86例双侧胸腔积液临床分析

目的探讨双侧胸腔积液病因及临床特点。方法对８６例双侧胸腔积液进行回顾性分析。结果①结核性４８例（５５．８％），肿瘤转移２８例（３２．５％），其他原因１０例（１１．７％）。②血性胸水在恶性胸水和结核性胸水中分别占５７％（１６／２８）和３１％（１５／４８）（Ｐ＜０．０５）。③胸水ＣＥＡ在恶性胸水和结核性胸水中阳性率分别占８０％（１６／２０）和２．５％（１／４０）（Ｐ＜０．０１）。④胸水ＡＤＡ值以≥２６Ｕ／Ｌ为阳性时，恶性胸水和结核性胸水阳性率分别占９％（２／２２）和４２．５％（１４／３３）（Ｐ＜０．０１）。⑤少量胸水占恶性胸水与结核性胸水中分别占５０％（１４／２８）和７５％（３６／４８）（Ｐ＜０．０５）。结论双侧胸腔积液多见于结核与肿瘤；少量积液多见于结核性胸水；血性胸水多见于肿瘤转移；胸水ＣＥＡ及ＡＤＡ测定对良、恶性胸水有鉴别价值。     

72例心包积液病因及误诊分析

目的 分析72例心包积液病因及误诊原因。方法 回顾分析2000年1月-2006年3月诊断有心包积液的病例72例。结果 心包积液病因依次是肿瘤性（22．2％）；结核性（16．7％）；心力衰竭性（12．5％）；非特异性（11．1％）；甲状腺机能减退性（8．3％）；其他病因及诊断不明的占29．2％。结论 肿瘤性心包积液发病率最高，且肿瘤性心包积液误诊为结核性及非特异性最高。     

86例双侧胸腔积液临床回顾分析

目的：探讨双侧胸腔积液病因及临床特点。方法；对８６例双侧胸腔积液进行回顾性分析，结果：（１）结核性４８例（５５．８％）肿瘤转移２８例（３２．５％）其他原因１０例（１１．７％）（２）血性胸水在恶性和结核性胸水中分别上占５７％（１６／２８）和３１％（１５／４８）（Ｐ〈０．０５），（３）胸水ＣＥＡ在恶性胸水和结核性胸水中阳性率分别为８０％（１６／２０）和２．５％（１／４０）（Ｐ〈０．０１），（４）胸水Ａ     

食管测压对反流性食管炎的诊断价值

目的探讨食管测压对反流性食管炎的诊断价值．方法使用专用软件控制的高分辨多道灌注测压系统（ＰＣｐｏｌｙｇｒａｆＨＲ瑞典产）测定了正常人１２例及反流性食管炎患者３２例的食管下括约肌动力指标、胸腹段长度及食管体动力参数．结果患者组ＬＥＳＰ，ＬＥＳＲＰ压力（ｋＰａ）明显低于对照组（１０±０７对２６±１０；０１±０４对０４±０２，Ｐ均＜００１）；食管中远段振幅（ｋＰａ）亦低于对照组（干咽：４６±３３对６５±２６，５３±３７对９１±３７，Ｐ均＜００５；湿咽：５３±３３对８９±３６，６１±４６对±１２４±４５，Ｐ均＜００５）．患者组ＬＥＳＬ１（ｃｍ）比对照组短（１７±０８对２６±０９，Ｐ＜００１）．结论反流性食管炎患者ＬＥＳＰ低下，ＬＳＥＬ１过短，食管体中远段动力低下，为临床选用动力药提供了客观依据     

