测诊断重度哮喘的AUC为0.938,明显高于两者单独检测。结论支气管哮喘患者血清TNC及POSTN水平与患者严重程度存在联系,可为评估重度支气管哮喘提供参考。     

血清HMGB1水平评价哮喘严重程度和控制水平的价值

目的观察哮喘患者血清HMGB1水平与患者严重程度及控制水平的关系。方法检测49例初诊哮喘患者(间歇/轻度20例、中度15例、重度14例)血清HMGB1的水平,并与36例完全控制哮喘组患者及20例正常人对照。结果间歇发作/轻度持续组,中度持续组与重度持续组哮喘患者血清HMGB1水平的差异有统计学意义(P值均<0.05)。完全控制哮喘组血清HMGB1水平显著低于初诊哮喘患者,但显著高于正常对照组(P值均<0.01)。结论血清HMGB1水平可以反应哮喘的严重程度和指导哮喘治疗。     

老年慢性心力衰竭患者血清瘦素水平变化及其与血压的关系

目的探讨慢性心力衰竭(CHF)患者血清瘦素水平变化及其与血压的关系。方法观察慢性心力衰竭患者35例及健康对照组30例血清瘦素、左心室射血分数(LVEF)及血压水平,分析瘦素水平与血压及LVEF之间的关系。结果CHF组与对照组比较,血清瘦素水平分别为(11.4±5.8)、(7.3±3.1)μg/L,收缩压分别为(142.1±19.7)(、127.0±17.6)mm Hg,舒张压分别为(85.0±12.9)、(78.4±9.7)mmHg,两组比较,差异有统计学意义(P<0.05和P<0.01)。CHF患者按LVEF程度分为2组,LVEF<30%组瘦素水平为(12.4±7.8)μg/L,30%~40%组瘦素水平为(10.8±1.8)μg/L,两组间比较差异有统计学意义(P<0.05),表明LVEF水平越低,瘦素水平越高。多元回归分析显示,CHF患者血清瘦素水平分别与体质指数(r=0.910,P<0.01)、收缩压(r=0.859,P<0.01)、舒张压(r=0.680,P<0.05)呈正相关,与LVEF呈负相关(r=-0.729,P<0.01)。结论老年CHF患者血清瘦素水平较健康对照组高,并与LVEF程度呈负相关;CHF患者血压明显高于健康对照组,且瘦素水平与血压呈正相关,提示血清瘦素水平与高血压之间存在密切联系,共同促进CHF发展。     

血清瘦素、脂联素与冠心病病变程度的相关性研究

目的探讨血清瘦素、脂联素(APN)水平与冠心病(CHD)病变程度的相关性。方法应用ELISA法对稳定型心绞痛(SA)组(21例)、不稳定型心绞痛(UA)组(23例)、急性心肌梗死(AMI)组(24例)和正常对照(CO)组(20例)进行血清瘦素、脂联素水平检测,并进行统计学分析。结果血清瘦素水平冠心病各组明显高于正常对照组(P<0.05),UA组及AMI组高于SA组(P<0.05),AMI组高于UA组(P<0.05),血清瘦素水平与冠心病病变程度呈正相关(r=0.60,P<0.05);血清APN水平UA组及AMI组明显低于SAP组和对照组(P<0.05),冠心病各组与正常对照组比较有统计学意义(P<0.05),AMI组与UA组比较有统计学意义(P<0.05),脂联素与冠心病病变程度呈负相关(r=-0.59,P<0.05)。结论血清瘦素、脂联素与冠心病发病密切相关,冠心病患者血清瘦素水平升高,血清瘦素水平与冠心病病变程度呈正相关。冠心病患者血清APN水平下降,血清脂联素与冠心病病变程度呈负相关。     

支气管哮喘患儿血清mir-98-5p及IL-13的表达水平及临床意义

目的探讨支气管哮喘患儿血清中mir-98-5p及IL-13的表达水平及临床意义。方法选取在我院确诊的支气管哮喘患儿60例为研究对象,其中哮喘急性期患儿30例,哮喘缓解期患儿30例;另选进行健康体检的健康儿童30例作为健康对照组。采集患儿及健康儿童清晨空腹静脉血检测血清miR-98-5p与IL-13的表达水平。结果支气管哮喘患儿血清IL-13水平显著高于健康对照组儿童(P0.01),哮喘急性期患儿血清IL-13水平显著高于哮喘缓解期患儿(P0.01)。支气管哮喘患儿血清miR-98-5p水平显著低于健康对照组儿童(P0.01),哮喘急性期组患儿血清miR-98-5p水平显著低于哮喘缓解期患儿(P0.01)。在哮喘急性期患儿中,中度组与重度组患儿血清IL-13水平显著高于轻度组患儿(P0.05),重度组显著高于中度组(P0.05);中度组与重度组患儿血清miR-98-5p水平均显著低于轻度组患儿(P0.05),重度组显著低于中度组(P0.05)。支气管哮喘患儿血清miR-98-5p的表达与IL-13的表达水平呈负相关(r=-0.863,P0.05)。结论支气管哮喘患儿血清miR-98-5p表达与IL-13的表达水平呈负相关,IL-13的过度分泌在哮喘的发病中起重要作用,miR-98-5p、IL-13的表达水平与患儿哮喘发病的严重程度有关,miR-98-5p可能会通过影响IL-13的表达水平而影响支气管哮喘的发生发展。     

