To the Editor: In relation to the recent article by Monreal et al,1Monreal MD Francisco Quilez RN Rey-Joly MD et al.Infusion phlebitis in patients with acute pneumonia.Chest. 1999; 115: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar we believe readers may be interested to learn of the results of a study carried out in our General Internal Medicine Service and communicated at the International Symposium on Thromboembolism held in Lisbon in June 1999.2Taboada-Cotón JM, Pose-Reino A. Factors related with the development of phlebitis after venopuncture. International Symposium on Thromboembolic Diseases: New Achievements and Challenges. Lisbon, Spain: 1999; A6Google Scholar In this work, we investigated the local complications of IV therapy in the 363 patients to whom it was applied in the Service over a period of 3 months, with emphasis on the frequency of phlebitis following venous catheterization and the risk factors favoring this complication; only first catheterizations were considered. Twenty-gauge catheters were used in 92% of cases, 22-gauge catheters in 3%, and 18-gauge catheters in 1.9%; needles were used in 1.7%, and in the remaining 1.4% of cases, central catheters were installed. Phlebitis arose in 35% of cases. Monreal et al1Monreal MD Francisco Quilez RN Rey-Joly MD et al.Infusion phlebitis in patients with acute pneumonia.Chest. 1999; 115: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar observed a slightly higher incidence, 39%, possibly because their study was limited to pneumonia patients and thus to patients receiving IV antibiotics, a known risk factor (see below); other authors have reported incidence rates from 20 to 70%.3Danchaivijirt S Srishapol N Pataworawuth S et al.Infusion-related phlebitis.J Med Assoc Thail. 1995; 78: S85-S90Google Scholar, 4Lipsky BA Peugeot RL Bokyo EJ et al.A prospective study of Staphylococcus aureus nasal colonization and intravenous therapy-related phlebitis.Arch Intern Med. 1992; 152: 2109-2112Crossref PubMed Scopus (11) Google Scholar5Maki DG Ringer M Risk factors for infusion-related phlebitis with small peripheral venous catheters.Ann Intern Med. 1991; 114: 845-854Crossref PubMed Scopus (423) Google Scholar, 6Hershey C Tomford JW McLaren CE et al.The natural history of intravenous catheter-associated phlebitis.Arch Intern Med. 1984; 144: 1373-1375Crossref PubMed Scopus (75) Google Scholar Onset was invariably within the first few days of catheterization (95% confidence interval, 2.7 to 3.5 days). There were no statistically significant differences among the different types of catheter (unsurprisingly, in view of the great predominance of 20-gauge catheters). Like Monreal et al1Monreal MD Francisco Quilez RN Rey-Joly MD et al.Infusion phlebitis in patients with acute pneumonia.Chest. 1999; 115: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar and others,6Hershey C Tomford JW McLaren CE et al.The natural history of intravenous catheter-associated phlebitis.Arch Intern Med. 1984; 144: 1373-1375Crossref PubMed Scopus (75) Google Scholar, 7Meguro S Kuraishi Y Kobayashi T et al.Phlebitis associated with the intravenous use of cephapirin and cephalotin in the combination therapy of antibiotics.Jpn J Antibiot. 1980; 33: 1163-1165Google Scholar8Lewis GBH Hecker JF Infusion thrombophlebitis.Br J Anaesth. 1985; 57: 220-233Crossref PubMed Scopus (107) Google Scholar we found that IV administration of antibiotics was the greatest risk factor. Furthermore, risk increased with the number of antibiotics administered. Also like Monreal et al,1Monreal MD Francisco Quilez RN Rey-Joly MD et al.Infusion phlebitis in patients with acute pneumonia.Chest. 1999; 115: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar we found that incidence was lower among patients who were receiving IV corticosteroids than among those who were not, with similar findings for diuretics and bronchodilators, although in none of these cases was the difference statistically significant. We regret not having investigated the influence of hemoglobin level, the pro-phlebitic effect of which was the most interesting finding of Monreal et al.1Monreal MD Francisco Quilez RN Rey-Joly MD et al.Infusion phlebitis in patients with acute pneumonia.Chest. 1999; 115: 1576-1580Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar In conclusion, we found a high incidence of phlebitis among patients receiving IV medication. There appears to be no doubt that IV administration of antibiotics is a risk factor, and the risk increases with the number of antibiotics administered. Possible prophylactic measures include the use of heparin and limitation of the level of insult by control of drug dilution and infusion rate.

