66例大量胸腔积液病因及诊断分析

目的分析大量胸腔积液的病因和诊断方法。方法回顾性分析66例大量胸腔积液住院患者的临床资料。结果 66例大量胸腔积液病因的前5位依次为恶性肿瘤（56.1%）,结核（24.2%）,肺炎旁积液和脓胸（6.1%）,肝硬化（4.5%）,外伤（3.0%）。大量良性胸腔积液以40岁以下患者为主;恶性胸腔积液以60岁以上患者居多。66例大量胸腔积液癌胚抗原水平均为恶性组高于良性组（P〈0.05）,腺苷脱氨酶水平均为恶性组低于良性组（P〈0.05）。结论大量胸腔积液主要病因是恶性肿瘤和结核,恶性肿瘤多见于60岁以上患者,结核病以40岁以下患者居多。胸腔积液癌胚抗原及腺苷脱氨酶含量鉴别良恶性胸腔积液有重要的价值。     

85例血性心包积液的病因及诊断方法分析

目的:总结分析血性心包积液的病因及其诊断方法,为诊断和鉴别诊断提供指导性资料。方法:对85例血性心包积液患者的临床表现、影像学检查、实验室检查结果进行回顾分析。结果:85例血性心包积液的病因中,肿瘤性41例(48.23%)、结核性27例(31.76%)、其他各种原因引起者17例(20.01%)。肿瘤性心包积液中癌胚抗原的平均值173μg/L,显著高于结核性心包积液的平均值0.62μg/L;结核性心包积液腺苷脱氢酶平均值44.5U/L,显著高于癌性心包积液平均值15U/L;结核性心包积液患者中心包积液和血液抗结核抗体(kjhkt)检测阳性率分别为62.5%和75%,显著高于肿瘤性心包积液患者(均为阴性)。结论:恶性肿瘤和结核是血性心包积液的主要病因。心包积液的脱落细胞学检查和腺苷脱氢酶、癌胚抗原、kjhkt等项实验室检查为血性心包积液病因诊断和鉴别诊断的主要手段,联合应用可提高诊断的准确性。     

γ-干扰素释放分析T-SPOT.TB在结核性胸腔积液中的诊断意义

目的 探讨γ-干扰素释放分析T-SPOT.TB的检测对结核性胸腔积液的诊断价值.方法 选取在本院住院的胸腔积液的患者78例,分为两组,每组患者39例,A组为疑是结核性胸腔积液,B组为临床确诊的癌性胸腔积液,两组患者均采用T-SPOT.TB试剂盒对外周血中释放γ-干扰素的结核分枝杆菌特异性T淋巴细胞进行检测,同时抽取胸水常规检测腺苷脱氨酶（ADA）及癌胚抗原（CEA）.结果 A组联合胸水常规ADA及 T-SPOT.TB检测结核性胸腔积液诊断敏感性高于单纯的ADA检测,差异有统计学意义（P〈0.05）,其CEA检测无明显升高,B组检测ADA 及T-SPOT.TB无升高情况.结论 联合胸水常规ADA及T-SPOT.TB检测对结核性胸腔积液诊断特异性高,对结核性疾病的诊断意义大,而对癌性胸腔积液无诊断意义.     

腺苷脱氨酶、γ-干扰素在结核性和癌性胸腔积液中的价值

目的探讨腺苷脱氨酶、γ-干扰素的检测对诊断结核性和癌性胸腔积液的价值。方法采用酶显色法和酶联免疫吸附法分别对结核性和癌性胸腔积液腺苷脱氨酶、γ-干扰素进行测定。结果腺苷脱氨酶：结核性胸膜炎组：43.85±12.32U/L,癌性胸膜炎组8.98±6.59U/L,两者之间有显著性差异（P〈0.01）;γ-干扰素：结核性胸膜炎组：521.31±82.35pg/ml,癌性胸膜炎组：48.62±30.37pg/ml,两者之间有显著性差异（P〈0.01）。结论腺苷脱氨酶、γ-干扰素的检测对结核性和癌性胸腔积液的鉴别有临床意义,可用于两者的鉴别诊断。     

腺苷脱氨酶与溶菌酶检测在诊断结核性胸腔积液中的价值

评价腺苷脱氨酶与溶菌酶检测时结核性胸腔积液的诊断价值。对108例诊断明确的胸腔积液患者进行胸水腺苷脱氨酶及胸水溶菌酶与血清溶菌酶之比值测定。结果结核性胸腔积液患者胸水中腺苷脱氨酶含量明显高于癌性胸腔积液组(P<0.05),胸水溶菌酶与血清溶菌酶之比明显高于癌性胸腔积液组(P<0.01)。     

