女性慢性阻塞性肺疾病研究进展

女性慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者人数呈逐年上升趋势.女性COPD患者临床表现及其对于治疗反应存在的性别差异可能与病理生理学、免疫反应和激素水平等方面相关.本文就女性COPD发病基础及临床表现特点的最新研究进展作一综述.     

支气管哮喘和慢性阻塞性肺疾病

目前认为支气管哮喘和COPD是均有气流阻塞的两种不同疾病,对两者的临床表现、病理改变和发病机制等方面的差异进行探讨。     

阻塞性睡眠呼吸暂停的个体化治疗：机遇与挑战

阻塞性睡眠呼吸暂停(OSA)是一种异质性疾病,其在临床表现、发病机制及治疗反应等方面存在个体差异。基于临床特征和病理生理机制分型可更好地识别不同患者,从而针对不同病因开展个体化综合治疗以提高治疗效果。目前,OSA的个体化治疗在国内的应用仍处于初级阶段,机遇与挑战并存。     

非阻塞性冠状动脉疾病发病机制及诊治

非阻塞性冠状动脉疾病（NOCAD）是指患者发生心绞痛甚至心肌梗死,且符合冠状动脉粥样硬化性心脏病的所有临床表现,排除非冠脉因素,行冠脉造影未见50%以上狭窄的临床综合征。在所有接受血管造影的冠状动脉疾病患者中,约有40%的患者表现为冠状动脉造影正常,考虑为NOCAD。发病机制主要包括易损斑块与血栓栓塞、冠脉微循环障碍和冠状动脉血管痉挛等。因行冠脉造影时往往未发现有意义的血管狭窄,使得本病易被忽视,且预后不佳。本文就可能的发病机制、诊断及治疗等方面进行综述。     

脉络膜前动脉梗死的研究进展

脉络膜前动脉梗死[anterior choroidal artery (AChA) infarction]是脑梗死的特定类型,又称为Abbie综合征,其病因及发病机制尚不完全明了,临床表现比较复杂,诊断和治疗难度相对较大。本研究介绍脉络膜前动脉(AChA)的解剖结构特征和血液供应分布,分析国内外对AChA梗死病因、发病机制、临床表现及治疗的研究进展。目前仍需要对AChA梗死的危险因素、发病机制及治疗等进行深入研究。     

《慢性阻塞性肺疾病》一书出版

由广西医科大学呼吸疾病研究所施焕中教授编著,解放军总医院呼吸科刘又宁教授主审的《慢性阻塞性肺疾病》一书近日由人民卫生出版社出版发行。本书系统阐述慢性阻塞性肺疾病的一般情况、流行病学、危险因素、发病机制、病理、病理生理、临床表现、实验室和其他检查、诊断和鉴别诊断、治疗以及教育管理等内容。本书可作为呼吸内科、危重监护病房、普通内     

阻塞性睡眠呼吸暂停综合征

阻塞性睡眠呼吸暂停综合征北京协和医院黄席珍阻塞性睡眠呼吸暂停综合征（ＯＳＡＳ）是发病率较高并具有一定潜在危险的疾患，近１０余年来国内外对该征的研究取得了较大的进展，本文对该综合征的定义，发病情况、病因及发病机理、临床表现、诊断和治疗作一简单的介绍。Ｏ...     

结直肠Dieulafoy病的诊断和治疗进展

Dieulafoy病,即黏膜下恒径动脉破裂出血,是消化道大出血少见而又致命的病因之一,可发生在整个消化道,其中4%位于结直肠,结直肠的病变则最常见于直肠和盲肠,目前病因及发病机制尚不明确.结直肠Dieulafoy病的临床表现为无先兆的、反复发作的、致死性的便血,间歇期可无任何临床表现,目前首选内镜下进行诊断及治疗,但由于操作难度、临床特点等因素,对于Dieulafoy病的诊断和治疗仍是个难题.本文就结直肠Dieulafoy病的病理、病因、发病机制、诊断和治疗进展作一概述.     

不可忽视的重症肝病——缺血性肝炎

缺血性肝炎在ICU临床日益多见,预后往往较差。其发病机制复杂,临床表现缺乏特异性,辅助检查方法有限,诊断标准及治疗方法尚未统一。早期识别和治疗对缺血性肝炎尤为重要。本文总结了缺血性肝炎的流行病学、发病机制、临床表现、辅助检查、诊断、治疗及相关研究进展,以期提高临床医师对该病的认识,促进对该病的及时诊断和治疗。     

阻塞性睡眠呼吸暂停综合征与难治性高血压

阻塞性睡眠呼吸暂停综合征(OSAS)与难治性高血压关系密切,它可通过交感神经兴奋增强、内皮功能损伤、肾素-血管紧张素-醛固酮系统紊乱等机制引起血压增高,而且临床表现有自己的特点。因此,对于难治性高血压患者应注意有无OSAS以及是否给予了相应治疗。     