Different systemic and local responses to mycobacterial antigens suggest an active compartmentalization of responsive lymphocytes to tubercular antigens. This fact, observed in pleuritic processes, raises doubts about the accuracy of information obtained in the study of cells taken solely from peripheral blood. For this reason we decided to study the concept of compartmentalization in 140 patients suffering from pleural effusions. Patients were classified into six groups according to the aetiology of the effusion: group I, tuberculous, n = 23; group II, paraneoplastic, n = 41; group III, metapneumonic empyematous, n = 5; group IV, transudate, n = 38; group V, miscellaneous exudate, n = 19; group VI, unknown aetiology, n = 14. In each group we studied the lymphocyte population by using flow cytometry with doubly fluorescent monoclonal antibodies: B [expressing human lymphocyte antigen (HLA)-DR on the surface], T (CD3 +), CD4 + and CD8 +, and the subpopulation of activated T lymphocytes (together expressing CD3 and HLA-DR on the surface) (CD3 + DR +). The study of these subpopulations in peripheral blood did not yield valuable results, but the CD3 + DR + population in pleural fluid demonstrated a diagnostic efficiency of 84% [positive predictive value (PPV) 51%, negative predictive value (NPV) 96%] at a cut-off value of 80.4 cells/mm 3 . The CD3 + DR + pleural fluid/peripheral blood ratio demonstrated an efficiency of 83% (PPV 50%, NPV 96%), and showed a statistically significant difference ( P < 0·02) with regard to all the diagnostic groups, with the exception of the paraneoplastic effusions. The lymphocytic subpopulations study confirms the concept of compartmentalization in tuberculous pleuritis, as shown by the greater number of activated T lymphocytes present in pleural fluid in comparison with peripheral blood in tuberculous pleuritis, a 98% efficiency of adenosine deaminase (ADA) determination in pleural fluid versus a 50% value in peripheral blood, predominance of helper cells (CD4 +) in pleural fluid and suppressor cells (CD8 +) in peripheral blood, a greater CD4 + /CD8 + ratio in pleural fluid than in peripheral blood, and a significant correlation of ADA-CD3 + DR + in pleural fluid, which does not occur in peripheral blood.

this patient's CD4' T-lymphocyte depletion, including HIV infection.Thus, our patient with idiopathic CD4+ T-lymphocytopaenia had suffered from miliary tuberculosis with acute respiratory failure.

OBJECTIVES:To determine the age at which tuberculous pleural effusions occur, the radiological and biochemical characteristics of the effusions, the sensitivities of the various diagnostic tests, and the utility of combining clinical, radiological, and analytic data in diagnosis.METHODS:We studied the case histories of 254 patients in whom tuberculous pleural effusions were diagnosed with certainty between January 1, 1989, and June 30, 1997, in a Spanish university hospital in a region with a high incidence of tuberculosis.RESULTS:The mean (+/-SD) age of the patients was 34.1+/-18.1 years, and 62.2% were younger than 35 years. The effusion was on the right side in 55.9% of patients, on the left side in 42.5% of patients, and on both sides in 1.6% of patients. In 81.5% of patients, less than two thirds of the hemithorax was affected. Associated pulmonary lesions were detected in 18.9% of patients, of whom 14.6% exhibited cavitation. In 93.3% of the effusions, more than 50% of leukocytes were lymphocytes, and almost all had the biologic characteristics of exudates (98.8% had high total protein contents, 94.9% had high cholesterol levels, and 82.3% had high lactate dehydrogenase levels). All but 1 effusion (99.6%) had an adenosine deaminase (ADA) concentration higher than 47 U/L, 96.8% (123/127) of the effusions had high ADA2 levels, and 89% (73/82) of the effusions had high interferon gamma levels. Adenosine deaminase 2 contributed 72.2%+/-12.5% (mean +/- SD) of total ADA activity. Total ADA activity was significantly correlated with ADA2 (r = 0.83) and with interferon gamma (r = 0.30) levels. Definitive diagnosis was based on the observation of caseous granulomas in pleural biopsy tissue samples in 79.8% of patients, on the results of biopsy cultures in 11.7% of patients, and on pleural effusion cultures in the remaining 8.5% of patients. Results of the tuberculin skin test were positive in only 66.5% of patients.CONCLUSIONS:In these patients, lymphocyte-rich exudative pleural effusions occurred, on average, at a young age, with no preference for either the right or the left side; normally affected no more than two thirds of the hemithorax; and were generally unaccompanied by pulmonary infiltrates. High ADA concentration was a highly sensitive diagnostic sign and was caused by a rise in ADA2 concentration. The most sensitive criterion based on pleural biopsy was the observation of caseous granulomas, and culture of biopsy material further increased overall sensitivity. Negative skin test results were no guarantee of the effusion being nontuberculous. This, together with the low mean age of the patients and the low frequency of associated pulmonary lesions, suggests that tuberculous pleural effusion is a primary form of tuberculosis in this region.

