结核性胸膜炎发生胸膜肥厚因素的探讨

目的 探讨结核性胸膜炎发生胸膜肥厚的因素。方法 对１９９３年至１９９５年收治的１１３例结核性胸膜炎发生胸膜肥厚的原因进行分析。结果 胸膜服厚的发生与就诊时间,胸水细胞数与蛋白含量及胸穿抽液是否及时有关,与胸水量无关。结论 降低结核性胸膜炎发生胸膜肥厚的重要措施是：（１）积极抗结核治疗及积极胸穿抽液;（２）归口管理。     

结核性胸膜炎发生胸膜肥厚因素的探讨

目的 探讨结核性胸膜炎发生胸膜肥厚的因素。方法 对１９９３年至１９９５年收治的１１３例结核性胸膜炎发生胸马厚的原因进行分析。结果 胸膜肥厚的发生与就诊时间、胸水细胞数与蛋白含量及胸穿抽液是否及时有关，与胸水量无关。结论降低结核性胸膜炎发生胸膜肥厚的重要措施。１．积极抗结核治疗及积极胸穿抽液，２．归口管理。     

利福平注射液胸腔注入治疗结核性胸腔积液

结核性胸腔积液的纤维蛋白沉积于胸膜形成胸膜肥厚,对心肺功能造成危害,胸穿抽液虽可以解除肺及心血管的受压,改善呼吸,但由于胸膜炎症的存在,胸穿抽液后胸水继续渗出。本文在常规治疗基础上,采用利福平注射液(商品名舒兰新,沈阳双鼎制药有限公司生产)胸腔注入治疗结核性胸腔积液,临床观察疗效显著,并发症少,无明显副作用。在胸腔积液消失率、胸水平均消失时间及平均胸腔穿刺次数等方面均明显优于对照组,且其胸膜肥厚粘连及胸腔感染等并发症亦均少于对照组。     

中心静脉导管胸腔闭式持续引流治疗结核性胸腔积液临床研究

临床上结核性胸膜炎较常见,常规胸穿抽液联合抗结核药化疗,部分患者会出现胸膜肥厚、粘连,形成胸液包裹。我科开展了中心静脉导管闭式引流术,并对2004年10月至2008年10月收住我科的结核性胸膜炎患者106例进行了置管持续引流与2001年至2004年132例常规穿刺抽液组,进行回顾性分析,发现发生胸腔积液包裹的病人明显减少,总结如下。     

在急诊室胸穿抽液治疗结核性胸膜炎的探讨

目的探讨急诊室对结核性胸膜炎进行胸穿抽液治疗的可行性。方法434例结核性胸膜炎患者经胸片或胸透检查及胸部B超定位后，在急诊室胸穿抽液治疗。术中、术后注意观察胸膜反应及创伤性气胸等并发症。结果全部病例胸液吸收。经胸片检查，多次胸穿抽液9例出现明显胸膜增厚，余425例胸片检查未见明显胸膜增厚。创伤性气胸及胸膜反应占总病例的4．4％；经治疗转归良好。结论急诊室对未能住院治疗的结核性胸膜炎病人及早进行胸穿抽液，取得较满意疗效，是一可行的治疗方法。     

胸腔置管引流并注入尿激酶治疗结核性胸腔包裹性积液的临床研究

目的探讨胸腔置管引流并注入尿激酶在治疗结核性包裹性胸膜炎的应用价值。方法 90例结核性包裹性胸膜炎病人作为研究对象,并随机分为A、B、C 3组,各30例;A组胸腔置管引流并注入尿激酶;B组胸穿抽液后注入尿激酶;C组单纯胸穿抽液;化疗方案等其它治疗方法相同。结果 A组在胸水消失时间、排液总量、胸膜厚度、肺功能FEV1%和FVC%改善方面均优于B组或C组。结论胸腔置管引流并注入尿激酶治疗结核包裹性积液引流彻底,安全有效,并发症少,能显著减轻胸膜肥厚,改善肺功能。     

胸腔内注入尿激酶预防结核性胸膜炎粘连肥厚的研究

目的探讨胸腔内注入尿激酶(urokinase,UK)对结核性胸膜炎所致胸膜粘连、肥厚的影响。方法40例结核性胸膜炎患者随机分成注药组(20例)和非注药组(20例),注药组每次抽液后注入尿激酶(3~5万u 生理盐水20ml),其他治疗相同。结果注药组抽液次数、抽液量、胸膜厚度、胸膜粘连度与非注药组相比(P值<0.01〉有显著差异。结论胸腔内注入尿激酶能显著增加胸液引流量、能有效降低胸膜粘连、肥厚的程度,与对照组相比差异有显著性。     