结核感染T细胞斑点试验联合胸腔积液腺苷脱氢酶检测对结核性胸腔积液的诊断价值研究

目的?分析结核感染T细胞斑点试验（tuberculosis infection T cell spot test, T-SPOT.TB）结合胸腔积液生化检测对结核性胸腔积液的诊断价值。方法?对2019年2月—2022年2月期间就诊于河北省胸科医院的126例有肺部病灶伴胸腔积液患者展开研究,所有患者均完成T-SPOT.TB试验和入院当天的胸腔积液生化检测,依据是否存在结核杆菌感染将其分为结核组（n=48,确诊为结核性胸腔积液）和对照组（n=78,确诊为非结核性肺部病灶伴胸腔积液）。统计并比较2组患者的各项一般资料和临床资料,Logistic多因素分析结核性胸腔积液的危险因素,并应用ROC曲线分析胸腔积液T-SPOT.TB和胸腔积液腺苷脱氨酶（adenosine deaminase, ADA）及2者联合对结核性胸腔积液的诊断价值。结果?Logistic多因素分析结果显示,结核病接触史、结核性胸腔积液结核菌素试验阴性率较高、胸腔积液T-SPOT.TB阳性、胸腔积液ADA≥45 U/L为发生结核性胸腔积液的危险因素（P均＜0.05）。ROC曲线分析显示胸腔积液T-SPOT.TB和胸腔积液ADA诊断结核性胸腔积液的最佳临界值分别为276.43×106/ml和45.36 U/L,AUC分别为0.67和0.63,灵敏度分别为74.26％和69.26％,特异度分别为72.17％和68.84％,2者联合诊断的AUC为0.86,灵敏度为81.65％,特异度为79.43％。结论?T-SPOT.TB结合胸腔积液检测对诊断结核性胸腔积液患者有较佳价值。     

内科胸腔镜检查对胸腔积液鉴别诊断的价值

目的探讨内科胸腔镜检查对胸膜积液病因诊断的重要价值,了解结核性与癌性胸腔积液的差异。方法回顾性分析经胸腔镜检查的231例胸腔积液患者的病因构成,重点比较结核性胸腔积液104例（结核组）和癌性胸腔积液114例（癌性组）患者临床资料与胸腔镜检查结果。结果①病因构成：231例胸腔积液患者中,结核性与癌性所占比例最大（45．02％,47．62％）;②临床资料：结核组患者年龄较癌性组年轻,病程较癌性组短（P〈0．001）,发热症状更多;结核组黄色胸水较多见（73．08％）,癌性组血性胸水较多见（76．36％）。两者胸腔积液量（超声测值）无显著性差异（P=0．351）。结核组腺苷脱氨酶（ADA）、乳酸脱氢酶（LDH）较癌性组高,癌胚抗原（CEA）较癌性组低（P〈0．001）;③内科胸腔镜下表现：结核组以胸膜粟粒结节、广泛粘连较多见;癌性组胸膜大小不等弥漫结节较多见。结论结核性及癌性胸水是胸腔积液的常见病因,内科胸腔镜检查联合临床症状及胸水生化检测,可大大提高胸腔积液病因的诊断率,其创伤小,安全性好,值得广泛推广。     

腹水铁蛋白、癌胚抗原及腺苷脱氨酶联合检测对鉴别良恶性腹水的价值

本文检测了104例腹水中铁蛋白、癌胚抗原及腺苷脱氨酶含量,结果表明恶性腹水铁蛋白、癌胚抗原含量显著高于结核性及肝硬化腹水,结核性腹水腺苷脱氨酶含量显著高于恶性腹水及肝硬化腹水.单独检测腹水铁蛋白及癌胚抗原对恶性腹水的敏感性分别为70.6%和60.5%,特异性均为100%;联合检测铁蛋白、癌胚抗原诊断恶性腹水的敏感性为87.6%,特异性为100%;检测腹水腺苷脱氨酶对结核性腹水的敏感性为95.4%,特异性为97.2%.     

联合检测腺苷脱氨酶与新蝶呤对鉴别诊断结核性胸腔积液的探讨

目的探讨腺苷脱氨酶和新蝶呤联合检测对鉴别诊断结核性胸腔积液的临床价值。方法选择2007年4月～2009年1月在我院住院的胸腔积液患者86例,其中结核性胸膜炎45例,恶性胸腔积液41例;常规穿刺抽取胸腔积液于无菌试管中,2500r/min,离心10min。取上清,1h内测定完毕。在日立7150全自动生化分析仪上采用酶显色法对ADA进行测定,精密度：批内CV%〈4.5%,批间CV%〈6.0%。新蝶呤测定采用反相液相色谱法,精密度：批内CV%〈2.0%,批间CV%〈5.0%。分析两组间各指标的差异性。结果结核性胸腔积液ADA活性高于恶性胸腔积液组,结核性胸腔积液组新蝶呤水平高于恶性胸腔积液组,差异有统计学意义。结论腺苷脱氨酶与新蝶呤联合检测可作为结核性胸腔积液鉴别诊断的有益补充,对鉴别结核性和恶性胸腔积液有重要的诊断意义。     