Approximately 20% of pleural effusions are caused by neoplastic processes. Although cytology is the most specific routine diagnostic procedure, its sensitivity of 50–60% is insufficient, and thus diagnosis is usually carried out by more invasive techniques such as pleural biopsy, thoracoscopy or thoracotomy. The object of this study is to evaluate the use of determining some tumour markers in pleural fluid obtained by thoracocentesis for diagnosis of neoplastic pleural effusion. Patients (271) with pleural effusions were classified in five groups: I: neoplasms n = 88; II: tuberculosis n = 63; III: parapneumonics n = 53; IV: miscellaneous exudates n = 39 and V: transudates n = 28. The tumour markers studied were: carcinoembryonic antigen (CEA), CA 125, squamous cell carcinoma antigen (SCC), and neuron specific enolase (NSE). The tumour makers had the following diagnostic efficiencies for neoplastic origin of the pleural effusion: CEA 76% (sensitivity 31%, specificity 93%); CA 125 66% (70% and 61%); SCC 65% (48% and 80%) and NSE 53% (30% and 89%). The diagnostic efficiencies for pulmonary neoplastic origins were 68% for NSE (sensitivity 83%, specificity 53%); 65% for SCC (54% and 75%); 63% for CEA (80% and 48%) and 61% for CA 125 (79% and 42%). We believe that the routine testing of tumour markers in pleural fluid obtained by thoracocentesis would greatly increase diagnostic effectiveness and could avoid the practice of more aggressive diagnostic techniques on the patient.

To investigate the etiology of pleural effusions in our region, we undertook a prospective study of patients with this condition in our centers. During a 5-year period, we studied 642 pleural effusion patients aged 57.1 +/- 21.1 years, of whom 401 were men aged 56.5 +/- 21 years and 241 were women aged 57.8 +/- 21.4 years; the male/female ratio was 1.6:1. The most frequent cause of pleural effusion was tuberculosis (25%), followed by neoplasia (22.9%) and congestive heart failure (17.9%). The etiology of 48 cases (7.5%) remained uncertain. In the neoplastic effusion group, the most frequent locations of the primary tumor were lung (32.6%), breast (11.5%), lymphoma (10.8%), and ovary (7.5%); in 21 cases (14.3% of the neoplastic group), it was not possible to identify the primary tumor. The 111 patients aged younger than 40 years with tuberculous effusions made up 69.4% of tuberculous effusion cases and the same percentage of patients younger than 40 years; the proportion of effusions that were tuberculous peaked in the 11- to 30-year-old age group and declined steadily thereafter. Of the patients with neoplastic effusions, 83% were older than 50 years; the proportion of effusions that were neoplastic rose steadily from zero in the 0- to 30-year-old age group to a peak among 60- to 70-year-olds. The age-wise distribution of effusions secondary to congestive heart failure was similar to that of neoplastic effusions. Of the effusions secondary to congestive heart failure, 86% (99/115) affected the right pleura or both, and 83% of effusions secondary to pulmonary thromboembolism (15/18) affected the right side. Neoplastic, tuberculous, parapneumonic, empyematous, and other exudative effusions showed no preference for either side. Of the 97 bilateral effusions, 77 (79.4%) were secondary to heart failure (59, 60.8%) or neoplasia (18, 18.6%). We conclude that in our region, the most frequent cause of pleural effusion is tuberculosis, followed by neoplasia and congestive heart failure. We suggest that all those interested in pleural disease should determine the etiologic pattern of pleural effusion in their region with a view to the adoption of regionally optimized diagnostic and therapeutic attitudes.