胸腔置管联合透明质酸钠防治结核性胸膜炎胸膜肥厚：成本效果分析

目的探索防治结核性胸膜炎胸膜肥厚成本低、效果好的治疗方法。方法64例中至大量游离结核性胸腔积液患者随机分为治疗组和对照组。治疗组胸腔置管完全引流积液后注入透明质酸钠,对照组常规胸穿抽液。统计治疗3个月后2组花费的成本,进行成本效果分析及敏感度分析。 结果59例患者参与最后结果分析。治疗3个月后治疗组、对照组胸膜肥厚发生率是6.7%、31.0%（有效率分别是：93.3%、69.0%）（P＜0.05）;成本效果比（C/E）是35.19,47.53,敏感度分析显示C/E 35.63,49.00。结论胸腔置管联合透明质酸钠防治结核性胸膜炎胸膜肥厚是成本低、效果好的方法。     

结核性脓胸40例临床分析

目的探讨结核性脓胸的发生原因、临床特点及治疗方法。方法寻找结核性脓胸的发生原因及临床特点;在应用抗痨药物的基础上,应用左氧氟沙星（LOFX）脓腔冲洗、尿激酶胸腔内注入（IPUK）等方法进行介入治疗。结果90%的结核性脓胸病人有渗出性结核性胸膜炎（TEP）病史,早期因胸水较少未行胸穿抽液,或胸穿抽液后胸水已少未再抽液;均为局限性脓胸。结论结核性脓胸主要由于TEP早期未积极胸穿抽液,遗留部分胸水转变所致。除合并支气管胸膜瘘外,局限性脓胸介入治疗效果优异,病人痛苦小,花费少,方法简便,安全可靠,值得临床推广。     

结核性胸膜炎合并活动性肺结核89例临床分析

目的总结结核性胸膜炎合并活动性肺结核的治疗方法和疗效评价。方法回顾性分析89例结核性胸膜炎合并活动性肺结核患者的临床资料。结果结核性胸膜炎合并活动性肺结核时,胸水吸收缓慢,易并发胸膜肥厚、粘连和多房性包裹性胸腔积液。结论强有力的抗结核治疗、积极胸腔穿刺抽液和抽液后胸膜腔内注药是治疗的有效方法。     

Subpleural mononuclear cell infiltration. Significance in the differential diagnosis of pleuritis showing nonspecific histologic findings

To determine if patients who had lymphocyte-rich pleural effusion and a pleural biopsy without any specific findings could be histopathologically differentiated between those with tuberculous and nontuberculous pleuritis, we histologically re-evaluated the pleural biopsies of all patients whose pleural effusion was predominant with lymphocytes and contained no malignant cells. A total of 40 patients with a nonspecific histologic findings of pleural biopsy specimen were categorized based on their ultimate diagnosis as having tuberculous (n = 15), carcinomatous (n = 10) or nontuberculous, benign pleuritis (n = 15). The pleural biopsy specimen of patients with nontuberculous, benign pleuritis frequently showed a band-like infiltration of mononuclear cells in the subpleural adipose tissue with minimal pleural inflammatory infiltrate (10 out of 15 patients), while the same finding was infrequent in those with tuberculous pleuritis (0 out of 15, p = 0.0001) and pleuritis associated with carcinoma (three out of 10, p = 0.082). Based on these results, the presence of band-like infiltration of mononuclear cells in the subpleural adipose tissue with minimal pleural inflammatory infiltrate in pleural biopsy specimens of patients with lymphocyte-rich pleural effusion suggests that the pleuritis is nontuberculous in its nature.     

Update on tuberculous pleural effusion

The possibility of tuberculous pleuritis should be considered in every patient with an undiagnosed pleural effusion, for if this diagnosis is not made the patient will recover only to have a high likelihood of subsequently developing pulmonary or extrapulmonary tuberculosis Between 3% and 25% of patients with tuberculosis will have tuberculous pleuritis. The incidence of pleural tuberculosis is higher in patients who are HIV positive. Tuberculous pleuritis usually presents as an acute illness with fever, cough and pleuritic chest pain. The pleural fluid is an exudate that usually has predominantly lymphocytes. Pleural fluid cultures are positive for Mycobacterium tuberculosis in less than 40% and smears are virtually always negative. The easiest way to establish the diagnosis of tuberculous pleuritis in a patient with a lymphocytic pleural effusion is to generally demonstrate a pleural fluid adenosine deaminase level above 40 U/L. Lymphocytic exudates not due to tuberculosis almost always have adenosine deaminase levels below 40 U/L. Elevated pleural fluid levels of γ‐interferon also are virtually diagnostic of tuberculous pleuritis in patients with lymphocytic exudates. In questionable cases the diagnosis can be established by demonstrating granulomas or organisms on tissue specimens obtained via needle biopsy of the pleura or thoracoscopy. The chemotherapy for tuberculous pleuritis is the same as that for pulmonary tuberculosis.     

