Association between inflammatory mediators and the fibrinolysis system in infectious pleural effusions

The response of the fibrinolytic system to inflammatory mediators in empyema and complicated parapneumonic pleural effusions is still uncertain. We prospectively analysed 100 patients with pleural effusion: 25 with empyema or complicated parapneumonic effusion, 22 with tuberculous effusion, 28 with malignant effusion and 25 with transudate effusion. Inflammatory mediators, tumour necrosis factor-alpha (TNF-alpha), interleukin-8 (IL-8) and polymorphonuclear elastase, were measured in serum and pleural fluid. Fibrinolytic system parameters, plasminogen, tissue-type plasminogen activator (t-PA) and urokinase PA, PA inhibitor type 1 (PAI 1) and PAI type 2 concentrations and PAI 1 activity, were quantified in plasma and pleural fluid. The Wilcoxon signed-rank test was used to compare plasma and pleural values and to compare pleural values according to the aetiology of the effusion. The Pearson correlation coefficient was used to assess the relationship between fibrinolytic and inflammatory markers in pleural fluid. Significant differences were found between pleural and plasma fibrinolytic system levels. Pleural fluid exudates had higher fibrinolytic levels than transudates. Among exudates, tuberculous, empyema and complicated parapneumonic effusions demonstrated higher pleural PAI levels than malignant effusions, whereas t-PA was lowest in empyema and complicated parapneumonic pleural effusions. PAI concentrations correlated with TNF-alpha, IL-8 and polymorphonuclear elastase when all exudative effusions were analysed, but the association was not maintained in empyema and complicated parapneumonic effusions. A negative association found between t-PA and both IL-8 and polymorphonuclear elastase in exudative effusions was strongest in empyema and complicated parapneumonic effusions. Blockage of fibrin clearance in empyema and complicated parapneumonic effusions was associated with both enhanced levels of PAIs and decreased levels of t-PA.     

探讨渗出性胸腔积液ADA、CEA对良恶性胸腔积液的诊断价值

目的 探究渗出性胸腔积液腺苷脱氨酶(ADA)、癌胚抗原(CEA)对良恶性胸腔积液的诊断价值.方法 选择2017年1月至2020年8月本院收治的106例渗出性胸腔积液患者,将患者分为恶性组(n=36)和良性组(n=70).对两组患者胸水ADA、胸水CEA、血清CEA水平进行比较,采用单因素、多因素Logistic回归分析...     

Pleural diseases.

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)     

神经元特异性烯醇化酶、细胞角质蛋白19片断、癌胚抗原联合LDH、ADA检测对良、恶性胸腔积液鉴别的意义

目的探讨血清、胸水中神经元特异性烯醇化酶（NSE）、细胞角质蛋白19片断（CYFRA21—1）、癌胚抗原（CEA）对良、恶性胸腔积液的鉴别价值。方法对40例经病理确诊的胸腔积液患者按胸水的性质分为恶性胸水组（23例）和良性胸水组（17例）。2组患者均采用电化学发光法检测血清及胸腔积液中NSE、CYFRA21—1、CEA的含量．生化检测胸腔积液中乳酸脱氢酶（LDH）和腺苷脱氨酶（ADA）。结果恶性胸水组的血清NSE、CYFRA21—1及CEA均显著高于良性胸水组（P=O,02、0．02及0．01）;胸水CYFRA21—1及CEA均明显高于良性胸水组（严如．01或P=0．04）,ADA显著低于良性胸水组（P=0．01）。2组胸水NSE、LDH比较差异无统计学意义（均P〉O．05）。结论血清、胸腔积液中NSE、CYFRA21—1、CEA和ADA联合检测,对良、恶性胸腔积液的鉴别诊断有重要价值,能提高准确率。     