The rise in adenosine deaminase (ADA) activity in the pleural fluid of tuberculous pleurisy patients, though used for diagnosis, is of unknown origin. In this work, we determined ADA activity and the activities of 2'-deoxyadenosine deaminase and ADA-2 in 350 patients. We also considered whether the results throw light on the origin of high pleural fluid ADA in tuberculous pleurisy and estimated the diagnostic efficiency of 2'-deoxyadenosine deaminase, ADA-2 and total ADA activities with and without the inclusion of the 2'-deoxyadenosine deaminase/ADA activity ratio in a combined criterion. The 350 pleural effusions were classified by previously established criteria as transudates (60 males/18 females) or as tuberculous (49 males/27 females), neoplastic (50 males/39 females), parapneumonic (36 males/19 females), empyematous (11 males/3 females), or miscellaneous (25 males/13 females) exudates. Total ADA, ADA-2 and 2'-deoxyadenosine deaminase activities were, respectively, 127.5 +/- 2.9, 103 +/- 29.5 and 42.8 +/- 14 U.L-1 in tuberculous exudates. With diagnostic thresholds of 47, 40 and 22 U.L-1 respectively, the sensitivities of ADA, ADA-2 and 2'-deoxyadenosine deaminase for tuberculosis were 100, 100 and 95%; their specificities 91, 96 and 92%; and their efficiencies 93, 97 and 93%, respectively. One hundred and one effusions (all 76 tuberculous, 12 neoplastic, 4 parapneumonic and 9 empyematous exudates) had total ADA levels > 47 U.L-1; of these, 8 neoplastic, 1 parapneumonic and all the tuberculous exudates had a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49. The criterion of simultaneously having ADA > 47 U.L-1, ADA-2 > 40 U.L-1 and a 2'-deoxyadenosine deaminase/ADA activity ratio < 0.49 was satisfied by all the tuberculous effusions but only eight others (all neoplastic) (sensitivity 100%, specificity 97%, efficiency 98%). We conclude that: 1) high total ADA activity in tuberculous pleural effusions is due mainly to an increase in ADA-2, and, therefore, originated from the only known source monocytes and macrophages; 2) ADA-2 was a more efficient diagnostic marker of tuberculous pleurisy than total ADA activity, although the difference was not statistically significant; and 3) among effusions with high total ADA the 2'-deoxyadenosine deaminase/ADA activity ratio differentiates tuberculous effusions from empyemas and parapneumonic effusions, but fails to discriminate well between tuberculous and neoplastic effusions.

Chylothorax, a condition featuring an infrequent form of pleural effusion, is generally caused by tumours or traumatism. Only about 1% of chylothorax cases are caused by cirrhosis of the liver. Two such cases are described in these case reports.

A lo largo de 15 meses se estudió, de forma prospectiva, la resistencia primaria de 100 cepas de Mycobacterium tuberculosis aisladas en enfermos diagnosticados de tuberculosis activa mediante confirmación bacteriológica. Se encontraron cepas resistentes, a uno o más fármacos, en el 5% de los pacientes. Tres enfermos presentaron resistencias a dos fármacos (isoniacida y estreptomicina en 2 casos y rifampicina e isoniacida en el otro), uno a tres (isoniacida, estreptomicina y etambutol) y otro únicamente a la pirazinamida. Debido al escaso número de resistencias primarias halladas, no fue posible establecer si alguno de los factores analizados en cada paciente se relacionaba con una mayor tasa de resistencias, si bien 4 de las 5 cepas con resistencia primaria procedían de muestras respiratorias. Concluimos que la tasa de resistencias primarias en nuestro medio es escasa, lo que nos permite, por una parte, prescindir del uso de un cuarto fármaco durante los dos primeros meses del tratamiento antituberculoso y, por otra, no realizar de forma sistemática pruebas de sensibilidad a pacientes que no refieran historia de tratamiento antituberculoso previo. The primary resistance of 100 specimens of Mycobacterium tuberculosis isolated in patients with active tuberculosis confirmed bacteriologically was studied prospectively over a period of 15 months. Strains resistant to 1 or more drugs were found in 5 patients. Three patients presented resistance to 2 drugs (isoniacide and streptomycin in 2 and rifampicin and isoniazid, streptomycin and ethambutol); and the fifth was resistant only to pyrazinamide. Owing to the few instances of primary resistance found, it was impossible to establish whether any of the factors analyzed in each patient was related to a higher index of resistance, although 4 of the 5 resistant strains came from respiratory specimens. We conclude that the index of primary resistance in our area is low and this allows us to do without prescribing a fourth drug in the first two months of anti-tuberculosis therapy, and makes routine sensitivity tests unnecessary for patients with no history of prior treatment for tuberculosis.

