The management of pleural space infections

Pleural infection is responsible for significant morbidity and mortality worldwide, and its clinical management is challenging. The diagnosis of empyema and tuberculous pleurisy may be difficult, and these conditions may be confused with other causes of exudative pleural effusions. Complicated parapneumonic effusion or empyema may present with 'atypical' clinical features; delays in diagnosis are common and may contribute to the high mortality of these infections. Pleural aspiration is the key diagnostic step; pleural fluid that is purulent or that has a pH < 7.2, or organisms on Gram stain or culture, is an indication for formal intercostal drainage. In order to achieve a definitive diagnosis of tuberculous pleurisy, Mycobacterium tuberculosis must be isolated in the culture of pleural fluid, pleural tissue or sputum; demonstration of granulomas in pleural tissue is also suggestive of tuberculosis. The use of pleural fluid biochemical markers, such as adenosine deaminase, in the diagnosis of tuberculous pleurisy varies among clinicians; the diagnostic value of such markers is affected by the background prevalence of tuberculosis and the likelihood of an alternative diagnosis. Uncertainties also remain regarding the treatment of pleural infection. Treatment of complicated parapneumonic effusion and empyema involves prolonged courses of antibiotics and attention to the patient's nutritional state. The role of intrapleural fibrinolytics and the optimal timing of surgical intervention are unknown. The lack of clear predictors of clinical outcome in empyema contributes to the difficulty in treating this condition. The pharmacological treatment of tuberculous pleurisy is the same as for pulmonary tuberculosis; the precise role of steroids in the treatment of tuberculous pleurisy remains uncertain.     

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.     

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.     

Discrimination of exudative pleural effusions based on multiple biological parameters.

Pleural effusion is a common complication of various diseases. Conventional methods are not always capable of establishing the cause of pleural effusion, so alternative tests are needed. The aim of this study was to explore means of discriminating between different pleural effusion groups, malignant, parapneumonic and tuberculous, based on the combined function of seven biological markers. Adenosine deaminase (ADA), interferon-gamma, C-reactive protein (CRP), carcinoembryonic antigen, interleukin-6, tumour necrosis factor-alpha and vascular endothelial growth factor concentration levels were measured in pleural fluid from 45 patients with malignant, 15 with parapneumonic and 12 with tuberculous pleural effusion. Receiver operating characteristic curve analysis, multinomial logit modelling and canonical variate analysis were applied to discriminate the pleural effusion groups. The three groups could be discriminated successfully using the measured markers. The most important parameters for discrimination were ADA and CRP concentration levels. An individual with an ADA concentration level of >45 U.L(-1) and a CRP concentration of <4 mg.dL(-1) was more likely to belong to the tuberculous pleural effusion group, whereas one with an ADA concentration level of <40 U.L(-1) and a CRP concentration of >6 mg.dL(-1) was more likely to belong to the parapneumonic pleural effusion group, and one with a CRP concentration of <4 mg.dL(-1) to the malignant pleural effusion group. The combination of adenosine deaminase and C-reactive protein levels might be sufficient for discriminating between the three different groups of exudative pleural effusion: malignant, tuberculous and parapneumonic.     

Differential diagnosis of tuberculous pleurisy by measurement of cytokine concentrations in pleural effusion

Study objective: Measurement of cytokine concentration in serum and pleural effusion may be useful in the differential diagnosis of tuberculous pleurisy.Patients and methods: We compared the biochemical properties and concentrations of cytokines in serum and pleural effusion samples of 18 patients with tuberculous pleurisy, 7 patients with parapneumonic pleurisy, and 25 patients with malignant pleurisy.Results: A high value of adenosine deaminase (ADA) was observed in pleural effusion of patients with tuberculosis. The serum concentrations of interleukin (IL)-1-beta, IL-2, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha were similar among the three groups. However, the concentration of IFN-gamma in pleural effusion was high in tuberculous patients, and that of TNF-alpha was high in tuberculous and parapneumonic pleural fluid, but both cytokines were low in malignant pleural fluid. The sensitivity, specificity and accuracy of IFN-gamma in the diagnosis of tuberculous pleurisy were 94%, 100% and 98%, respectively. Similarly, those of TNF-alpha for the diagnosis of infectious pleurisy including tuberculous and parapneumonic pleurisy were 88%, 80% and 84%, respectively.Conclusions: Our results indicate that simultaneous measurement of IFN-gamma and TNF-alpha in pleural effusion is a useful diagnostic tool for differentiating tuberculous pleurisy from parapneumonic and malignant pleurisy.     