慢性阻塞性肺病合并睡眠呼吸暂停综合征的研究

为研究慢性阻塞性肺病（COPD）合并阻塞性睡眠呼吸暂停综合征（OSAS）的临床特点，对50例COPD患者据其第1次睡眠呼吸监测结果分为COPD组和COPD合并OSAS组，两组各选10例在吸氧下行第2次睡眠呼吸监测，其中COPD合并OSAS组在持续正压通气（CPAP）和双水平正压通气（BiPAP）治疗下行第3、4次睡眠呼吸监测，10例COPD合并OSAS患者在吸氧同时加用CPAP和BiPAP治疗下行第5、6次睡眠呼吸监测。结果显示，在COPD合并OSAS发病率为24％。COPD合并OSAS患者体重大，夜间打鼾，缺氧明显，呼吸衰竭和心力衰竭发生率高，睡眠潜伏期短（SLT），呼吸紊乱指数（RDI）大。睡眠时氧可使两组患者RDI增大。COPD合并OSAS组50％耐受CPAP通气治疗，皆能耐受BiPAP治疗，吸氧同时加用机械通气可取得更理想疗效。提示COPD合并OSAS患者病情危重，对其氧疗的同时给予CPAP和BiPAP通气是抢救成功的关键。     

Increased prevalence of obstructive lung disease in patients with obstructive sleep apnea

Study purposes

This study aims to determine whether there is an increased prevalence of obstructive lung diseases (OLDs) in patients with obstructive sleep apnea (OSA). We also determined whether among the OLD patients there is a difference in the prevalences of specific chronic disease co-morbidities between patients with and without OSA.

Methods

The prevalences of COPD, asthma, and COPD combined with asthma (ICD-9 coding) were compared between 1,497 adult OSA patients and 1,489 control patients, who were matched for age, gender, geographic location, and primary care physician. The prevalences of specific co-morbidities were measured in the OLD groups between patients with OSA and the matched control group.

Results

COPD, asthma, and COPD combined with asthma were found to be more prevalent among OSA patients compared to the matched controls. Prevalences among patients with and without OSA, respectively, were COPD—7.6 and 3.7 % (P?<?0.0001), asthma—10.4 and 5.1 % (P?<?0.0001), COPD plus asthma—3.3 and 0.9 % (P?<?0.0001). The Charlson Comorbidity Index was greater for OSA patients (2.3?±?0.2) than for controls (1.9?±?1.8; P?<?0.0001). These trends held for all severity ranges of OSA. Patients with OSA and COPD were characterized by more severe hypoxia at night compared with the OSA patients without OLD.

Conclusion

OSA was associated with an increased prevalence of OLDs.     

Studies in obstructive jaundice

Acute obstruction of the extrahepatic ducts causes gross proximal duct dilatation, and elevated levels of ornithine carbamyl transferase, bilirubin, and alkaline phosphatase.Slow progressive obstruction causes variable proximal duct dilatation and in these cases bilirubin, alkaline phosphatase, and ornithine carbamyl transferase return to normal, despite the presence of severe though incomplete obstruction of the common duct and microscopic findings of biliary cirrhosis. In the early phases, ornithine carbamyl transferase is a slightly more sensitive indicator of biliary obstruction than alkaline phosphatase or bilirubin, but the values still return to normal in the face of a persistent stricture.If a patient who has previously had common duct surgery develops recurrent episodes of fever which suggest cholangitis, it should be assumed that he has a recurrent stricture, even though a cholangiogram and liver function may be normal or only slightly altered. A delay until the liver function studies show consistently raised levels may result in severe biliary cirrhosis and decreased hepatic reserve.     

The obstructive subaortic conus

Eleven children are reported who had stenosis under a malposed aorta with gradients of 20 to 76 mm Hg between the right ventricle and aorta. The subaortic obstruction was caused by hypertrophy of the foreshortened infundibulum and malalignment of the infundibular septum relative to the remainder of the ventricular septum. Of these 11 patients, nine had a ventricular septal defect and seven had coarctation of the aorta. Rightward deviation of the infundibulum and aorta produced an unusually long left main coronary artery that was compressed by the stent of a bioprosthetic conduit valve in one patient. Serial cardiac catheterization studies in four patients showed progressive stenosis in each. Subaortic stenosis can develop in patients with malposition of the aorta and the frequency may be greater than 5% since milder forms are likely to occur. The obstruction can be progressive. The left coronary artery may be particularly vulnerable to compression after operative repair with an extracardiac conduit.     

Post-surgical and obstructive gastroparesis

Post-surgical gastroparesis (PSG) is recognized as a consequence of vagal nerve injury following upper abdominal surgery. It has been well documented following vagotomy for peptic ulcer surgery. With the increasing role of surgical treatment in the management of GERD and morbid obesity, PSG is now being diagnosed after fundoplication and bariatric surgery. PSG has also been reported after heart and lung transplantation, possibly due to opportunistic viral infection or motor-inhibitory effects of the immunosuppressive drugs, in addition to vagal nerve injury. Initial postoperative management of PSG should be conservative as many symptoms following abdominal surgery resolve with time. This occurs possibly because the enteric nervous system is able to adapt to the loss of vagal input or vagal reinnervation occurs. Persistent symptoms are difficult to manage and require a multidisciplinary team approach. Gastric electrical stimulation has shown promise in small series.