纳洛酮治疗COPD慢性呼吸衰竭60例的临床疗效

目的观察纳洛酮在COPD呼吸衰竭患者出现呼吸抑制的临床疗效。方法120例入选者随机分为对照组和治疗组(在对照组治疗的基础上加用纳洛酮),对比观察抢救成功率和死亡率及治疗前后血气变化。结果治疗组抢救成功率达85%,死亡率15%,与对照组相比有显著差异(P<0·01)。讨论纳洛酮抢救慢性呼衰患者的呼吸抑制不失为一种安全有效的方法,值得临床推广应用。     

醒脑静联合纳洛酮治疗急性重度乙醇中毒的临床观察

目的探讨醒脑静注射液联合盐酸纳洛酮注射液两种药物应用治疗急性重度乙醇中毒的疗效。方法治疗组26例采用醒脑静注射液联合盐酸纳洛酮注射液，对照组22例采用盐酸纳洛酮注射液，其他常规治疗相同，比较两组平均催醒时间和平均呼吸改善时间等指标。结果治疗两组意识转清醒时间（P≤0．05）和平均呼吸改善时间及酒后症状消失时间均短于单用纳洛酮组，两组比较差异均有非常显著性（P≤0．01）。结论醒脑静注射液和盐酸纳洛酮注射液两种药物联合应用治疗急性重度乙醇中毒，疗效明显优于单用盐酸纳洛酮注射液，能明显缩短患者催醒时间和呼吸改善时间及酒后症状消失，提高抢救成功率，临床应用安全、副作用少，值得推广应用。     

纳洛酮加用葛根素治疗急性乙醇中毒的疗效观察

目的 观察纳洛酮与葛根素注射液联用治疗急性乙醇中毒的临床疗效。方法 将56例急性乙醇中毒患者随机分为治疗组和对照组。治疗组30例用纳洛酮与葛根素注射联合治疗；对照组26例单用纳洛酮治疗。观察两组患者症状消失和重症患者清醒时间。结果 治疗组症状消失时间、重症清醒时间均明显短于对照组。结论 纳洛酮与葛根素注射液联用是治疗急性乙醇中毒的有效药物，使用方便，作用迅速，疗效可靠，能提高抢救成功率，降低病死率。     

纳洛酮在37例心肺脑复苏中的应用疗效

目的探讨纳洛酮在37例心肺脑复苏中的应用疗效。方法 2012年2月到2014年3月我院收治突发心跳骤停患者共73例,并随机分为对照组（n=36例）和观察组（n=37例）。两组均给予常规心肺复苏措施,在此基础上给予观察组纳洛酮治疗。对比两组的复苏情况、复苏成功率以及48h生存率。结果观察组在自主循环恢复率、自主呼吸恢复率均高于对照组（χ2自主循环恢复率=7.439,P=0.006;χ2自主呼吸恢复率=7.820,P=0.005）,意识恢复时间低于对照组（t意识恢复时间=6.250,P=0.000）。观察组的复苏成功率、48h生存率分别为51.4%、45.9%,对照组分别为22.2%、16.7%,观察组均显著高于对照组（χ2复苏成功率=6.643,P=0.010;χ2生存率=7.249,P=0.007）。结论在心肺脑复苏过程中,应用纳洛酮能够改善患者的呼吸循环,提高复苏成功率和生存率,应大力推广。     

血栓通联合纳洛酮治疗急性脑梗死30例疗效观察

目的观察血栓通联合纳洛酮治疗急性脑梗死的临床疗效。方法将60例进展型脑梗死患者随机分为常规治疗组（对照组）和血栓通联合纳洛酮治疗组（治疗组）各30例。分别对两组患者治疗前、治疗14d后的神经功能缺损及临床疗效进行评价。结果两组治疗后14d的神经功能缺损较治疗前均有明显改善（P〈0．01）,治疗组与对照组比较有显著性差异P〈0.01。治疗14d后,治疗组总有效率（83．33％）明显高于对照组（66．67％）,P〈0．05。结论血栓通联合纳洛酮治疗急性脑梗死有良好疗效,值得临床推广应用。     

纳洛酮治疗重度有机磷中毒呼吸抑制的疗效观察

纳洛酮自应用于临床后,其治疗范围在不断地拓展,在危重急症患者的抢救中,已显示出广泛的用途和独特的疗效。本文就我院1998年以来,应用纳洛酮抢救重度有机磷农药中毒所致呼吸抑制,收到了明显疗效,报告如下。临床资料一般资料　符合诊断标准[1]的口服有机磷农药中毒58例,分为两组:对照组28例,为1996年6月至1997年12月的住院病例;治疗组30例,为1998年1月至1999年6月的住院病例。两组患者在年龄、性别、毒物种类、中毒量、中毒时间均基本相似,具有可比性。治疗方法　对照组在常规解毒剂治疗的基础上,对28例呼吸抑制的患者给予可拉明、洛贝林交…     

七叶皂甙钠联合纳洛酮治疗外伤性脑梗死

目的 观察七叶皂甙钠联合纳洛酮治疗外伤性脑梗死（TCI）的临床疗效。方法 将52例TCI病人随机分为两组。治疗组28例采用七叶皂甙钠和纳洛酮治疗，对照组24例采用常规治疗，观察两组的生活能力状态及疗效。结果 治疗组总有效率82．14％，明显优于对照组的62，50％（X^2=6．44，P〈0．05），生活能力状态优于对照组（X^2=4，18，P〈0，05）。结论 七叶皂甙钠和纳洛酮合用治疗TCI可提高疗效。     

纳洛酮和奥扎格雷钠联合治疗急性脑梗死临床观察

目的探讨纳洛酮联合奥扎格雷钠治疗急性脑梗死的临床疗效。方法将68例急性脑梗死患者随机分为两组，对照组应用纳洛酮注射液治疗，治疗组联用纳洛酮注射液和奥扎格雷钠注射液。1个疗程后比较两组临床疗效、神经功能缺损评分和血液流变学的变化。结果治疗组总有效率为94．3％，明显优于对照组的70．0％（P〈0．05）；治疗后治疗组神经功能缺损评分、血液流变学各项指标改善均优于对照组（P〈0．05）。结论纳洛酮联合奥扎格雷钠能提高脑梗死患者的临床治疗效果。     

高压氧联合纳洛酮治疗一氧化碳中毒疗效观察

目的 观察高压氧联合纳洛酮治疗急性一氧化碳中毒的疗效。方法42例符合急性一氧化碳中毒的患者随机分为2组，治疗组22例，对照组20例。在常规治疗的基础上，治疗组给予高压氧联合纳洛酮治疗，对照组只给予高压氧治疗；每10d为一疗程，4个疗程后评价疗效。结果治疗组治愈19例（86．36％），显效3例（13．64％），无效0例（0％）；对照组治愈10例（50．00％），显效7例（35．00％），无效3例（15．00％），差异有统计学意义（P〈0．05）；两组后遗症比较差异有统计学意义。结论高压氧联合纳洛酮治疗急性一氧化碳中毒疗效显著。     

纳洛酮治疗早产儿原发性呼吸暂停疗效观察

目的观察纳洛酮治疗早产儿原发性呼吸暂停的临床疗效。方法将诊断为原发性呼吸暂的78例早产儿随机分为两组,对照组38例给予常规治疗,治疗组40例在常规治疗基础上用纳洛酮,比较两组患者的疗效。结果治疗组和观察组间差异有统计学意义(P<0.05)。结论纳洛酮治疗早产儿原发性呼吸暂停疗效显著。     

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.