Der tuberkulöse Pleuraerguss

Approximately one third of the world’s population is infected with Mycobacterium tuberculosis and among communicable diseases tuberculosis is the second leading cause of death. The most common type of tuberculosis is pulmonary tuberculosis. Among the extrapulmonary manifestations, tuberculous pleuritis ranks second only after lymphatic tuberculosis. Tuberculous pleuritis is most commonly a disease with acute onset which is self-limiting in the majority of cases. A large proportion of patients though develop some form of active tuberculosis after a latency period. Therefore the correct diagnosis and the initiation of treatment are of the utmost importance. The easiest way to establish the diagnosis of tuberculous pleuritis is to demonstrate an elevated ADA (adenosine deaminase) in a lymphocytic effusion. Should pleural fluid analysis be nondiagnostic, the diagnosis of tuberculous pleuritis can be established with percutaneous closed needle biopsy in over 80% of cases. All patients with an undiagnosed pleural effusion after closed needle biopsy require thoracoscopy with selected biopsies taken under direct vision. The diagnostic yield of thoracoscopy is close to 100% in tuberculous pleuritis.     

Diagnostic significance of interferon-gamma in tuberculous pleural effusions

STUDY OBJECTIVES: Tuberculosis (TB), the single most frequent infectious cause of death worldwide, also is a major cause of pleural effusion, which in TB usually has lymphocytic and exudative characteristics. Differential diagnosis between TB and nontuberculous pleural effusion can be sometimes difficult, representing a critically important clinical problem. METHODS: We studied 46 patients presenting with pleural effusion to the National Sanyo Hospital between April 2000 and January 2001 (34 men and 12 women; mean age, 64 years). Ten patients (22%) had tuberculous pleurisy, 19 patients (41%) had malignant pleuritis, and 17 patients (37%) had pleural effusion due to an etiology other than tuberculosis or cancer. Pleural fluid concentrations of four suggested markers were measured using commercially available kits. RESULTS: The pleural fluid levels (mean +/- SE) of adenosine deaminase (83.3 +/- 18.2 U/L vs 25.8 +/- 20.4 U/L, p < 0.0001), interferon-gamma (137 +/- 230 IU/mL vs 0.41 +/- 0.05 IU/mL, p < 0.0001), immunosuppressive acidic protein (741 +/- 213 micro g/mL vs 445 +/- 180 micro g/mL, p < 0.001) and soluble interleukin 2 receptor (7,618 +/- 3,662 U/mL vs 2,222 +/- 1,027 U/mL, p < 0.0001) were significantly higher for tuberculous pleuritis than for other causes of effusion. Receiver operating characteristic analysis demonstrated that pleural fluid content INF-gamma was the best indicator of tuberculous pleurisy among four relevant biological markers. CONCLUSIONS: INF-gamma in pleural fluid is the most sensitive and specific among four biological markers for tuberculous pleuritis. Thus, our results suggest that determination of INF-gamma at the onset of pleural effusion is informative for the diagnosis of tuberculous pleuritis. Further studies including larger numbers of patients are needed to verify this result.     

Evaluation of a new inflammatory molecule (triggering receptor expressed on myeloid cells-1) in the diagnosis of pleural effusion

BACKGROUND AND OBJECTIVE: The triggering receptor expressed on myeloid cell-1 (TREM-1) is a newly discovered molecule that is associated with the inflammatory response to microorganisms. We investigated the role of surface and soluble TREM-1 in differentiating different disease entities in pleural effusion formation. METHODS: Sixty-seven patients with pleural effusion due to transudate (14), malignancy (15), tuberculous pleuritis (16), para-pneumonic effusion (10) and empyaema (12) were included in this study. Surface TREM-1 was measured by flow cytometry and was expressed as mean fluorescence intensity and soluble TREM-1 was measured by ELISA and expressed as pg/mL. Results are given as mean levels +/- SEM. RESULTS: Surface TREM-1 was measured in 24 patients and the levels were highest in para-pneumonic effusion (30.0 +/- 8.4) and lowest in malignant pleural effusion (5.2 +/- 1.1) and tuberculous pleuritis (5.2 +/- 2.4). Soluble TREM-1 was highest in effusions of infectious aetiology (para-pneumonic effusion (979.4 +/- 229.6) and empyaema (1712.6 +/- 299.5)) and lowest in non-infectious effusions (transudate (81.2 +/- 4.5 pg/mL) and malignancy (111.3 +/- 20.7). At a cut-off value of 114 pg/mL, soluble TREM-1 yielded a sensitivity of 87.5% and a specificity of 89.7% in differentiating non-infectious effusion from tuberculous pleuritis. At a cut-off value of 374 pg/mL, sTREM-1 yielded a sensitivity of 93.8% and a specificity of 90.9 in differentiating tuberculous pleuritis from bacterial pleural effusion. Conclusion: Soluble and surface TREM-1 are valuable markers in establishing the aetiology of pleural effusions.     