老年与老年前期消化性溃疡临床对比分析

目的研究老年人消化性溃疡的临床特点。方法回顾性分析我院１９９１年至１９９５年收治的２４６例老年人消化性溃疡，与同期住院的２８７例老年前期患者作对比。结果老年胃溃疡占同期胃溃疡住院人数的构成比已由１９９１年的２６．１％上升至１９９５年的３５．６％。老年组无规律性上腹痛，恶心呕吐，腹胀，体重减轻，黑便分别为４８．０％，５６．９％，４７．２％，３３．３％，４１．１％，高于对照组（分别为２５．８％，３３．５％，２５．１％，１７．１％，２８．９％）（Ｐ＜０．０１）。老年组并发大出血２１．６％，急性穿孔２１．３％，幽门梗阻９．８％；对照组分别为１０．１％，１３．９％，１７．４％。２组相比有显著性差异（Ｐ＜０．０１或Ｐ＜０．０５）。老年组溃疡大于２．５ｃｍ者占２３．２％，多于对照组（１２．５％）（Ｐ＜０．０１）。结论老年人胃溃疡发病率逐年上升，症状体征不典型，并发出血及穿孔多且严重，巨大溃疡较多     

第1批肺结核短程化疗研究5年随防报告

本文采用６及９个月ＨＲＥ短化方案与３ＳＨＰ／１５ＨＰ标化方案进行近、远期疗效的对照研究。前次报告已验证两个短化方案与标化方案的近期疗效极为相似。满疗程的４８１例进行随防观察，５年中失访５６例。复发１５例，其中１２例在停药后１年半内复发。６及９个月短化方案的细菌及Ｘ级总复发率分别为５．８％和１．１％，与标化组（３．９％）比较无显著性差异（Ｐ＞０．０５）；但６ＨＲＥ组复发高于９ＨＲＥ组（Ｐ＜０．０５）     

115例心包积液患者病因及误诊分析

目的分析115例心包积液患者的病因变化及误诊原因。方法收集我院1995～2004年收治的115例心包积液患者的临床资料并进行回顾性分析。结果心包积液常见病因依次为肿瘤性(19.1%)、结核性(18.3%)、非特异性(13.9%)、心力衰竭性(12.2%)、尿毒症性(6.1%)和结缔组织疾病(5.2%),其他各种原因引起者占14.8%,肿瘤已成为心包积液的首要病因。误诊8例。结论肿瘤是心包积液的首要病因。误诊的主要原因是将肿瘤性心包积液诊断为其他性质的心包积液。     

Inoue气囊经皮瓣膜成形术治疗成人肺动脉瓣狭窄

１９８５年１２月至１９９４年８月，５３例成人先天性肺动脉瓣狭窄（ＰＳ）患者用Ｉｎｏｕｅ气囊进行经皮肺动脉瓣成形术（ＰＢＰＶ），成功率为１００％，无严重并发症。术后ＰＶＤ口压力阶差从９０．９±４５．９ｍｍＨｇ减至３８．１±３２．３ｍｍＨｇ（Ｐ＜０．００１）。ＰＶ口直径从８．９±３．６ｍｍ增至１７．４±４．６ｍｍ（Ｐ＜０．００１）。在６．４±２．８（０．８至９．５）年的随访期，心功能保持在Ⅰ级至Ⅱ级，其中９例重行心导管术检查，术前术后及随访的ＰＶ压力阶差分别为１０６．９±４７．７ｍｍＨｇ、５０．１±２９．２ｍｍＨｇ及２９．６±１６．０ｍｍＨｇ（术前比术后及随访Ｐ＜０．０５）；ＰＶ口径分别为８．２６±１．４、１７．２±２．０５及１８．７±１．３ｍｍ（Ｐ＜０．００１）（术前比术后及随访Ｐ＜０．０５）．认为Ｉｎｏｕｅ气羹ＰＢＰＶ对ＰＳ是有效和安全的方法，远期疗效满意。     

溶栓治疗老年急性心肌梗塞患者的利弊分析

将１０６例急性心肌梗塞（ＡＭＩ）患者分为两组,≥７０岁组３１例,＜７０岁组７５例,均在发病６小时内接受尿激酶静脉溶栓治疗。结果：≥７０岁组与＜７０岁组比较,血管再通率分别为６７．７％及７０．６％（Ｐ＞０．０５）,４周病死率分别为６．５％及５．３％（Ｐ＞０．０５）,左室射血分数（ＬＶＥＦ）分别为０．４９±０．１２及０．５１±０．１４（Ｐ＞０．０５）,出血并发症分别为４５．１％及２０％（Ｐ＜０．０１）。血管再通者与血管未通者比较,病死率分别为２．７％及１２．５％（Ｐ＜０．０５）,ＬＶＥＦ分别为０．５６±０．１４及０．４４±０．１１（Ｐ＜０．０１）。因此认为,溶栓治疗ＡＭＩ的疗效与年龄无关,而与血管是否再通密切相关。老年ＡＭＩ患者行溶栓治疗虽出血等并发症高,但其利大于弊。     