Role of biochemical tests in the diagnosis of exudative pleural effusions

OBJECTIVES: To examine the diagnostic utility of pleural adenosine deaminase (PADA), pleural lactate dehydrogenase (PLDH), and several other biochemical tests in bronchogenic carcinoma and malignant mesothelioma, and to compare biochemical characteristics of their fluid with nonmalignant pleural effusions. DESIGN AND METHODS: This study consisted of 226 patients diagnosed with malignant (75), tuberculous (65), and parapneumonic pleural effusions (86). We examined the following biochemical parameters in the pleural fluid and serum: adenosine deaminase, lactate dehydrogenase, glucose level, protein level, pleural fluid/serum ADA ratio (P/S ADA), P/S LDH ratio, and P/S protein ratio. RESULTS: Parapneumonic pleural effusions had a significantly higher level of PLDH and of P/S LDH than malignant and tuberculous pleural effusions (P = 0.000), and malignant pleural effusions had a higher level of PLDH than tuberculous pleural effusions. Tuberculous and parapneumonic effusions had significantly higher levels of PADA than those of malignant effusions (P = 0.000). When the 54 patients having bronchogenic carcinoma were compared to the remaining 21 mesothelioma patients, the former had a lower median level of PADA (P = 0.001) with a higher level of PLDH (P = 0.05). CONCLUSION: Our results show that high pleural LDH and low PADA levels are suggestive of pleural effusion due to bronchogenic carcinoma, whereas high levels of PADA alone can be indicative of tuberculous pleural effusion and high levels of both markers can show complicated parapneumonic effusions or empyema.     

Usefulness of monitoring β-glucuronidase in pleural effusions

Background: The objective of the study was to evaluate the additional value of β-glucuronidase (BGD), a lysosomal enzyme in the analysis of transudative and exsudative pleural effusions, especially between malignant and non-malignant effusions.

Design and methods: Pleural fluid samples obtained from four respective diagnostic groups: transudates parapneumonic effusions, malignant effusions or pleuritis carcinomatosa, and empyema were evaluated.

Results: Beta-glucuronidase was significantly different between transudative and exsudative effusions (p < 0.001) as well as between parapneumonic and malignant effusions (p < 0.03), parapneumonic effusions and empyema (p < 0.002), and malignant and empyema (p < 0.002), respectively. Logistic regression analysis yielded a weak discrimination between the parapneumonic and malignant groups.

Conclusions: Beta-glucuronidase activity differed between pleural effusions of various origin. However, including BGD in the biochemical work-up of pleural effusions did not reveal discriminatory value in the assessment of the classification of these effusions.     

Measurement of vitamin D-binding protein in pleural fluids and sera by means of a turbidimetric immunoassay measuring system

BACKGROUND: Vitamin D-binding protein (DBP) has been recognized as a multifunctional plasma protein that can modulate certain immune and inflammatory responses. There may be differences between the DBP concentrations in pleural fluids from various diseases involving a variety of possible responses in the pleural cavity. METHODS: An anti-DBP polyclonal antibody was prepared using commercially available DBP to establish a quantitative measuring system for DBP. With a rabbit antibody, a turbidimetric immunoassay (TIA) was developed for DBP with an automatic analyzer. Using this measuring system, the concentrations of DBP were compared with the protein concentration in pleural fluid and serum specimens from patients with various diseases. RESULTS: The fluid DBP concentrations in transudative (n=11) and exudative (n=41) effusions were 71.9+/-21.2 and 180.7+/-43.7 mg/l, respectively. Among the exudative effusions, the fluid DBP concentrations in the bacterial (n=10), tuberculous (n=13), and malignant (n=18) effusions were 218.8+/-37.3, 186.7+/-26.2, and 155.1+/-41.3 mg/l, respectively. The DBP fluid/serum ratio and the fluid DBP/protein ratio in bacterial effusions were significantly higher than those in tuberculous (p<0.005, p<0.05, respectively) and malignant effusions (p<0.0005, p<0.005, respectively), although no statistically significant differences in the serum DBP/protein ratio between those effusions were found. CONCLUSIONS: Using the TIA assay, the DBP concentrations in bacterial pleural effusions were significantly higher than in tuberculous and malignant effusions.     

髓系细胞触发受体-1和CRP在胸腔积液中的表达及意义

目的：探讨髓系细胞触发受体-1（TREM-1）、CRP在不同性质的胸腔积液中表达水平和意义。方法收集胸腔积液患者,检测胸腔积液和血清中TREM-1、CRP水平,检测胸腔积液细胞膜TREM-1 mRNA的表达。统计不同类型胸腔积液TREM-1、CRP表达水平的差异。结果（1）TREM-1检测显示：与结核性、肿瘤性和漏出性三组胸腔积液比较,肺炎旁胸腔积液sTREM-1表达显著增高。肺炎旁胸腔积液组血清sTREM-1与肿瘤性、漏出性胸腔积液组比较,表达均显著增高,但与结核性胸腔积液组比较无明显差异。（2）CRP检测显示：结核性和肺炎旁胸腔积液CRP水平均显著高于肿瘤性和漏出性胸腔积液。但结核性胸腔积液和肺炎旁胸腔积液CRP水平无显著差异。结核性胸腔积液组和肺炎旁胸腔积液组血清CRP水平均显著高于肿瘤性胸腔积液组和漏出性胸腔积液组,但结核性胸腔积液组和肺炎旁胸腔积液组血清CRP水平无显著差异。结论胸腔积液sTREM-1水平可以作为判断肺炎旁胸腔积液的重要参考指标。     