血管内皮生长因子在心包积液病因鉴别中的价值

目的：探讨血管内皮生长因子（VEGF）在心包积液病因鉴别中的作用。方法：将渗出性心包积液分成恶性肿瘤组和非肿瘤组，采用双抗体夹心酶联免疫吸附法检测心包积液中VEGF、乳酸脱氢酶（LDH）和腺苷脱氨酶（ADA），并行心包积液常规和细胞学检查，分析比较两组临床特点。结果：恶性心包积液20例，其中肺癌11例，乳腺癌3例，淋巴瘤3例，纵隔肿瘤、直肠癌和黑色素瘤各1例。非恶性心包积液26例，其中结核性16例，结缔组织病7例，甲状腺机能减退2例，射频消融术后1例。恶性心包积液组VEGF水平明显高于非恶性心包积液组（4．53±3．72pg／μl vs 1．10±0．74pg/μl，P〈0．01），而两组之间LDH、ADA和常规检查无明显差异，ADA、LDH和VEGF之间亦无明显相关性。结论：VEGF在鉴别良恶性心包积液中具有一定的价值。     

Pericardial effusion: clinical and analytical parameters clues

Prospectively, clinical and biochemical data of 83 patients with a diagnosis of pericardial effusion were studied. The etiologies were as follows: Idiopathic: 42 cases (50%); Tuberculous: 18 cases (22%); Neoplastic: 14 cases (17%); Other: 9 cases (11%) with a miscellaneous etiology. Sedimentation rate resulted significantly higher in Tuberculous group (67-102), p<0.05. The highest values of adenosine deaminase in pericardial fluid were observed in Tuberculous group (110 U/l), p<0.001. Diagnosis of tuberculosis was established by culture of the bacillus in sputum in 8 cases and by pericardial biopsy in 11 patients. Analysis of the pericardial fluid leads to diagnosis in 25 cases (30%). The pericardial biopsy resulted as the most reliable method for the diagnosis of tuberculous pericarditis.     

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.     

A case of tuberculous pericarditis—Use of adenosine deaminase activity (ADA) in early diagnosis

Pericardial tuberculosis is rare, and because of the difficulty in isolating the causative organism, the diagnosis is often missed. Adenosine deaminase, an enzyme associated with purine metabolism, shows markedly high levels of activity in tuberculous effusion. We report a case of tuberculous pericarditis diagnosed by high levels of adenosine deaminase activity, and where the pericardial fluid cultures revealed acid-fast organisms.     

The use of adenosine deaminase and interferon-gamma as diagnostic tools for tuberculous pericarditis

BACKGROUND: Traditional diagnostic tests for pericardial tuberculosis (TB) are insensitive and often require long culture periods, and this has led to more emphasis being placed on biochemical tests such as the pericardial adenosine deaminase (ADA) test. However, controversy exists as to its diagnostic utility. In addition, the use of interferon (IFN)-gamma, which is a reliable indicator of pleural and peritoneal TB, has not been explored in pericardial effusions. We investigated ADA and IFN-gamma levels in pericardial effusions of different etiologies. METHODS AND RESULTS: A prospective study was carried out from February 1995 to February 1998 at Tygerberg Hospital (South Africa), with pericardial taps being performed under echocardiographic guidance. During this period, 110 consecutive patients presenting with large pericardial effusions were included in the study. Diagnoses were made according to predetermined criteria, and they included TB (n = 64), malignancy (n = 12), nontuberculous infections (n = 5), other effusions (n = 19), and effusions of uncertain origin (n = 10). The median ADA level in the tuberculous group was 71.7 U/L (range, 10.3 to 303.6 U/L), which was significantly higher than that in any other group (p < 0.05). With a cutoff level for ADA activity of 30 U/L, sensitivity was 94%, specificity was 68%, and positive predictive value was 80%. IFN-gamma levels were determined in 30 subjects. The median IFN-gamma concentration in the tuberculous group was > 1,000 pg/L, which was significantly higher than in any other diagnostic group (p < 0.0005). A cutoff value of 200 pg/L for IFN-gamma resulted in a sensitivity and specificity of 100% for the diagnosis of pericardial TB. CONCLUSION: Pericardial fluid levels of ADA and IFN-gamma are useful in the diagnosis of tuberculous pericarditis.     