家兔急性缺血性心力衰竭心机械功能动态变化特征及其对临床的启示

为探讨急性缺血性心力衰竭（ＨＦ）形成过程中心机械功能变化特征及其意义，观察８只家兔，于冠状动脉左室支结扎后，不同时间点的左室收缩、舒张及射血功能的变化趋势，并与７只假手术家兔比较。结果:与假手术兔比较，ＨＦ兔于拮扎后５ｍｉｎ，１５ｍｉｎ，３０ｍｉｎ，６０ｍｉｎ，１２０ｍｉｎ和１８０ｍｉｎ，左室内压上升最大速率分别降低:２２．３％，１８．３％，８．４％，７．４％，２３．８％和４１．８％（均Ｐ＜０．０５）；左室收缩峰压分别降低:２３．８％（Ｐ＜０．０５），１０．７％（Ｐ＜０．０５），６．４％，６．９％，１３．９％（Ｐ＜０．０５）和４０．８％（Ｐ＜０．０５）；左室内压下降最大速率分别降低３２．９％，２０．０％，１３．９％，１１．８％，２８．８％和４５．５％（均Ｐ＜０．０５）；左室舒张末压分别升高:３８０．０％，２５０．０％，２６０．０％，２４３．８％，７２６．７％和１４５０％（均Ｐ＜０．０５）；心输出量分别降低:０．４％，４．０％，７．４％，１２．４％（Ｐ＜０．０５），２３．４％（Ｐ＜０．０５）和３６．９％（Ｐ＜０．０５）。结果表明，心脏收缩与舒张功能于冠脉结扎后呈急剧下降－缓慢恢复－再继续下降的变化，尤以舒张功?     

基质金属蛋白酶9和基质金属蛋白酶组织抑制物1在不同性质胸腔积液诊断和鉴别诊断中的应用

目的 探讨基质金属蛋白酶9(MMP-9)、基质金属蛋白酶组织抑制物1(TIMP-1)及MMP-9/TIMP-1比值在结核性和仲瘤性胸腔积液形成过程中的作用及在上述胸腔积液诊断和鉴别诊断中的价值.方法 采用ELISA法测定36例结核性胸膜炎、38例恶性肿瘤和14例漏出液患者胸水中MMP-9和TIMP-1的浓度.结果 ①结核性胸腔积液组胸水中MMP-9浓度、TIMP-1浓度和MMP-9/TIMP-1比值均高于恶性胸腔积液组和漏出液组(P值均＜0.05),恶性胸腔积液组上述指标均高于漏出液组(P值均＜0.05).②恶性胸水脱落细胞学检查阳性组MMP-9浓度、MMP-9/TIMP-1 均高于细胞学检查阴性组(P值均＜0.05),TIMP-1浓度低于细胞学检查阴性组(P＜0.05).③MMP-9和TIMP-1之间呈正相关(r=0.239,P=0.025);MMP-9、MMP-9/TIMP-1分别与胸水乳酸脱氢酶、腺苷脱氨酶、蛋白质、白细胞总数、淋巴细胞比例之间显著正相关(P值均＜0.01);MMP-9、MMP-9/TIMP-1分别与胸水葡萄糖、氯化物之间呈显著负相关(P值均＜0.01);TIMP-1与乳酸脱氢酶、腺苷脱氨酶、蛋白质、淋巴细胞比例之间呈显著正相关(P值均＜0.01).④胸水中MMP9、TIMP-1、MMP-9/TIMP-1比值在恶性胸腔积液诊断中的敏感性分别为63.2%、71.1%和65.8%,特异性分别为83.3%、63.9%和80.6%.采用胸水MMP-9和TIMP-1串联联合检测的敏感性和特异性分别为39.5%和91.7%,并联联合检测的敏感性和特异性分别为94.7%和55.6$%.结论 MMP-9和TIMP-1与结核性胸膜炎和恶性胸腔积液的形成密切相关,MMP-9/TIMP-1比例的失衡在此过程中扮演了重要角色,胸水MMP-9、TIMP-1及MMP-9/TIMP-1比值的检测有助于结核性胸膜炎和恶性肿瘤所致胸腔积液的鉴别诊断.     