BACKGROUND:Pleural biopsy is usually considered important for the diagnosis of pleural effusions, especially for distinguishing between tuberculosis and neoplasia, even though tuberculous pleural fluid contains sensitive biochemical markers. In regions with a high prevalence of tuberculosis, and in patient groups with a low risk of other causes of pleurisy, the positive predictive value of these markers is increased. The criteria for performing a pleural biopsy under these circumstances have been investigated, using adenosine deaminase (ADA) as a pleural fluid marker for tuberculosis. METHODS:One hundred and twenty nine patients with a pleural effusion aged < or = 35 years (mean (SD) 25.2 (4.9) years) were studied. Seventy three were men. Eighty one effusions (62.8%) were tuberculous, 12 (9.3%) parapneumonic, and 10 (7.7%) neoplastic, five were caused by pulmonary thromboembolism, four by systemic lupus erythematosus, seven by empyema, three following surgery, one was the result of asbestosis, and one of nephrotic syndrome. In five cases no definitive diagnosis was reached. ADA levels were determined by the method of Galanti and Giusti. RESULTS:The diagnostic yield of procedures not involving biopsy was 94.5% (122/129). Pleural biopsy provided a diagnosis in a further two cases, but not in the remaining five. All tuberculous cases had pleural fluid levels of ADA of > 47 U/l (mean (SD) 111.1 (36.6) U/l). The only other cases in which ADA exceeded this level were six of the seven patients with empyema. Cytological examination of the pleural fluid diagnosed eight of the 10 neoplastic cases, compared with six diagnosed by pleural biopsy. CONCLUSIONS:In a region with a high prevalence of tuberculosis procedures not involving pleural biopsy have a very high diagnostic yield in patients with a pleural effusion aged < or = 35 years, making biopsy necessary only in cases in which pleural levels of ADA are below 47 U/l, pleural fluid cytology is negative and, in the absence of a positive basis for some other diagnosis, neoplasia is suspected.

Bronchiolitis obliterans organizing pneumonia (BOOP) is a clinicopathological entity with well-defined diagnostic criteria, the aetiology of which is generally unknown. Among the adverse pulmonary effects of the drug amiodarone, BOOP is the least commonly reported in the literature. In this article we describe a case of amiodarone-induced BOOP.

We report a rare case of acute respiratory failure in a previously asymptomatic patient showing clinical signs of inferior cranial nerve palsy together with weakness and muscular atrophy of the upper limbs. Magnetic resonance imaging revealed Arnold-Chiari malformation associated with platybasia, basilar impression, syringomyelia and Klippel-Feil syndrome. Episodes of apnoea required tracheostomy and recurred upon tentative closure of the tracheostome, but remitted upon decompression of the posterior fossa. This case involved both obstructive mechanisms and dysfunction of the respiratory centre. Patients with respiratory failure not explained by pulmonary pathology should be checked for underlying neurological disease.

The primary resistance of 100 specimens of Mycobacterium tuberculosis isolated in patients with active tuberculosis confirmed bacteriologically was studied prospectively over a period of 15 months. Strains resistant to 1 or more drugs were found in 5 patients. Three patients presented resistance to 2 drugs (isoniazide and streptomycin in 2 and rifampicin and isoniazid, streptomycin and ethambutol); and the fifth was resistant only to pyrazinamide. Owing to the few instances of primary resistance found, it was impossible to establish whether any of the factors analyzed in each patient was related to a higher index of resistance, although 4 of the 5 resistant strains came from respiratory specimens. We conclude that the index of primary resistance in our area is low and this allows us to do without prescribing a fourth drug in the first two months of anti-tuberculosis therapy, and makes routine sensitivity tests unnecessary for patients with no history of prior treatment for tuberculosis.