Diagnosis and treatment of tuberculous pleurisy--with special reference to the significance of measurement of pleural fluid cytokines

Tuberculous pleurisy as well as malignant pleuritis is a representative disease presenting pleural effusion. The diagnosis of tuberculous pleurisy is made from examination of pleural effusion, but the sensitivity of smear or culture of Mycobacterium tuberculosis from pleural fluid is generally low. Although the pleural fluid concentration of adenosine deaminase (ADA) is useful in terms of sensitivity or specificity, the value could be high in empyema or rheumatoid pleuritis. Thoracoscopic biopsy of pleura is more sensitive rather than conventional percutaneous needle biopsy, but is more invasive. Tuberculous pleural effusion is caused by delayed allergy which macrophage and T-helper 1 cells mainly relate and the stimuli of bacterial body consecutively induces T-helper 1 cytokines. Pleural fluid interferon-gamma (INF-gamma) is important not only in pathogenesis but also in diagnosis. We demonstrated that INF-gamma is a more sensitive and specific indicator for tuberculous pleurisy than ADA using receiver operating characteristics (ROC) analysis. Cytometric bead array (CBA) is a tool to simultaneously measure abundance of various cytokines and is expected to be a very useful method to provide informations for understanding a feedback mechanism of cytokine network. It is needed to clear the immunity in pleural fluid and to establish the less invasive and more useful method to diagnose tuberculous pleurisy.     

结核性与癌性胸腔积液的实验室检测比较研究

目的比较研究实验室检测腺苷脱氨酶(ADA)、乳酸脱氢酶(LDH)、癌胚抗原(CEA)、蛋白(TP)、葡萄糖(GLU)等多项指标对结核性与癌性胸腔积液的鉴别诊断价值。方法对151例明确诊断为结核性或癌性胸腔积液分别测定胸水ADA、LDH、CEA、TP、GLU和血清TP,并进行统计分析。结果结核性胸腔积液中ADA、LDH、TP含量都明显高于癌性胸腔积液,其中胸水ADA以28U/L作为诊断结核性胸水的临界值则其敏感性和特异性均极高,结核性胸水中GLU含量则低于癌性胸水,癌性胸水CEA的阳性率高达76.0%,而结核性胸水CEA均阴性。结论联合检测胸水ADA、LDH、CEA、TP和GLU可以作为结核性与癌性胸腔积液的诊断和鉴别诊断依据,其中ADA28U/L可以考虑作为结核性胸腔积液的单独诊断依据。     

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.     

Diagnostic value of adenosine deaminase in nontuberculous lymphocytic pleural effusions.

Adenosine deaminase (ADA) can aid in the diagnosis of tuberculous pleural effusions, but false-positive findings from lymphocytic effusions have been reported. The purpose of this study is to assess the ADA levels in nontuberculous lymphocytic pleural effusions (lymphocyte count > 50%) of different aetiologies. Altogether, 410 nontuberculous lymphocytic pleural fluid samples were consecutively selected. These included malignant effusions (n = 221), idiopathic effusions (n = 76), parapneumonic effusions (n = 35), postcoronary artery bypass graft surgery effusions (n = 6), miscellaneous exudative effusions (n = 21) and transudative effusions (n = 51). The ADA level reached the diagnostic cut-off for tuberculosis (40 U x L(-1)) in seven of the 410 cases (1.71%). The negative predictive value of ADA for the diagnosis of pleural tuberculosis was 99% (403 of 407 cases) in the group of lymphocytic pleural effusions. In five of these seven patients ADA1 and ADA2 were measured, and in all these cases (100%) ADA1/ADA(p) correctly classified these lymphocytic effusions as nontuberculous (ratio < 0.42). This prospective study provides additional evidence that adenosine deaminase levels in nontuberculous lymphocytic pleural effusions seldom exceed the cut-off set for tuberculous effusions. The pleural fluid adenosine deaminase levels were significantly higher in different types of exudative effusions than in transudates. An adenosine deaminase level < 40 IU x L(-1) virtually excluded a diagnosis of tuberculosis in lymphocytic pleural effusions. Adenosine deaminase1/adenosine deaminase(p) correctly classified all nontuberculous lymphocytic pleural effusions with high adenosine deaminase levels.     

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.     

Adenosine deaminase activity in pleural fluid--a diagnostic test of tuberculous pleural effusion.