大量心包积液病因影响因素的回顾性分析

目的 收集并分析41例大量心包积液患者病因的影响因素，为诊治大量心包积液提供更为清晰诊疗思路。方法 根据2015年欧洲心血管病学会《心包疾病的诊断和治疗指南》诊断大量心包积液的标准，收集2017.1.1-2019.10.1期间入住福建省立医院及福建省立金山医院的大量心包积液患者41例，根据其病因诊断将所有入组对象分为4组：结核性心包积液组（TB组）、恶性肿瘤性心包积液组（MT组）、非TB感染性心包积液组（NTB组）及其他病因心包积液组（OE组）。采用SPSS统计软件分析所有入组患者心包积液患者病因的影响因素。结果 41例大量心包积液患者中男性24人，女性17人，平均年龄为60.3±14.9岁。TB组、MT组、NTB组及OE组患者分别占24.4%，24.4%，29.3%，21.9%。按照Light标准的定义，大量心包积病例中97.6%为渗出液。结核性心包积液的腺苷脱氨酶水平最高，达57.0±37.3U/L，远高于其他病因所致的心包积液（P<0.01）。腺苷脱氨酶诊断结核性心包积液的ROC曲线下面积0.961，最佳诊断切点为20.5U/L，此时敏感性达100%，特异性达80.6%。多元Logistics回归分析显示大量心包积液病因的主要影响因素有血红蛋白、心包积液腺苷脱氨酶水平和心包积液癌胚抗原水平。结论 本研究发现大量心包积液最常见病因是结核和恶性肿瘤，腺苷脱氨酶是诊断结核性心包积液的敏感指标，Light标准无法鉴别大量心包积液的病因，血红蛋白、心包积液腺苷脱氨酶和心包积液癌胚抗原是影响大量心包积液病因判定的重要指标，具有一定临床指导意义。     

恶性胸膜间皮瘤误诊为结核性胸膜炎17例原因分析

目的 探索恶性胸膜间皮瘤(malignant pleural mesothelioma,MPM) 的临床特点,分析其与结核性胸膜炎(tuberculous pleural effusion,TPE)的临床差异,以减少误诊。方法 回顾性分析盘锦市传染病医院2010—2017年收治的 17例 MPM 误诊为TPE的患者临床资料,以了解误诊原因及提出避免措施。结果 本组MPM患者以男性(70.6%,12/17)、>40岁者(70.6%,12/17)多见,仅1例患者明确有石棉接触史;右侧(52.9%,9/17)多于左侧(35.3%,6/17);临床表现以胸痛(82.4%,14/17)最多见,发热(17.6%,3/17)较少见;误诊时间6d至18个月,平均(80.6±132.6)d。初诊时17例胸腔积液脱落细胞、抗酸杆菌检查均为阴性,结核菌素皮肤试验(PPD试验)阳性8例(47.1%),其中强阳性2例;血T-SPOT.TB阳性6例(35.3%)。胸腔积液生化检测:胸腔积液均为渗出性,11例(64.7%)为黄色,白细胞(WBC)计数以淋巴细胞为主(50%~86%),计数为1300~7500×10⁶/L(正常值<100×10⁶/L);乳酸脱氢酶(LDH)[280~1520U/L(正常值<200U/L),平均(439.76±301.82)U/L]均升高,腺苷脱氨酶(ADA)升高6例(35.3%)[32~56U/L(正常值4~24U/L),平均(26.76±11.96)U/L];血癌胚抗原(CEA)均未见升高,胸腔积液CEA升高2例(11.8%)[分别达8.6μg/L和9.2μg/L(正常值≤5μg/L)];CT检查均有胸膜增厚,11例(64.7%)胸膜增厚超过1cm。最终17例患者均经过组织病理检查确诊,其中胸腔穿刺胸膜活检确诊7例、胸腔镜取组织活检确诊9例、开胸手术病理检查确诊1例;病理检查结果多为MPM上皮样型11例(64.7%)。 结论 MPM的临床表现、实验室检查、早期CT表现同TPE患者相比较缺乏特异性,易误诊为TPE;确诊需依靠组织病理活检或手术病理检查。     