Diagnostic value of leptin in tuberculous pleural effusions

It is suggested that leptin may be involved in inflammation. Although relation between leptin levels and active pulmonary tuberculosis has been studied, there is no information about relation between leptin levels and tuberculous pleural effusions (TPE). We evaluated the diagnostic value of pleural fluid and serum leptin levels in TPE and compared them with adenosine deaminase (ADA). Forty-five patients, 17 tuberculous effusion and 28 nontuberculous effusion, with exudative pleural effusions were included. Leptin and ADA levels were measured from serum and pleural fluid in all patients. There were no statistically significant differences between tuberculous and nontuberculous groups with respect to the serum ADA activity and pleural fluid/serum leptin ratio. On the contrary, pleural fluid leptin level, pleural fluid ADA activity, serum leptin level and pleural fluid/serum ADA activity ratio were statistically different between tuberculous and nontuberculous groups. When leptin levels were corrected for body mass index, serum leptin levels did not reach statistical significance. Cut-off points to predict tuberculosis were calculated as 9.85 ng/ml and 35.55 U/l for pleural fluid leptin level and pleural fluid ADA activity, respectively. Sensitivity, specificity and area under the curve +/- standard error were 82.4%, 82.1%, 0.83 +/- 0.07 for pleural fluid leptin levels and 100%, 100%, 1.00 +/- 0.00 for pleural fluid ADA activity, respectively; the difference between these curves was significant (p = 0.01). Pleural fluid leptin levels were lower in tuberculous effusions than in other exudates. Pleural fluid leptin has a diagnostic value for TPE but not as good as that of ADA.     

Pleural fluid protein is inversely correlated with age in uncomplicated parapneumonic pleural effusions

ObjectivesAssess whether age influences standard biochemical parameters used in the differential diagnosis of transudative and exudative pleural effusions.Design and methodsWe retrospectively analyzed data from the database of our clinic from 225 patients with pleural effusions categorized based on their final diagnosis in 5 groups: transudates 41 (18%), uncomplicated parapneumonic 26 (12%), complicated parapneumonic 20 (9%), tuberculosis 35 (15%) and lung cancer 103 (46%). We tested whether age correlated with pleural fluid protein or lactate dehydrogenase.ResultsThere was a statistically significant inverse correlation only between the age and the pleural fluid protein content in patients with uncomplicated parapneumonic effusions with correlation coefficient r = ? 0.6 [(95% CI = ? 0.8 to ? 0.28); p = 0.001]. Linear regression analysis showed that this association is given by the equation: age = 101.998 ? 10.03 protein. In the same group of patients age was not correlated with serum protein content.ConclusionsOur study shows that age may be a confounding factor in the differential diagnosis of transudative and exudative pleural effusions. Clinicians should be aware of this finding especially when dealing with elders.     

Procalcitonin as a diagnostic marker in differentiating parapneumonic effusion from tuberculous pleurisy or malignant effusion

Objectives

Differential diagnosis of exudative pleural effusions can be difficult, despite the use of several biomarkers. Serum procalcitonin (s-PCT) is a well-known biomarker for systemic bacterial infections. However, the usefulness of pleural fluid procalcitonin (pf-PCT) in clinical practice has not been established. This study evaluated the usefulness of PCT measurements in differentiating parapneumonic effusion (PPE) from tuberculous (TB) pleurisy or malignant effusion.

Design and methods

Ninety eight adult patients diagnosed with exudative pleural effusion were enrolled and allocated into the PPE group (n = 32), TB pleurisy group (n = 40), or malignant effusion group (n = 26). Both s-PCT and pf-PCT concentrations were measured at admission using an immunoluminometric assay.

Results

Both s-PCT and pf-PCT were significantly increased in the PPE group compared with the TB pleurisy or malignant effusion groups (p < 0.001). The optimal cut-off value for s-PCT in the diagnosis of PPE was 0.18 ng/mL (sensitivity 83.3%, specificity 81.0%). The pf-PCT cut-off value was 0.16 ng/mL (sensitivity 81.5%, specificity 72.1%). Serum PCT exhibited better diagnostic accuracy than pf-PCT, with areas under the receiver operating characteristic curves of 0.842 for s-PCT and 0.784 for pf-PCT (p = 0.015). In addition, s-PCT and pf-PCT showed better diagnostic accuracy than serum C-reactive protein (p = 0.005 and p = 0.023, respectively).

