Tuberculous Effusion Research Articles

Diagnostic dilemma in tuberculous pleural effusion

AimTo evaluate the clinical use of interferon gamma release assays (QuantiFERON-TB Gold (In-Tube Method)) for the diagnosis of pleural tuberculosis and comparing it with ADA as a method for diagnosis TB effusion. Patients and methods40 patients presenting with pleural effusions were classified according to their final diagnosis in two groups.Group I: Include 20 cases with tuberculous pleural effusions, group II: Control group: 20 cases divided into 2 subgroups: Subgroup11a: para pneumonic pleural effusions: 8 cases, Subgroup11b: malignant pleural effusions: 12 cases. ResultsTuberculous pleural effusion showed statistically significantly lower mean age than non-tuberculous effusion. Tuberculous group showed statistically significantly highest mean ADA. This was followed by para pneumonic group then malignant group. ADA showed sensitivity (98%), specificity (55%), diagnostic accuracy (75%), negative predictive value (PV−) (67.9%) and positive predictive value (PV+) (91.7%) in diagnosing tuberculous effusion QuantiFERON-TB Gold showed sensitivity 65%, specificity 70%, PPV (68.4%), NPPV (66.7%) and diagnostic accuracy (67.5%) in diagnosing tuberculous effusion. ConclusionIt was concluded that ADA measurement in the pleural fluid is an appropriate, fast diagnostic tool for the diagnosis of tuberculous pleural effusion, with higher sensitivity (98%) and diagnostic accuracy (75%). QuantiFERON-TB Gold which is technically more complicated, expensive and has lower sensitivity (65%) and diagnostic accuracy (67.5%) than ADA.

Tuberculous pericarditis: An exceptional STEMI association: Case report

Among all the complications of myocardial infarction, pericardial effusion remains correlated with a high morbidity and mortality rate. Tuberculosis in Morocco is a public health problem with 25,000 new cases per year, 47% of which are extra pulmonary, we present an exceptional case of a 70 year old man presenting with an extensive anterior myocardial infarction complicated with tuberculous pericarditis effusion, highlighting the importance of thinking of this aetiology in a specific context.

Vascular endothelial growth factor in diagnosis of pleural effusion

BackgroundVascular endothelial growth factor (VEGF) is a glycoprotein which is an important mediator of angiogenesis and vascular permeability. Different VEGF levels were found in carcinomatous, inflammatory and tuberculous pleural effusions, implying a varying degree of influence on the process of fluid accumulation in the pleural space in different disease states. Aim of the work: to assess the role of serum and pleural fluid VEGF levels to evaluate its value as a marker in diagnosis of pleural effusion of different etiologies. MethodsForty patients with pleural effusion, 19 males and 21 females, with a mean age of 55.960±6.835years, were classified into transudative and exudative groups. All patients were subjected to thorough history, clinical examination, radiological examination, laboratory investigations, sputum for acid fast bacilli, tuberculin test, thoracocentesis and occasionally pleural biopsy or thoracoscopy and both serum and pleural fluid VEGF were measured in all patients. ResultsThere was a significant difference between exudate and transudate regarding serum and pleural fluid VEGF levels that were higher in exudates than transudate. In comparison between the subtypes of exudative effusion, there was higher concentration of VEGF in pleural of malignant than tuberculous, parapneumonic, and collagen exudative effusion. ConclusionVEGF pleural fluid level could differentiate between malignant and non malignant effusion, while could not differentiate between tuberculous and nontuberculous, or between parapneumonic and nonparapneumonic exudative effusions.

Tuberculous Pleuro-Pericardial Effusion with Adenitis

Background: Hydra-headed clinical presentations of tuberculosis could be confusing even in immunocompetent, for example pleuro-pericardial effusion with adenitis. From our literature search, this is rare. Case presentation: A 61-year-old clergyman presented with a 3-week history of cough, fever and a 5-day history of progressive dyspnoea. There was associated anaemia, weight loss but no history of drenching night sweat, hemoptysis, exposure to tuberculosis, diabetes or other suggestion of immunosuppression. Examination revealed multiple matted left axillary lymph nodes. Erythrocyte sedimentation rate (ESR) was 70 mm/hr; and negative for Hepatitis B, C and HIV. Chest X-ray showed left lower lung zone homogenous opacity with obliteration of the left cardiac border. Lymph node aspirate and pleural fluid analyses confirmed a tuberculous aetiology. Conclusion: Tuberculous pleuro-pericardial effusion with adenitis occurs in immunocompetent. High index of suspicion in endemic areas as well as early anti-tubercular treatment could be life-saving.