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。     

Relevance of adenosine deaminase and lysozyme measurements in the diagnosis of tuberculous pericarditis

OBJECTIVE: To assess the value of pericardial fluid adenosine deaminase (ADA) and pericardial lysozyme (Lys) as tools in diagnosing tuberculous pericarditis. METHODS: Forty-one patients (age range 17--77 years) with significant pericardial effusion were included in the study. Diagnostic pericardiocentesis and pericardial biopsy were performed while serum and pericardial fluid ADA and Lys were measured in all patients. Grouping of patients resulted as follows: group I = 7 patients with tuberculous pericarditis; group II = patients with neoplastic pericarditis; group III = 30 patients with idiopathic pericarditis. RESULTS: Pairwise multiple comparison procedures revealed a significant difference of ADA in group I versus group III (p < 0.05) but not versus group II. Furthermore, pericardial Lys in group I was higher than in groups II and III (p < 0.05). A strong correlation between pericardial ADA and Lys was found (r = 0.733, p = 0.01) for all the patients. Receiver operating curves showed a value of 72 U/l as cutoff point of pericardium ADA, with a sensitivity of 100% and a specificity of 94% in the diagnosis of tuberculous pericarditis. Similarly for pericardial Lys, a value of 6.5 microg/dl had a sensitivity and specificity of 100 and 91.17%, respectively. CONCLUSIONS: Both measurements of pericardial ADA and Lys need to be taken into account when attempting the early diagnosis of tuberculous pericarditis.     

Adenosine deaminase and tuberculous pericarditis--a systematic review with meta-analysis

BACKGROUNDS: Adenosine deaminase (ADA) activity in pericardial fluid is a valuable aid in the diagnosis of tuberculous pericarditis (TP), but there is no systematic review performed to evaluate the benefits of ADA activity as an adjunctive test for TP diagnosis. The objective of this systematic review was to evaluate the utility of ADA activity as a diagnostic marker of TP on patients presenting with pericardial effusion. METHODS: MEDLINE, LILACS and Cochrane Library databases (1980-2005) searches to identify articles related to adenosine deaminase activity on TP diagnosis. Articles with patients with at least one TP diagnostic criteria were included. The controls were patients with other pericardial diseases with moderate or large pericardial effusion. To calculate the sensitivity, specificity, as well as positive and negative likelihood ratios we extracted the total number of confirmed TP cases over all patients with pericardial effusion as well as the number of cases with ADA activity values of 40 U/L and over. RESULTS: Thirty one studies met our initial inclusion criteria and five articles were selected. The heterogeneity limited the specificity analysis (p=0.004). The method yielded a sensitivity and specificity of 88% and 83%, respectively. The SROC curve presented an area with a tendency towards 1 (value of 0.9539) and corroborates the diagnostic value of ADA activity. CONCLUSIONS: The present study confirms the clinical value of ADA activity as adjunctive diagnostic marker of TP among other causes of pericardial effusion.     

Evaluation of usefulness of pleural fluid adenosine deaminase in diagnosing tuberculous pleural effusion from empyema

ObjectiveTo evaluate the utility of adenosine deaminase activity in the pleural fluid for the diagnosis of tuberculous pleural effusion from empyema of non-tubercular origin.MethodA retrospective analysis of data was performed on patients who were diagnosed to have tuberculous pleural effusion and empyema of non tubercular origin. Among 46 patients at Kasturba Hospital, Manipal University, Manipal, Karnataka, India, from November 2012 to February 2013 who underwent pleural fluid adenosine deaminase estimation, 25 patients with tuberculous pleural effusion and 21 patients with empyema were diagnosed respectively. Adenosine deaminase in pleural fluid is estimated using colorimetric, Galanti and Guisti method.ResultsPleural fluid Adenosine Deaminase levels among tuberculous pleural effusion(109.38±53.83), empyema (141.20±71.69) with P=0.27.ConclusionPleural fluid adenosine deaminase alone cannot be used as a marker for the diagnosis of tuberculous pleural effusion.     

A case of tuberculous pericarditis,the diagnosis of which was complicated by the delay in the rise of adenosine deaminase in the pericardial effusion

An 81-year-old man was admitted to our hospital because of pericardial effusion and sputum PCR positive for Mycobacterium (M.) tuberculosis. Since adenosine deaminase (ADA) value of the pericardial effusion was not high and the sputum smear and culture were negative, anti-tuberculous therapy was not started. Two months later he was admitted again because of high fever and cardiomegaly. Chest computed tomography showed deterioration and the sputum culture revealed M. tuberculosis. The ADA value of the pericardial effusion which was not high at the first admission, was elevated in the second admission, and the diagnosis was made as tuberculous pericarditis two months later. We had better start anti-tuberculous therapy at the first admission, in spite of low value of ADA, as his pericardial effusion showed lymphocyte predominance.