Conclusions

Measurement of s-PCT and pf-PCT is useful in differentiating PPE from TB pleurisy and malignant effusion. Both s-PCT and pf-PCT may be useful biomarkers in the differential diagnosis of exudative pleural effusions.     

Pleural effusions caused by infection

Diagnostic thoracentesis is imperative when pneumonia is accompanied by an effusion (parapneumonic effusion). Examination of the pleural fluid is the only way to differentiate empyema and complicated parapneumonic effusions from uncomplicated parapneumonic effusions, and this differentiation is vital in deciding whether chest tube drainage is needed. If the aspirated pleural fluid contains pus or bacteria, closed chest tube drainage and antibiotic therapy should be started promptly. The same management approach is indicated if the pleural fluid pH is less than 7.00 or the glucose level is less than 40 mg/ml, since these effusions almost invariably are complicated parapneumonic effusions that do not resolve without fluid drainage. If the pleural fluid pH is greater than 7.20 and glucose level is more than 40 mg/ml, antibiotic therapy alone will suffice. Management of parapneumonic effusions with a pH of 7.00 to 7.20 should be based on serial observations of clinical status and pleural fluid findings.     

Concurrent measurement of adenosine deaminase and dipeptidyl peptidase IV activity in the diagnosis of tuberculous pleural effusion

Measurement of pleural fluid adenosine deaminase (ADA) levels aids diagnosing tuberculous pleural effusion (TPE). Dipeptidyl peptidase IV (DPP) enzyme is closely related to ADA. Our aim was to determine the value of concurrent measurement of these T-cell–associated enzymes, ADA and DPP levels in the diagnosis of TPE. Patients with pleural effusion were grouped as TPE, parapneumonic, malignant, congestive heart failure related, and miscellaneous pleural effusions. Pleural and serum ADA and DPP levels were measured. Pleural and serum levels of ADA and pleural DPP were higher in TPE group than the rest. In 7 patients, pleural biopsy revealed granulomatous pleuritis. All of these patients had TPE and had elevated serum and pleural ADA levels. Serum and pleural ADA or DPP levels and pleural ADA and DPP levels correlated with each other. Selecting cutoff values of 40 and 27 IU/L for pleural ADA and DPP, respectively, the sensitivity of concurrent measurement of both enzymes was 77%, specificity 94%, and diagnostic efficiency 91%. ADA and DPP play an important role in tuberculous immunopathogenesis. The utility of DPP in the diagnosis of TPE has never been determined before. Concurrent measurement of ADA–DPP can aid in diagnosing TPE with higher specificity, sensitivity, and efficiency.     

Pleural effusion: comparison of clinical judgment and Light's criteria in determining the cause

Pleural fluid analysis is often the initial diagnostic test used to determine the cause of a pleural effusion. We prospectively studied 33 consecutive patients with pleural effusions to determine whether the fluid arose from a transudative or an exudative process. Clinical judgment by an internist before thoracentesis and both serum and pleural fluid protein and lactic dehydrogenase levels (commonly referred to as "Light's criteria") were compared to the patient's final diagnosis. The internist correctly classified 15 of 17 exudative processes and all 16 transudative processes; the presence of any one of Light's three criteria correctly classified 15 of 17 exudative processes, whereas the absence of all three criteria correctly classified 14 of 16 transudative processes. Clinical judgment and Light's criteria are comparable in their ability to predict whether an exudative or transudative process was responsible for the effusion. Both methods are associated with errors, though of different kinds; these errors occurred infrequently. Recognizing the limitations of these methods will permit the most accurate effusion categorization.     

A novel biomarker for pleural effusion diagnosis: Interleukin‐36γ in pleural fluid