结核γ-干扰素酶联免疫斑点检测在结核性心包积液诊断中的应用

目的 探讨结核菌特异性γ-干扰素（interferon-gamma,IFN-γ）酶联免疫斑点（enzyme-linked immunosorbent spot,ELISPOT）检测对结核性心包积液的诊断价值.方法 采用结核菌特异性IFN-γ ELISPOT技术同时检测20例结核性心包积液患者（TP组）和14例非结核性心包积液患者（Non-TP组）外周血单核细胞（peripheral blood mononuclear cells,PBMC）及心包积液单核细胞（pleural effusion mononuclear cells,PEMC）中结核菌特异性IFN-γ水平.结果 TP组PBMC和PEMC结核菌特异性IFN-γ水平均显著高于Non-TP组,差异有统计学意义（P＜0.01,P＜0.01）.TP组心包积液中结核菌特异性IFN-y水平显著高于外周血IFN-γ水平,差异有统计学意义（P＜0.01,P＜0.01）.PBMC ELISPOT检测结核性心包积液的敏感性和特异性分别为80.0％和85.7％;而PEMC ELISPOT敏感性和特异性为90.0％和85.7％.结论 结核菌特异性IFN-γELISPOT技术对结核性心包积液诊断和鉴别诊断具有很好的辅助价值.     

Etiology and prognostic implications of a large pericardial effusion in men

To assess the etiology and prognosis of a large pericardial effusion, we reviewed 25 consecutive patients who presented with a large pericardial effusion and underwent a drainage procedure. Large pericardial effusion was defined as: (1) an echo-free space greater than or equal to 10 mm anteriorly and posteriorly by M-mode echocardiography and (2) removal of greater than or equal to 350 ml of fluid at pericardial drainage. The etiologies of large pericardial effusion were: neoplastic (36%), idiopathic (32%), uremic (20%), postmyocardial infarction (8%), and acute rheumatic fever (4%). Of our patients, 44% presented with cardiac tamponade, while 25% of patients with idiopathic pericarditis had hemorrhage effusion and cardiac tamponade. At follow-up, 37 +/- 17 months after pericardial drainage, 68% had died from complications of their underlying disease. There were no deaths attributed to pericardial disease. While 88% of patients with idiopathic large pericardial effusion were alive at follow-up, none of the neoplastic large pericardial effusion patients survived longer than 5 months after initial pericardial drainage (p less than 0.001). Additionally, the survival of patients with uremic large pericardial effusion was better than patients with neoplastic large pericardial effusion (p less than 0.05). We conclude: (1) neoplastic, idiopathic, and uremic pericarditis are the most common causes of large pericardial effusion in men, (2) idiopathic pericarditis can be hemorrhagic and cause cardiac tamponade, and (3) the prognosis of large pericardial effusion is related to patients' underlying disease.     

Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?