Adenosine deaminase (ADA) activity in pleural fluids was studied in 47 patients with pleural effusion of different etiology. Patients were divided into two groups: Group I - Tuberculous pleural effusion (21 patients): Group II - Non tuberculous effusion (26 patients) and these included malignant pleural effusion (9 cases), synpneumonic pleural effusion (9 cases) and transudative pleural effusion (8 cases). The mean ADA activity was 64.67 IU/L +/- 21.68 in group I and 6.99 +/- 3.69 in Group II. Increased mean pleural fluid ADA activity in tuberculous pleural effusion was highly significant (p < 0.001) when compared with pleural effusion of non-tuberculous etiology. Based on lowest value of ADA activity found in tuberculous pleural effusion (30 IU/L), the test has a sensitivity and specificity of 1.     

Clinical evaluation of pleural effusion--carcinoembryonic antigen (CEA) and adenosine deaminase (ADA) activities in pleural fluids

We reviewed 327 patients with pleural effusion who had been examined at our department for identification of its cause during the 14 years between 1974 and 1987, and studied the percentages of definitive diagnosis by examining the pleural fluids of patients with malignant tumor and tuberculosis. We also measured the levels of carcinoembryonic antigen (CEA) and adenosine deaminase (ADA) in the pleural fluids of these patients and evaluated their diagnostic usefulness. We further carried out a detailed clinical study of the factors affecting the CEA and ADA activities in the pleural fluids, which are considered to be particularly important in differential diagnosis of patients with pleural effusion. Of 327 patients with pleural effusion, malignancy-related pleurisy was observed in 166 patients (50.8%), and tuberculous pleurisy in 85 (26.0%). The rate of definitive diagnosis based on the examination of the pleural effusion in these patients indicated that 20-30% of them pose difficulty in clinical diagnosis. CEA was positive in 64.7% of patients with malignancy-related pleurisy, and ADA was positive in 97.7% of those with tuberculous pleurisy. These suggested their usefulness as supportive diagnostic methods of those diseases. In addition, CEA was elevated in patients with complications such as empyema, suggesting an effect of non-specific cross-reacting antigen (NCA). ADA showed high values in patients with conditions related to cell-mediated immunological responses as well as empyema and hemolysis. It suggested the release of ADA from blood cells due to hemolysis. These factors must be carefully evaluated in the interpretation of the CEA and ADA activities in pleural effusion.     

The diagnostic values of serum, pleural fluid and urine neopterin measurements in tuberculous pleurisy.

SETTING: Pulmonary department of a medical academy in Ankara, Turkey. OBJECTIVE: Neopterin is a marker of cell-mediated immunity, and it has been demonstrated that neopterin levels of various body fluids could be elevated in tuberculosis. We aimed to investigate diagnostic values of serum, pleural fluid and urine neopterin measurements in tuberculous pleurisy (TP). DESIGN: Serum, pleural fluid and urine neopterin levels were measured in 34 patients with TP and in 29 patients with pleural effusion of non-tuberculous origin as controls. RESULTS: Neopterin levels in serum, pleural fluid and urine (38.28 +/- 14.18 nmol/l, 38.97 +/- 14.18 nmol/l and 759.15 +/- 622.74 micromol/mol, respectively) were significantly higher in patients with TP than those with non-tuberculous pleural effusion (22.57 +/- 6.02 nmol/l, 21.88 +/- 6.90 nmol/l and 343.10 +/- 233.65 micromol/mol, respectively). Pleural fluid neopterin > or =30 mol/l gave the best diagnostic yield, with 85% sensitivity, 93% specificity, 94% positive predictive value, 84% negative predictive value and 89% diagnostic accuracy, although it is not superior to pleural fluid adenosine deaminase determination. CONCLUSION: We have suggested that elevated serum, pleural fluid and urinary neopterin levels in TP with respect to pleural effusions of non-tuberculous origin may reflect activation of cell-mediated immunity and that pleural fluid neopterin measurement may be of value in the differential diagnosis of TP.     