Tuberculous pleuritis with onset of refractory pleural effusion after chemoradiotherapy for esophageal cancer

A 75-year-old man received chemoradiotherapy (CRT) for stage IVa esophageal cancer and complete response (CR) was obtained. However, he was referred to our department for recurrence in an area of esophagus not included in the previously irradiated field. Left pleural effusion increased after admission. Tuberculous pleuritis was eventually diagnosed by thoracoscopic pleural biopsy. It is necessary to accurately diagnose the cause of pleural effusion after CRT, because treatment strategies greatly depend on it. It is also necessary to consider the possible onset of tuberculous pleuritis, in particular, in patients with a history of tuberculosis infection.     

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.     

The usefulness of pleural biopsy in benign or malignant pleurisy

Retrospective studies of pleural biopsy, cytology and ADA in pleural effusion were performed in 116 patients with pleural effusion between 1980 and 1988. Pleural malignant disease was diagnosed in 25 patients (75.8%) by cytology, in 19 patients (57.6%) by pleural biopsy. Thus, cytology should be performed first in patients with pleurisy. Both of cytologic study and CEA in pleural effusion were negative in 3 cases of squamous cell carcinoma. Tuberculous pleuritis was diagnosed in 24 patients (50.0%) by pleural biopsy, in 5 patients (10.4%) by isolation of Mycobacterium tuberculosis. Both pleural biopsy and adenosine deaminase activity (ADA) were examined in 19 cases of tuberculous pleuritis and ADA was elevated in 16 patients (84.2%). These data suggested that pleural biopsy was useful for diagnosis of pleuritis and the combination of cytology, tumor markers and ADA with biopsy improved diagnostic rates of pleuritis.     

胸腔积液中IL-27及Gene Xpert MTB/RIF联合检测有助于结核性胸膜炎的快速诊断

目的：观察胸腔积液中白介素-27（IL-27）、结核杆菌利福平耐药基因（Gene Xpert MTB/RIF）表达水平在结核性胸膜炎快速诊断中的应用价值。方法：回顾性分析128例结核性胸膜炎患者的临床资料，另选择同期收治的128例非结核性胸膜炎胸腔积液患者为对照（恶性胸腔积液组、类肺炎性胸腔积液组与漏出性胸腔积液组分别61例、36例与31例），采用酶联免疫吸附法检测患者胸腔积液中IL-27水平，并予以Gene Xpert MTB/RIF试验，以临床综合诊断结果为金标准，评估IL-27、Gene Xpert MTB/RIF水平在结核性胸膜炎诊断中的应用价值。结果：结核性胸膜炎组胸腔积液中IL-27水平显著高于恶性胸腔积液组、类肺炎性胸腔积液组与漏出性胸腔积液组（F=112.944，P均<0.05）；IL-27诊断结核性胸膜炎的AUC值为0.875，敏感度为73.43%、特异性为85.16%；Gene Xpert MTB/RIF诊断结核性胸膜炎敏感度、特异性分别为77.34%、100.00%；两者联合诊断结核性胸膜炎的敏感度为86.72%，特异性为100.00%。结论：胸腔积液中IL-27、Gene Xpert MTB/RIF水平对结核性胸膜炎的诊断有一定意义，联合检测有助于结核性胸膜炎的诊断。     

良性血性胸腔积液42例临床诊断分析

目的 探讨不同病因引起的良性血性胸腔积液的临床特点.方法 分析我院收治的42例良性血性胸腔积液患者的临床资料.结果 42例患者中有结核性胸膜炎27例,占62.8%,其他良性疾病15例(其中肺炎旁4例,系统性红斑狼疮性3例,类风湿性关节炎2例,充血性心力衰竭2例,结节病1例,肝硬化2例,慢性胰腺炎1例),这些患者在既往史、症状及实验室检查等方面各有其特点.结论 良性血性胸腔积液以结核性胸膜炎为主,亦见于其他良性疾病,如果排除恶性肿瘤,且抗结核治疗效果欠佳,则需仔细询问患者既往史,完善有针对性的实验室检查尽早明确病因,积极治疗原发病以改善预后.