STUDY OBJECTIVES: The decrease in incidence of tuberculosis, along with the increase in invasive cardiovascular procedures, may have changed the frequency of causes of bloody pericardial effusion associated with cardiac tamponade, although this is not yet recognized by medical textbooks. We analyzed the causes of bloody pericardial effusion in the clinical setting of cardiac tamponade in the 1990s; patients' survival; the effect of laboratory results on discharge diagnosis; and how often bloody pericardial effusion is a presenting manifestation of a new malignancy or tuberculosis. DESIGN: Retrospective, observational, single-center study. SETTING: A community hospital. PATIENTS: The charts of all patients who underwent pericardiocentesis for cardiac tamponade and had bloody pericardial effusion were retrospectively reviewed. RESULTS: Of 150 patients who had pericardiocentesis for relieving cardiac tamponade, 96 patients (64%) had a bloody pericardial effusion. The most common cause of bloody pericardial effusion was iatrogenic disease (31%), namely, secondary to invasive cardiac procedures. The other common causes were malignancy (26%), complications of atherosclerotic heart disease (11%), and idiopathic disease (10%). Tuberculosis was detected as a cause of bloody pericardial effusion in one patient and presumed to be the cause in another patient. Bloody pericardial effusion was found to be a presenting manifestation of a newly diagnosed malignancy in two patients. The patients in the idiopathic and iatrogenic groups were all alive and had no recurrence of pericardial effusion at 24 +/- 27 and 33 +/- 21 months after hospital discharge, respectively, whereas 80% of patients with malignancy-related bloody effusions died within 8 +/- 6 months. CONCLUSIONS: In a patient population that is reasonably representative of that in most community hospitals in the United States, the most common cause of bloody pericardial effusion in patients with signs or symptoms of cardiac tamponade is now iatrogenic disease. Of the noniatrogenic causes, malignancy, complications of acute myocardial infarction, and idiopathic disease predominated. Hemorrhagic tuberculous pericardial effusions are uncommon and may likely reflect a low incidence of cardiac tuberculosis in community hospitals in the United States.     

Pericardial effusion in the course of myocardial infarction: incidence, natural history, and clinical relevance

Incidence and significance of pericardial effusion in patients with acute myocardial infarction (AMI) have not been established. To evaluate these issues, we studied prospectively 138 consecutive patients with AMI. An echocardiogram was obtained in each 1, 3, and 10 days and 3 and 6 months after admission. Fifty four patients with unstable angina and 57 without heart disease were studied as controls. Echocardiographic diagnostic criteria of pericardial effusion were established from 33 additional patients undergoing surgery. Pericardial effusion was found in 28% of patients with AMI. Twenty-five percent of patients with AMI had pericardial effusion on the third day, vs 8% of patients with unstable angina (p less than .02) and 5% of patients without heart disease (p less than .01). At 1, 3, and 10 days and 3 and 6 months prevalence of pericardial effusion was 17%, 25%, 21%, 11%, and 8%, respectively. There was no case of tamponade. Pericardial effusion was more common in anterior AMI (p less than .02) and in patients with heart failure (p less than .05) but it was not significantly associated with early pericarditis, peak creatine kinase-MB, the level of anticoagulation, or mortality. Thus, pericardial effusion is a common event in patients with AMI (incidence of 28%), but does not result in specific complications. The reabsorption rate of pericardial effusion is slow and, in our experience, mild or moderate pericardial effusion does not preclude heparin therapy.     

Adenosine deaminase 2 in the diagnosis of tuberculous pleuritis

PURPOSE: We examined the usefulness of adenosine deaminase 2 (ADA2) in the diagnosis of tuberculous pleuritis. SUBJECTS: A hundred cases, 78 male and 22 female, with pleural effusion were examined. With regard to pleural effusion, 18 cases were transudate and 82 cases (9 tuberculous pleuritis, 27 lung cancer, 8 mesothelioma, 5 malignant diseases except lung cancer and mesothelioma, 5 benign asbestos pleurisy, 10 empyema, 10 parapneumonic effusion, one SLE, one parasitic infection, and 6 undetermined etiology) were exudates. The last 6 cases with unknown origin were excluded in this study. RESULTS: Pleural adenosine deaminase (ADA) was 90.4 +/- 22.4 U/l (mean +/- SD) and pleural ADA2 was 80.4 +/- 21.9 U/l in tuberculous pleuritis, both were significantly higher than those in non-tuberculous exudates (p < 0.001). In the diagnosis of tuberculous pleuritis, pleural ADA showed 100% sensitivity and 88% specificity, whereas pleural ADA2 showed 100% sensitivity and 91% specificity. CONCLUSION: Pleural ADA2 is useful in the diagnosis of tuberculous pleuritis, which has similar sensitivity and a little better specificity compared with pleural ADA.