肝细胞生长因子与冠状动脉狭窄程度的相关性研究

目的:探讨肝细胞生长因子(HGF)、血管内皮生长因子(VEGF)、肿瘤坏死因子-α(TNF-α)与冠心病病变程度的相关性。方法:63例冠心病患者根据冠状动脉狭窄程度分为3组:轻度组18例,中度组22例,重度组23例,采用酶联免疫吸附法检测外周血HGF、VEGF、TNF-α水平,与20例年龄和性别相当的健康者(对照组)进行比较。冠心病患者按心绞痛分级Ⅰ级12例,Ⅱ级14例,Ⅲ级15例,Ⅳ级22例,与HGF、VEGF、TNF-α水平进行相关分析。结果:血清HGF水平重度组、中度组及轻度组明显高于对照组,有极显著性差异(P<0.01);血清VEGF、TNF-α水平重度组、中度组均明显高于轻度组及对照组,有极显著性差异(P<0.01);HGF、VEGF、TNF-α水平与心绞痛分级呈正相关(r1=0.864P<0.01;r2=0.682P<0.01;r3=0.403P<0.01)。结论:HGF、VEGF、TNF-α与心绞痛程度呈显著正相关,其中HGF较其他两项指标相关性更好。     

支气管哮喘患者血清脂氧素A4水平与肺功能相关性分析

目的通过检测不同严重程度支气管哮喘患者及正常对照组之间血清脂氧素A4(LXA4)和肺功能的水平,探讨支气管哮喘急性发作期患者血LXA4与肺功能之间的关系,以期进一步阐明血清脂氧素在支气管哮喘患者中诊疗的意义。方法选择酶联免疫吸附法(ELISA法)对45例不同程度支气管哮喘患者组与正常对照组25例的血清LXA4水平进行检测,同时收集哮喘患者的肺功能指标,分析血清LXA4与肺功能的相关性。结果 (1)不同严重程度的哮喘急性发作组血清LXA4水平高于对照组(P0.01);中、重度组血清LXA4水平亦高于轻度组(P0.01);而重度组血清LXA4水平[(271.22±26.99)]ng/L却显著低于中度组[(302.4±31.18)]ng/L(P0.01);(2)支气管哮喘患者急性发作期各亚组血清LXA4水平随FEV1占预计值的百分比(FEV1%pred)的降低而升高,呈负相关性(r=0.-314,P0.01)。结论支气管哮喘急性发作期各亚组血清脂氧素A4水平均显著高于对照组,且与肺功能呈负相关,提示脂氧素作为天然的白三烯拮抗物质可能参与支气管哮喘的发病机制。     

血清hscTnT、Hcy、hsCRP联合检测与冠心病诊断阳性率的相关性

目的:探析血清超敏肌钙蛋白T (hscTnT)、同型半胱氨酸(Hcy)、超敏C反应蛋白(hsCRP)联合检测与冠心病诊断阳性率的相关性。方法:选择95例冠心病患者,其中稳定型心绞痛(SAP)35例,不稳定型心绞痛(UAP)30例,急性心肌梗死(AMI)30例。根据冠脉造影结果,患者被分为:轻度狭窄组(31例),中度狭窄组(34例)和重度狭窄组(30例),并另选95例健康体检者作为健康对照组。检测并比较各组hscTnT、Hcy、hsCRP水平及单独检测和联合检测的阳性率,并分析冠状动脉病变程度与血清hscTnT、Hcy、hsCRP水平及联合检测的相关性。结果:冠心病患者的血清hscTnT、Hcy、hsCRP水平均显著高于健康对照组(P均=0.001)。UAP与AMI组的Hcy阳性率明显高于SAP组(63.33%、70.00%比14.29%,P均=0.001)。SAP、UAP及AMI患者的联合检测阳性率(91.43%、93.33%、96.67%)之间无统计学意义(P均0.05),但均显著高于单一指标阳性率(P0.05或0.01)。hscTnT与hsCRP诊断SAP的阳性率显著高于Hcy(68.57%、71.43%比14.29%,P均=0.001)。与轻度狭窄组比较,中度、重度狭窄组患者的血清hscTnT、Hcy、hsCRP水平明显升高,且重度狭窄组的明显高于中度狭窄组的(P均=0.001)。二变量Spearman分析显示,冠心病患者血清hscTnT、Hcy、hsCRP水平及联合检测结果与冠状动脉病变程度之间均呈明显正相关(r=0.512～0.813,P均0.01)。结论:冠心病患者的血清hscTnT、Hcy、hsCRP联合检测阳性率均高于单一指标阳性率,联合诊断结果与冠脉病变程度呈明显正相关。     