We compared the parameters pleural adenosine deaminase (PADA, determined in 405 patients), the PADA/serum ADA ratio (P/SADA; 276 cases), pleural lysozyme (PLYS, 276 cases), the PLYS/serum LYS ratio (P/SLYS; 276 cases), and pleural interferon gamma (IFN, 145 cases) regarding their ability to differentiate tuberculous pleural effusions from others. The 405 pleural effusions were classified by previously established criteria as tuberculous (91), neoplastic (110), parapneumonic (58), empyemas (10), transudates (88), or miscellaneous (48). The intermean differences between the tuberculous group and each of the others were statistically significant for all five parameters (p < 0.01 for PLYS and P/SLYS with respect to the empyema group; p < 0.001 otherwise), except for PADA and P/SADA with respect to the empyema group. All the tuberculous pleurisy cases had PADA values of 47 U/L or more, as compared to only 5 percent of the other cases (sensitivity, 100 percent; specificity, 95 percent). P/SADA was above 1.5 in 85.7 percent of tuberculous effusions and 11 percent of the others (sensitivity, 85.7 percent; specificity, 89 percent). PLYS, with a diagnostic threshold of 15 g/ml, had a sensitivity of 85.7 percent and a specificity of 61.6 percent; P/SLYS, with a threshold of 1.1, had a sensitivity of 67.3 percent and a specificity of 90.3 percent; and IFN, with a threshold of 140 pg/ml, had a sensitivity of 94.2 percent and a specificity of 91.8 percent. The lowest misclassification rate was achieved by PADA, with statistically significant differences (p < 0.001) with respect to P/SADA, PLYS, and P/SLYS, but not with respect to IFN. The only significant pairwise correlations among these parameters were between P/SLYS and PADA and between P/SLYS and P/SADA. We conclude that PADA and IFN are useful parameters for early diagnosis of tuberculous pleurisy, and that the other parameters considered have no advantages over PADA and IFN for this purpose (though the high specificity of P/SLYS may be noted).

Iron levels in samples from certain treated tuberculous patients are underestimated by the Ferrochem II analyser. Of the tuberculostatic drugs examined for a possible interference, isoniazid, ethambutol, rifampicin, pyrazinamide and Rifater (a mixture of rifampicin, isoniazid and pyrazinamide), only pyrazinamide and Rifater (due to its pyrazinamide content) were associated with iron levels differing significantly (p < 0.001) from those of controls, with means of -317.2 and -185.6 mumol l-1 for pyrazinamide and Rifater respectively as against 9.91 mumol l-1 for the controls. The negative interference (I) due to pyrazinamide was independent of iron level in the samples but dependent on pyrazinamide concentration in the same (P) (r = 0.9993), I = -0.4380P-0.4276.

Sixteen patients who had massive pulmonary thromboembolism and shock had no history of cardiopulmonary disease. We present an evaluation of the short-term effects of fibrinolytic treatment consisting of intrapulmonary administration of a bolus of 500,000 IU of urokinase followed by infusion of 1 x 10(6) IU into the right auricle over 12 h and subsequent intravenous infusion of heparin. For each patient, the effectiveness of treatment was evaluated by comparing pretreatment angiographic and hemodynamic parameters with those measured 48 h after the start of treatment. The Miller index fell from 22.9 +/- 5.9 to 9.8 +/- 3.3 (p less than 0.001), with a mean improvement of 57.2 percent. All the hemodynamic parameters studied (cardiac output and index, total pulmonary vascular resistance, and systolic, diastolic, and mean pulmonary vascular pressure) also exhibited statistically significant differences between pretreatment and posttreatment values (p less than 0.001 for each parameter), with a mean improvement of over 30 percent in each case. All the patients survived, and in no case did treatment fail; only one patient (6.2 percent) suffered severe hemorrhage. We conclude that this form of administration of urokinase is useful for patients with critical massive pulmonary thromboembolism.

Conventional tests are not always helpful in making a diagnosis of tuberculous pleurisy. Many studies have investigated the usefulness of adenosine deaminase (ADA) in pleural fluid for the early diagnosis of tuberculous pleurisy. We conducted a meta-analysis to determine the accuracy of ADA measurements in the diagnosis of tuberculous pleurisy.After a systematic review of English language studies, sensitivity, specificity, and other measures of accuracy of ADA concentration in the diagnosis of pleural effusion were pooled using random effects models. Summary receiver operating characteristic curves were used to summarize overall test performance.Sixty-three studies met our inclusion criteria. The summary estimates for ADA in the diagnosis of tuberculous pleurisy in the studies included were sensitivity 0.92 (95% confidence interval 0.90–0.93), specificity 0.90 (95% confidence interval 0.89–0.91), positive likelihood ratio 9.03 (95% confidence interval 7.19–11.35), negative likelihood ratio 0.10 (95% confidence interval 0.07–0.14), and diagnostic odds ratio 110.08 (95% confidence interval 69.96–173.20).ADA determination is a relative sensitive and specific test for the diagnosis of tuberculous pleurisy. Measurement of ADA in pleural effusion is thus likely to be a useful diagnostic tool for tuberculous pleurisy. The results of ADA assays should be interpreted in parallel with clinical findings and the results of conventional tests.