BackgroundNumerous studies have described the critical importance of interleukin (IL) ‐36γ in host defense against lung infections, but it is unknown whether it plays a role in infectious pleural effusion (IPE). This study aimed to examine the levels of IL‐36γ in pleural effusions of different etiologies and evaluate the diagnostic accuracy of IL‐36γ in the differential diagnosis of IPE.MethodsA total of 112 individuals was enrolled in this research. IL‐36γ levels in pleural fluids of all 112 patients were measured by enzyme‐linked immunosorbent assay (ELISA). We also characterized these markers'' diagnostic values across various groups.ResultsPatients with tuberculous pleural effusion (TPE) and parapneumonic effusion (PPE) had exhibited markedly higher IL‐36γ levels in their pleural fluid than the malignant pleural effusion (MPE) and transudative effusion patients. Furthermore, the IL‐36γ concentrations in TPE patients were evidently higher than in uncomplicated parapneumonic effusion (UPPE) patients but significantly lower than in complicated parapneumonic effusion (CPPE)/empyema patients. Pleural fluid IL‐36γ is a useful marker to differentiate TPE from UPPE, at a cut‐off value for 657.5 pg/ml (area under the curve = 0.904, p < 0.0001) with 70.0% sensitivity and 95.7% specificity.ConclusionsThe elevated IL‐36γ in pleural effusion may be used as a novel biomarker for infectious pleural effusion diagnosis, particularly in patients with CPPE/empyema, and is a potentially promising biomarker to differentiate between TPE and UPPE.     

内科胸腔镜胸膜活检术与血清肿瘤标志物在不明原因胸腔积液中的诊断价值*

目的探讨内科胸腔镜下胸膜活检术和肺部肿瘤标志物对不明原因胸腔积液的临床应用价值。方法回顾性分析该院2014年1月-2016年3月76例不明原因胸腔积液的患者,采用内科胸腔镜进行胸膜活检送病理,且在入院时即采集患者静脉血10 ml送检,查血清肿瘤标志物[癌胚抗原(CEA)、鳞状细胞癌抗原(SCC-Ag)、胃泌素释放肽前体(Pro GRP)、细胞角蛋白19片段(CYFRA21-1)]进行测定。结果 76例不明原因胸腔积液的患者中有良性病变32例(肺结核14例,炎性病变9例,肉芽肿性炎6例,脓胸2例,错构瘤1例);恶性病变44例(腺癌18例,鳞癌13例,小细胞肺癌6例,腺鳞癌3例,间皮瘤2例,大细胞癌1例,胸腺瘤1例)。检测血清肿瘤标志物发现,血清中CEA、SCC-Ag、Pro GRP、CYFRA21-1水平在恶性胸腔积液组与良性胸腔积液组之间差异具有统计学意义(P=0.021、P=0.006、P=0.003和P=0.010),恶性胸腔积液患者血清各项肿瘤标记物水平明显高于良性胸腔积液的患者。根据病理结果将44例恶性胸腔积液中非肺癌所致胸腔积液的患者剔除(即2例间皮瘤及1例胸腺瘤患者),将剩下的41例肺癌所致胸腔积液患者,根据病理类型分为非小细胞肺癌(NSCLC)与小细胞肺癌(SCLC)。分析结果显示CEA、Pro GRP和CYFRA21-1水平在NSCLC与SCLC中差异具有统计学意义(P=0.036,P=0.005,P=0.008),而SCC-Ag差异无统计学意义(P=0.811)。结论内科胸腔镜在不明原因胸腔积液中具有检出率高、准确性高的特点,尤其是对胸膜转移瘤的恶性胸积液的诊断具有重要的意义。但血清学指标可以在病理结果出来之前为医师提供重要的参考价值,是临床诊断肺癌所致恶性胸腔积液的一种重要的手段,值得在临床推广应用。     

Pleural effusions in right-sided endocarditis: characteristics and pathophysiology.

The incidence, characteristics, and pathogenesis of pleural effusions in patients with right-sided endocarditis (RSE) are poorly defined. We have recently observed four patients with a history of intravenous drug abuse and bacteremia due to Staphylococcus aureus who had pleural effusions during an episode of RSE. We report the pleural fluid characteristics of five effusions in these four patients and attempt to define the pathogenesis of each. We found that (1) an exudative, sterile, serosanguineous, or bloody effusion is common in RSE, (2) empyema occurred in only one patient, and (3) transudative effusions due to CHF were not observed. Possible mechanisms of pleural fluid formation in RSE include parapneumonic effusion, septic pulmonary emboli with or without infarction, and empyema. Congestive heart failure does not appear to be a common cause of pleural effusion in pure right-sided endocarditis.     