胸水M1/M2型巨噬细胞比例在结核性胸膜炎与恶性胸腔积液鉴别中的价值

目的探讨巨噬细胞极化在结核性胸膜炎与恶性胸腔积液鉴别中的价值。方法前瞻性收集2018年10月至2019年9月到我院就诊的新发结核性胸膜炎或恶性胸腔积液患者,在治疗前采集胸腔积液与外周血,流式细胞术检测M1型(CD14^+CD86^+)与M2型(CD14^+CD163^+)单核巨噬细胞。并测定外周血细胞计数、血沉、γ-干扰素释放试验及胸腔积液腺苷脱氨酶。结果纳入结核组51例,肿瘤组39例。结核组外周血CD14^+巨噬细胞高于肿瘤组,胸水M1型巨噬细胞高于肿瘤组,M2型巨噬细胞低于肿瘤组(P<0.05)。胸水M1/M2>0.92诊断结核性胸膜炎的敏感性86.3%,特异性94.6%,阳性预测值86.3%,阴性预测值81.7%(曲线下面积0.946)。结论结核性胸水中巨噬细胞向M1极化,恶性胸水巨噬细胞向M2极化,胸水M1/M2>0.92可作为结核性胸膜炎与恶性胸水鉴别的免疫学指标。     

Determination of adenosine deaminase activity and its isoenzymes for diagnosis of pleural effusions

OBJECTIVE: We aimed to investigate adenosine deaminase (ADA) activity and the activities of its ADA1 and ADA2 isoenzymes in pleural effusions and also sera with different aetiological origins. METHODOLOGY: The pleural effusions of 87 patients were examined. The patients were separated into four groups: transudates, parapneumonic, malignant, and tuberculous effusions. The cases were also designated as tuberculous or non-tuberculous group. Adenosine deaminase activity was determined by the colorimetric method described by Giusti and Galanti. RESULTS: The intermean differences were statistically significant for total ADA, ADA1 and ADA2, except for pleural fluid ADA1 in the malignant group when compared to the tuberculous effusion group. The intermean differences between the tuberculous and non-tuberculous group were statistically significant for all three parameters except for pleural fluid and serum ADA1 activity. The sensitivities of total ADA, ADA1 and ADA2 activities for tuberculosis were 91, 57 and 93%, respectively; their specificities 89, 88 and 92%, respectively; their positive predictive values 82, 70 and 86%; and their diagnostic accuracies 89, 76 and 92%, respectively, in pleural fluid. CONCLUSIONS: Determination of ADA and its isoenzymes can help to differentiate the causes of pleural effusion. Increased ADA2 activity is a striking marker of tuberculous effusions. In contrast, increased ADA1 activity was significantly elevated in parapneumonic effusions.     

Polymorphonuclear elastase in the early diagnosis of complicated pyogenic pleural effusions

BACKGROUND: Polymorphonuclear elastase (PMN-E) is a neutrophilic marker that has been implicated in acute inflammatory responses. OBJECTIVES: To evaluate the accuracy of PMN-E in the diagnosis of complicated pyogenic effusions. PATIENTS AND METHOD: We studied 536 patients with pleural effusion of various etiologies. There were 125 pyogenic bacterial effusions (42 typical parapneumonic, 17 borderline complicated parapneumonic and 66 complicated parapneumonic or empyema), 83 tuberculous, 91 malignant, 42 paramalignant, 95 transudates, 28 miscellaneous and 72 effusions of unknown origin. Classic markers (pH, glucose, proteins, adenosine deaminase, LDH, leukocytes and differential count) and the PMN-E level were quantified in pleural fluid. The accuracy of PMN-E as an early marker in the diagnosis of complicated pyogenic infectious effusions was evaluated among pleural effusions that were not diagnosed with classic biochemical markers, radiological findings or Gram stain. Since results of pleural fluid culture and cytological examination are generally available after a 48-hour delay, they were not included as early markers in the initial diagnosis of pleural effusions. RESULTS: Early diagnosis of complicated pyogenic bacterial effusions was achieved in only 48 of 66 cases with classic markers. Among those that were not diagnosed with these parameters, a pleural PMN-E value >3,500 microg/l discriminated between complicated and noncomplicated pyogenic bacterial effusions with a sensitivity of 67% and a specificity of 97%. CONCLUSIONS: PMN-E is useful in the early diagnosis and management of complicated pyogenic infectious effusions, which may be delayed with classic markers.     

Role of pleural viscosity in the differential diagnosis of exudative pleural effusion

