重视慢性阻塞性肺疾病的合并症

根据2011年慢性阻塞性肺疾病全球防治创议（global initiative for chronic obstructive lung disease,GOLD）,慢性阻塞性肺疾病（chronic obstructive pulmonary disease, COPD）是一种可预防和治疗的常见疾病。该病以持续性、不完全可逆的气流受限为特征,通常呈进行性发展,并与气道和肺对有害颗粒或气体产生的慢性炎症反应增强有关,急性加重与合并症的发生影响病情的严重程度。     

慢性阻塞性肺疾病并发直肠癌患者围手术期护理及训练

随着医疗技术的不断发展进步,合并慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）直肠癌手术患者日趋增多.由于COPD患者肺部通气功能障碍,对麻醉和手术的耐受性减弱,术后常并发肺栓塞、肺不张,肺炎和呼吸衰竭,因此对合并COPD的直肠癌患者进行正确的围手术期的护理及呼吸训练,具有重要的临床意义.     

慢性阻塞性肺疾病评估测试的研究进展

慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）是一种以持续存在并呈进行性发展的气流受限为特征的慢性呼吸系统疾病,具有发病率、致残率和病死率均较高的特点。预计到2020年,     

认知行为治疗对慢性阻塞性肺疾病患者睡眠障碍的改善作用

慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）通常伴有不同程度的睡眠障碍和夜间低氧血症。夜间睡眠质量的下降严重的影响着COPD患者的生活质量以及疾病康复。镇静催眠药物可以引起低氧血症和高碳酸血症,而且COPD患者常伴有抑郁症状,其安全性差。     

对慢性阻塞性肺疾病的认识和再认识

全球慢性阻塞性肺病倡议组织（global obstructive lung disease，GOLD）宣布2005年11月16日举行世界慢性阻塞性肺病（chronic obstructive pulmonary disease，COPD）日纪念活动，主题为“轻松呼吸，不再无助”，藉以增强大众对COPD的认识，并提高对COPD的预防、诊断和治疗水平。借此机会谈谈我对COPD的认识。     

慢性阻塞性肺疾病急性加重表型的研究进展

<正>慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)是一种以进行性气流受限为特征的慢性肺部炎症性疾病~([1-2])。慢性阻塞性肺疾病急性加重(acuteexacerbation of chronic obstructive pulmonary disease,AECOPD)是患者呼吸道症状恶化超出日常变化范围并需要改变临床用药方案的急性临床事件。AECOPD可加速肺功能的恶化,降低患者生活质量~([3-4])。表型是指能将生物体分     

祛痰治疗在慢性阻塞性肺疾病中临床应用

气道黏液高分泌是慢性阻塞性肺疾病（ chronic obstructive pulmonary disease, COPD）等气道炎症性疾病的重要临床表现之一。气道黏液高分泌主要由受到中性粒细胞（polymorphonuclear neutrophil,PMN）弹性蛋白酶（alkaline elastase）、     

慢性阻塞性肺疾病合并心血管疾病的研究进展

慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）是一种以不完全可逆性气流受限为特征的慢性炎症反应性疾病.COPD除了肺脏本身受损外,局部炎症介质“溢出”进入血循环还可引起明显的全身效应.全身效应可进一步诱发或加重COPD的合并症,如心血管疾病（cardiovascular disease,CVD）、骨质疏松、焦虑和抑郁、感染、代谢综合征及糖尿病等,其中以CVD尤为突出.COPD合并症不仅增加住院率和医疗费用,而且增加病残率和病死率.现就近年来COPD合并CVD的研究进展作一综述.     