类肺炎性胸腔积液68例临床分析

目的 总结类肺炎性胸腔积液的临床特征及治疗。 方法 对我院收治的68例类肺炎性胸腔积液的临床资料进行回顾性分析,根据辅助检查及实验室检查等,将类肺炎性胸腔积液分成单纯性类肺炎性胸腔积液（uncomplicated parapneumonic effusion,UCPE）及复杂性类肺炎性胸腔积液(complicated parapneumonic effusion,CPE)。比较其临床特点、治疗方法及预后。 结果 68例类肺炎性胸腔积液中,UCPE 51例, CPE 17例。类肺炎性胸腔积液以发热、咳嗽、胸痛为主要临床特点,与单纯肺炎症状相同。复杂性类肺炎性胸腔积液其发热时间较单纯性类肺炎性胸腔积液长,毒血症状重,白细胞计数高,胸水量大。51 例UCPE中,43例经全身应用抗生素治疗治愈,胸水量少不宜定位未能抽取胸水自行吸收、临床症状消失。8例经全身应用抗生素治疗+胸腔穿刺抽液1~2次而治愈;17例CPE中,经抗生素治疗+胸腔穿刺2次或以上者5例,胸腔闭式引流胸水者12例;10例治愈;7例临床症状好转、胸水明显减少出院、随访3月,其中3例胸水完全吸收,2例失访, 2例死亡。复杂性类肺炎性胸腔积液往往多见于年龄大、使用激素等免疫抑制剂及有基础疾病者或就医比较晚者。 结论 区分类肺炎性胸腔积液的分型对治疗相当重要、胸部X线或CT加B超检查可作为首先的检查方法,尽早胸腔穿刺抽取胸水或微管引流胸水,可减少患者发热时间、缩短病程,减少住院天数,明显提高治愈率。     

渗出性胸腔积液135例诊断分析

目的 探讨腺苷脱氨酶(ADA)、癌胚抗原(CEA)、糖类抗原153(CA153)、神经元烯醇化酶(NSE)、糖类抗原199(CA199)对渗出性胸腔积液鉴别诊断的价值.方法 应用电化学发光法测定胸腔积液患者的血清及胸水CEA、CA153、NSE、CA199水平,采用酶偶联速率法测定胸水ADA水平,并评价联合检查对胸腔积液的诊断价值.结果 结核性胸腔积液组胸水ADA含量为(65.89±19.81)U/L,恶性组为(27.44±22.64)U/L,炎性组为(17.33±16.58)U/L,结核组显著高于其余2组(q=12.19、10.72,P均＜0.01).结性胸腔积液组ADA阳性29例(82.88%),恶性组11例(13.41%),炎性纽2例(11.11%),组间比较差异有统计学意义(X~2=59.07,P＜0.01).恶性胸腔积液组CEA、CA153、NSE、CA199含量和阳性率均高于结核组,差异均有统计学意义(P均＜0.05),炎性组和恶性组相比差异无统计学意义.82例恶性胸腔积液患者血清4项肿瘤标记物联检阳性率为74.3%(61/82),胸腔积液中阳性率为82.9%(68/82).结论 ADA、CEA、CA153、NSE、CA199联合检测对胸腔积液的鉴别诊断具有一定意义.     

Differentiating transudative from exudative pleural effusion: should we measure effusion cholesterol dehydrogenase?

INTRODUCTION: Pleural effusions are often classified into transudates and exudates based on Light's criteria. In this study, the diagnostic properties of Light's criteria were compared to those of several other analytes for the classification of pleural fluids into transudative and exudative. METHODS: A total of 471 patients with pleural effusions were evaluated. In pleural effusions and simultaneously drawn blood samples, lactate dehydrogenase (LDH), total protein, albumin, cholesterol, amylase, glucose, pH and the cell number were measured. Retrospectively, the clinical records were used to establish a clinical diagnosis. The diagnostic properties of the biochemical tests were calculated using the clinical diagnoses as gold standard. RESULTS: By clinical diagnosis, 108 patients had transudative and 300 patients had exudative pleural effusions. In addition to pleural LDH activity (accuracy 89%, sensitivity 86%, specificity 97%) and fluid to serum LDH ratio (accuracy 89%, sensitivity 91%, specificity 85%), pleural cholesterol concentration readily identified exudates (accuracy 82%, sensitivity 76%, specificity 98%). Combination of these three parameters achieved a higher overall accuracy (accuracy 95%, sensitivity 93%, specificity 100%) than the Light's criteria (accuracy 93%, sensitivity 100%, specificity 73%). Combination of effusion cholesterol concentration and effusion LDH activity had the highest discriminatory potential (accuracy 98%, sensitivity 98%, specificity 95%). CONCLUSIONS: Including effusion cholesterol, concentration in the routine biochemical work-up of pleural fluid allows for correct classification of more pleural effusions than achieved by use of Light's criteria. Combination of cholesterol and LDH had the highest discriminatory potential and the added advantage that no patient plasma is needed for correct classification.