OBJECTIVE AND BACKGROUND: Determining the aetiology of an effusion involves assessing if it is an exudate or a transudate. However, a reliable test for determining the aetiology of a pleural effusion is lacking. Pleural viscosity has a high sensitivity and specificity and a high positive and negative predictive value for discriminating exudative and transudative pleural effusions. The aim of this study was to use pleural fluid viscosity to discriminate between various aetiologies of exudative effusions, namely malignant, parapneumonic and tuberculous. METHODS: Seventy consecutive patients (24 women, 46 men, mean age = 67 years) with exudative pleural effusion due to pneumoniae in 24 patients, tuberculous pleurisy in 21 and lung cancer in 25 were studied prospectively. Measurements of pleural fluid and plasma viscosity were performed using Brookfield DV-II viscometer. RESULTS: Pleural viscosity and pleural LDH were highest in the tuberculous pleurisy patients and lowest in the lung cancer patients. Pleural viscosity > or = 1.57 was found to be indicative of tuberculous pleurisy with a sensitivity of 100% and specificity of 95%. Pleural viscosity < 1.39 was found to be indicative of lung cancer with a sensitivity of 100% and specificity of 94%. Pleural viscosity was significantly correlated with pleural albumin (r = 0.34, P = 0.004), protein (r = 0.40, P = 0.001), LDH (r = 0.70, P < 0.001) and plasma viscosity (r = 0.44, P < 0.001), having the most significant value with pleural LDH. CONCLUSION: The pleural fluid viscosity of patients with parapneumonic, tuberculous and malignant effusions are significantly different from each other. Among these groups, tuberculous effusions had the highest viscosity, and malignant effusions from lung cancer the lowest.     

Tuberculous pleural effusion

Tuberculous effusion is a common disease entity with a spectrum of presentations from a largely benign effusion, which resolves completely, to a complicated effusion with loculations, pleural thickening and even frank empyema, all of which may have a lasting effect on lung function. The pathogenesis is a combination of true pleural infection and an effusive hypersensitivity reaction, compartmentalized within the pleural space. Diagnostic thoracentesis with thorough pleural fluid analysis including biomarkers such as adenosine deaminase and gamma interferon achieves high accuracy in the correct clinical context. Definitive diagnosis may require invasive procedures to demonstrate histological evidence of caseating granulomas or microbiological evidence of the organism on smear or culture. Drug resistance is an emerging problem that requires vigilance and extra effort to acquire a complete drug sensitivity profile for each tuberculous effusion treated. Nucleic acid amplification tests such as Xpert MTB/RIF can be invaluable in this instance; however, the yield is low in pleural fluid. Treatment consists of standard anti‐tuberculous therapy or a guideline‐based individualized regimen in the case of drug resistance. There is low‐quality evidence that suggests possible benefit from corticosteroids; however, they are not currently recommended due to concomitant increased risk of adverse effects. Small studies report some short‐ and long‐term benefit from interventions such as therapeutic thoracentesis, intrapleural fibrinolytics and surgery but many questions remain to be answered.     

ADA、CRP和CEA在胸腔积液诊断中的意义

目的探讨腺苷脱氨酶（ADA）、C反应蛋白（CRP）、癌胚抗原（CEA）在胸腔积液中鉴别诊断的意义。方法收集已确诊的胸腔积液标本76例（结核性胸腔积液29例、癌性胸腔积液38例和化脓性胸腔积液9例）,检测胸腔积液中ADA、CRP和CEA数值,并进行各组间统计学分析。结果ADA在结核性胸腔积液及化脓性胸腔积液明显升高,在癌性胸腔积液明显偏低（P〈0．01）。CRP在化脓性胸腔积液升高最明显,在结核性胸腔积液次之,在癌性胸腔积液中值最低,三者之间比较有显著差异（P〈0．01）。CEA在癌性胸腔积液中均值明显高于结核性胸腔积液和化脓性胸腔积液组（P〈0．01）。结论ADA、CRP和CEA联合监测对胸腔积液的鉴别诊断有较好的意义。     

胸水和血清ADA、TB-Ab-IgG联合检测对结核性胸膜炎的诊断探讨

目的 探讨胸水/血清腺苷脱氨酶(ADA)、结核抗体(TB-Ab-IgG)联合检测对结核性胸膜炎的诊断价值.方法 采用斑点金免疫渗滤试验(DIGFA)和酶连续监测法对234例胸腔积液进行胸水/血清ADA和TB-Ab-IgG检测结果进行分析.结果 结核性胸膜炎患者174例其胸水、血清中TB-Ab-IgG的阳性率分别为62.0%和70.1%,特异性分别为93.1%(56/60)和86.6%(52/60).ADA活性在结核性和癌性胸腔积液中分别为(59.58±29.85)U/L和(15.31±7.36)U/L(P<0.01).以P-ADA>40 U/L做为诊断结核的临界值,其敏感性为79.3%,特异性为86.4%;以P-ADA/S-ADA>1为临界值,其敏感性为97.7%,特异性为95.5%.结论 胸水和血清ADA、TB-Ab-IgG联合检测在结核性胸膜炎与非结核性胸膜炎上具有诊断与鉴别诊断价值.