慢性阻塞性肺疾病运动耐力下降的机制及治疗进展

慢性阻塞性肺疾病（chronic obstructive pulmonary disease，COPD）患者的运动耐力下降与气流受限、呼吸肌疲劳、呼吸驱动调节异常、营养不良等因素有关，改善COPD患者的运动耐力，对提高患者的生活质量有重要意义。     

慢性阻塞性肺疾病急性加重期的定义及治疗

慢性阻塞性肺疾病（chronic obstructive pulmonary disease,COPD）是一种以不完全可逆性气流阻塞为特征的疾病状态,通常呈进行性加重。     

Pathology of chronic hepatitis B and chronic hepatitis C

Histologic evaluation of the liver is a major component in the medical management and treatment algorithm of patients with chronic hepatitis B (HBV) and chronic hepatitis C (HCV). Liver biopsy in these patients remains the gold standard, and decisions on treatment are often predicated on the degree of damage and stage of fibrosis. This article outlines the clinical course and serologic diagnosis of HBV and HCV for the clinician and the pathologist, who together have a close working relationship in managing patients with acute and chronic liver disease. The salient histologic features are elucidated in an attempt to provide the clinician with an understanding of the basic histopathology underlying chronic HCV and HBV.     

Sweet's syndrome during the chronic phase of chronic myeloid leukaemia

We report the case of a 52 year-old male in the chronic phase of chronic myeloid leukaemia, with Philadelphia chromosome due to t(9;22) in the karyotype. He was treated with courses of busulfan and hydroxyurea. Fourteen months after initial presentation, the patient developed fever, non-productive cough, maculonodular violaceous painful skin lesions and bilateral pulmonary infiltrates visible on a chest roentgenogram. Laboratory data, repeated bone marrow aspiration and biopsy and karyotype analysis showed findings similar to those of the initial diagnosis. A biopsy taken from one of the trunk lesions was consistent with Sweet's syndrome. Oral methylprednisolone therapy was initiated at doses of 64 mg daily, and the skin lesions and fever were rapidly resolved. When we reduced the steroid dose, skin lesions and fever recurred. Two further courses of steroid therapy were given with similar results. Finally we treated him with naproxen (750 mg daily for 1 month) with a rapid and stable response. This drug should be considered as an alternative treatment for patients with Sweet's syndrome not responding to corticosteroids or for immunocompromised hosts.     

Etiologic theories of chronic prostatitis/chronic pelvic pain syndrome

The etiology of chronic prostatitis/chronic pelvic pain syndrome is unknown. Whereas infection causes category I and II prostatitis, the evidence for an ongoing infection in category III patients is lacking. Immunologic, neurologic, and psychologic factors likely play a role in the development and maintenance of symptoms in these men. The traditional concept of pain as a simple response to a noxious stimulus has some merit, but modern research indicates that the response is much more complex, and we must look at a patient’s physiology and psychology to be able to interpret each individual’s pain response. It is some advance in the field to realize that we probably need to look beyond the prostate and address the entire biopsychosocial problem to be able to offer successful treatment to these men.     

Diagnosis and treatment of chronic gastroparesis and chronic intestinal pseudo-obstruction

Chronic gastroparesis and CIP are debilitating disorders that are difficult to treat with currently available therapies. Failure of proper migration and differentiation of enteric neurons or ICC can result from specific genetic mutations and lead to phenotypes of CIP with or without concomitant gastroparesis. Intestinal dysfunction in diabetes may reflect a depletion of NO production (and perhaps other neurotransmitters or modulators), which is manifest as a syndrome of gastroparesis, diarrhea, or constipation in individual patients. As the key molecular changes underlying these disorders are defined, clinicians will begin to understand their precise etiology and rational medical therapy may become possible. In the future, testable hypotheses regarding the etiology of other functional bowel disorders (e.g., functional dyspepsia, irritable bowel syndrome, and so forth) may be developed.     

Epidemiology of chronic bronchitis and acute infective exacerbations of chronic bronchitis

Acute exacerbations of chronic bronchitis (AECBs) are one of the major causes of morbidity and mortality in the United States, resulting in significant cost to the health care system. Epidemiological information on chronic bronchitis is abundant and has been collected in most industrialized countries. The epidemiology of AECB, however, is less forthcoming. The causes of AECB are multifactorial and include environmental pollutants, allergic responses, and viral and bacterial infections. The role of bacterial infection in AECB is controversial but is believed to account for half of AECB. Because the medical and economic implications of treatment failure in these patients are substantial, an aggressive approach to stratify and treat these patients is necessary. Epidemiological data on chronic bronchitis and acute infective exacerbations of chronic bronchitis will allow us to more precisely define the role of bacterial infection in AECB, and this information may help guide antimicrobial therapy.