MicroRNA-16及Let-7a在支气管哮喘患者中表达水平及与严重程度的关系

目的探讨微RNA-16(microRNA-16,miR-16)及Let-7a在支气管哮喘患者中表达水平及与严重程度的关系。方法选取2017年7月至2019年7月我院收治的128例支气管哮喘患者作为研究对象,按照严重程度将患者分为轻、中度组(n=85)和重度组(n=43)。选取同期120例体检健康者作为对照组。采用实时荧光定量PCR(RT-qPCR)检测血清miR-16和Let-7a相对表达量,并分析模型A(miR-16+Let-7a)、模型B(IL-13+IgE+EOS计数)及模型C(miR-16+Let-7a+IL-13+IgE+EOS计数)评估重度支气管哮喘的效能。结果轻、中度组及重度组血清miR-16和Let-7a相对表达量低于对照组,重度组血清miR-16和Let-7a相对表达量低于轻、中度组,差异均有统计学意义(P0.05)。miR-16、Let-7a评估重度支气管哮喘的AUC分别为0.802、0.808。Logistic回归分析显示IL-13、IgE、EOS计数、miR-16、Let-7a与支气管哮喘病情加重密切相关。模型C评估重度支气管哮喘的效能高于模型A及模型B。结论血清miR-16和Let-7a与支气管哮喘严重程度关系密切,检测血清miR-16和Let-7a相对表达量有助于评估患者病情。     

血清可溶性转铁蛋白受体水平与慢性阻塞性肺疾病患者认知障碍程度的相关性研究

背景目前,血清可溶性转铁蛋白受体(sTFR)水平与慢性阻塞性肺疾病(COPD)患者认知障碍的关系尚未完全明确。目的探讨血清sTFR水平与COPD患者认知障碍程度的相关性。方法选取2017年2月-2019年7月在西安交通大学第一附属医院就诊的COPD患者248例作为观察组,另选取同期健康体检者250例作为对照组;另根据贫血程度将COPD患者分为轻度组38例、中度组45例、重度组19例及非贫血组146例。比较对照组、观察组及轻度组、中度组、重度组、非贫血组患者血清sTFR、内皮素1 (ET-1)、铁调节素(hepcidin)、8-羟基脱氧尿苷酸(8-OHdG)、低氧诱导因子1α(HIF-1α)水平及蒙特利尔认知评估量表(MoCA)评分;血清sTFR水平、MoCA评分与COPD患者血清ET-1、hepcidin、8-OHdG、HIF-1α水平间的相关性分析及血清sTFR水平与COPD患者MoCA评分的相关性分析均采用Pearson相关分析。结果 (1)观察组患者血清sTFR、ET-1、hepcidin、8-OHdG、HIF-1α水平高于对照组,MoCA评分低于对照组(P<0.05)。(2)轻度、中度、重度组患者血清sTFR、ET-1、hepcidin、8-OHdG、HIF-1α水平高于非贫血组,MoCA评分低于非贫血组(P<0.05);中度、重度组患者血清sTFR、ET-1、hepcidin、8-OHdG、HIF-1α水平高于轻度组,MoCA评分低于轻度组(P<0.05);重度组患者血清sTFR、ET-1、hepcidin、8-OHdG、HIF-1α水平高于中度组,MoCA评分低于中度组(P<0.05)。(3) Pearson相关分析结果显示,血清sTFR水平与COPD患者血清ET-1 (r=0.482)、hepcidin(r=0.682)、8-OHdG(r=0.513)、HIF-1α(r=0.441)水平均呈正相关(P<0.05),MoCA评分与COPD患者血清ET-1 (r=-0.461)、hepcidin (r=-0.515)、8-OHdG(r=-0.485)、HIF-1α(r=-0.437)水平均呈负相关(P<0.05);血清sTFR水平与COPD患者MoCA评分呈负相关(r=-0.481,P<0.05)。结论随着贫血程度加重,COPD患者血清sTFR水平升高、认知障碍程度加重,且血清sTFR水平与COPD患者认知障碍程度有关。     

Growth effects of asthma and asthma therapy.

A small effect (1 cm) of inhaled corticosteroids (ICS) on the 1-year growth of asthmatic children was observed in studies published during the 1990s. A high volume of literature published during the past year confirmed mild growth suppression at one year, but provided information on the effects of longer-term treatment. These developments are important, since the effect was previously unknown and the findings have major implications for asthma caregivers and the communication that they have with asthmatic children and their parents. The possibility that this is an idiosyncratic effect received conflicting support. These studies collectively provide support for ICS use and ease the minds of caregivers, parents, and children. The risk of growth retardation can be lessened and managed by the employment of several simple strategies: (1) monitor growth; (2) use the minimal effective dose; (3) optimize steroid-sparing strategies (smoke and allergen environmental controls, vaccinate for influenza, diagnose and treat rhinitis, sinusitis, and gastroesophageal reflux disease, use add-on therapy with a second controller rather than doubling the ICS dose if control is inadequate); and (4) use spacing devices (for pressurized metered-dose inhalers) and mouth rinsing. Open and accurate communication with patients and parents about this possible effect is essential to minimize nonadherence. Ultimately, no child whose disease severity warrants ICS therapy should be denied the tremendous benefits that this therapy can provide because of relatively minor concerns about growth effects.     

Allergen-induced asthma

It was only in the late 19th century that specific allergens, pollen, animal antigens and, later, house dust mite, were identified to cause upper and lower airway disease. Early allergen challenge studies, crudely monitored before measurement of forced expiratory volume in 1 s became widespread in the 1950s, focused on the immediate effects but noted in passing prolonged and/or recurrent asthma symptoms. The late asthmatic response, recurrent bronchoconstriction after spontaneous resolution of the early responses occurring 3 h to 8 h or more postchallenge, has been identified and well characterized over the past 50 years. The associated allergen-induced airway hyper-responsiveness (1977) and allergen-induced airway inflammation (1985) indicate that these late sequelae are important in the mechanism of allergen-induced asthma. Allergens are now recognized to be the most important cause of asthma. A standardized allergen inhalation challenge model has been developed and is proving to be a valuable research tool in the investigation of asthma pathophysiology and of potential new pharmacological agents for the treatment of asthma.     

Urban asthma

PURPOSE OF REVIEW: To review the possible reasons why the prevalence and morbidity of asthma are greater in those living in an urban setting. RECENT FINDINGS: Urban asthma is associated with exposure to air pollution, urban allergens, and violence. Outdoor air pollution is a particular problem in urban areas and affects children more than adults. Asthma has been shown to be exacerbated by ozone, respirable particulates, and nitrogen dioxide. Exposure to high point sources of pollutants such as heavy traffic is of particular concern. Urban allergens include cockroach, mouse, and rat. Cockroach exposure increases the risk of asthma exacerbations and may increase the risk of developing asthma. Although mouse allergen is also found in suburban homes, the concentration is a log-fold higher in inner-city homes at levels known to elicit symptoms in workers in animal facilities. Rat allergen is found in a third of inner-city homes and is associated with asthma morbidity. A recent interventional study showed that comprehensive environmental control of cockroach allergen reduced asthma morbidity. Finally, stress elicits asthma symptoms and exposure to violence is associated with greater asthma morbidity. SUMMARY: The increase in prevalence and morbidity of asthma associated with urban living is associated with at least three plausible causative factors each of which is amenable to intervention, raising the issue of environmental justice issues: controlling air pollution in general and exposure to point sources in particular; reducing cockroach, mice, and rat infestations; and preventing violence.     

Difficult asthma

The correct diagnosis of asthma is usually easily made and most patients with asthma respond to therapy. Approximately 5% of patients with asthma, however, have disease that is difficult to control despite taking maximal doses of inhaled medications. Patients with therapy-resistant or difficult-to-control asthma require a rigorous and systematic approach to their diagnosis and treatment. The first step is evaluation and testing directed at determining that asthma is the correct diagnosis. Many diseases mimic asthma and these alternate diagnoses should be considered. The second step is to identify and eliminate triggers that worsen asthma. Cigarette smoking, occupational exposures, and allergic rhinitis contribute to worsening disease. Most patients with "difficult asthma" require treatment with high-dose inhaled corticosteroids and long-acting inhaled beta(2)-agonists. Despite maximal inhaled therapy, these patients will require either frequent bursts or chronic daily therapy with oral corticosteroids. These patients may have "resistant" inflammation with a persistent inflammatory state. Numerous studies also suggest that compliance with asthma therapy is poor. Combination therapy with inhaled corticosteroids and long-acting beta(2)-agonist in a single inhaler may improve patient compliance. In selected patients, additional therapy with leukotriene modifiers or anti-IgE antibody can result in improved asthma control and may allow tapering of corticosteroids. Use of methotrexate is not justified based on current data. Emerging evidence suggests that different phenotypes of difficult or therapy-resistant asthma exist. Recognition of these subgroups allows tailored therapy and prevents overmedication in an attempt to normalize lung function in patients with irreversible airflow obstruction.