Adenosine deaminase in pleural effusions with special reference to tuberculous effusions

Adenosine deaminase in pleural effusions with special reference to tuberculous effusions

Comparison of the diagnostic utility of ADA and CA125 in tuberculous effusion

BackgroundPleural effusion can be due to various pleural infections like TB as well as neoplasia. CA125 is a tumor marker found on the surface of ovarian and other normal cells as pleural cells. CA125 has been found to increase in serum and hence pleural fluid of patients with pleural effusion due to malignancy as well as due to TB.This study was conducted to evaluate the utility of CA125 in the diagnosis of pleural effusion resulting from TB, malignancy and pneumonia as well as to evaluate and compare the diagnostic utility of CA125 and ADA in the diagnosis of TB effusion. Patients and methods20 patients with tuberculous effusion (group I), 20 patients with malignant effusion (group II) and 20 patients with parapneumonic effusions (group III) were evaluated for the levels of CA125 and ADA in their pleural fluid. In malignant cases, diagnosis was made through microscopic inspection of pleural biopsy samples and cytology of pleural fluid. For diagnosis of tuberculosis, Ziehl Neelsen sputum smear, pleural fluid smear and/ or culture. Parapneumonic effusions were confirmed by pleural fluid cell count and culture & sensitivity. ResultsThe mean±SD level of CA125 in pleural fluid was 41.732±20.744U/ml, 309.27±79.564U/ml and 7.040±5.601U/ml in tuberculous, malignant and parapneumonic effusions respectively; which showed a statistically significant difference between the three groups (p<0.01). Pleural fluid CA125 was significantly higher in group II than group I (P1=0.000), and group III (P3=0.000). Pleural fluid CA125 was significantly higher in group I than group III (P2=0.000). Pleural fluid ADA was significantly higher in group I than group II (P1=0.000) and group III (P2=0.000). For diagnosing TB, CA125 showed a sensitivity and specificity of 74.1%, 76.9%, respectively while ADA demonstrated a sensitivity and specificity of 75% and 75% respectively. ConclusionCA-125 levels in pleural fluid may be used for differentiation between TB, pneumonic, and malignancy-induced effusions.Also CA125 may be added to the diagnostic workup of pleural fluid for accurate diagnosis of TB effusion.

Laboratory Diagnosis of Tuberculosis- an Update

Annually about two million deaths occur globally due to tuberculosis (TB). Bangladesh ranks the sixth position among 22 highest burden TB countries in the world and also one of the 27 high multidrug resistant tuberculosis (MDR-TB) burden countries where about 70,000 people die every year due to TB. Among six key components of Stop TB Strategy (STS) Plan, the first one includes increase case notification of all forms of TB and improve diagnosis of new smear negative, extrapulmonary cases and TB in children by 2016. As TB can affect any organ in human body, the TB cases are managed by any discipline in medical community. Unfortunately diagnostic accuracy is not satisfactory and is not only due to uniform unavailability of the latest diagnostic facilities but also due to inadequate knowledge of the professionals about currently available modern laboratory techniques to diagnose TB. Light-emitting diode (LED) microscopy with fluorescence (auramine-rhodamine staining) should be preferred than conventional microscopy with Zeihl-neelsen (acid fast) staining to identify TB bacilli. Mantoux test (MT) indicates only infection by TB bacilli, does not necessarily the active disease. It may be positive in latent TB and in BCG (Bacillus Calmette-Guerin) vaccinated cases. Antibodies from Lymphocyte Secretion or Antibodies in Lymphocyte Supernatant (ALS) assay can detect active TB cases within three days of sample collection. The test is very useful to diagnose TB in children where sputum collection is difficult. Interferon gamma release assay (IGRA) tests are not advocated in low and middle-income countries, typically those with a high TB and/or HIV burden. Anti TB IgG/IgM/IgA tests should be avoided because these are being misinterpreted by someone as active TB cases. Adenosine Deaminase Assay (ADA) is a reliable test to diagnose tuberculous pleural effusion together with other evidences. ADA in pleural fluid &lt;40 IU/L is considered negative for TB. The more the ADA level, the more possibility to be tuberculous effusion. Level &gt;100 IU/L is highly specific for TB origin. Gene Xpert MTB/RIF, an Xpert test for mycobacterium tuberculosis (MTB) and Rifampicin (RIF) resistance, is used for rapid identification for TB bacilli, specially when MDR-TB is suspected, in human immunodeficiency virus ( HIV) infected cases and highly suspected sputum negative cases ( as a follow on test ) where microscopy frequently failed due to low bacterial load. The test exhibits high sensitivity and specificity for detecting pulmonary TB.Faridpur Med. Coll. J. Jul 2015;10(2): 71-75

Expressions and diagnostic value of the cytokines in tuberculous and malignant pleural effusion

Objective To analyze the levels of pro-inflammatory cytokines, anti-inflammatory cytokines and chemokines in tuberculous and malignant pleural effusion using Luminex method, and to evaluate their diagnostic value in tuberculous pleural effusion. Methods Fifty-three patients with tuberculous pleural effusion and 28 patient with malignant pleural effusion were included in this study. Luminex method was applied to detect the levels of pro-inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-12, interferon [IFN]-γ and tumor necrosis factor [TNF]-α), anti-inflammatory cytokines (IL-1 receptor antagonist [IL-1ra], IL-4, and IL-10), and chemokines (IFN-γ inducible protein [IP]-10, macrophage inflammatory protein [MIP]-1α, MIP-1β, and monocyte chemo-attractant protein [MCP]-1) in all patients. The levels of cytokines were compared using Mann-Whitney test. Results The levels of IFN-γ (1 064.33 pg/mL vs 294.78 pg/mL, U=130.5, P<0.01) and IP-10 (39 179.86 pg/mL vs 9 411.73 pg/mL, U=98.0, P<0.01) in tuberculous pleural effusion were significantly higher than those in malignant pleural effusion, while the IL-10 level (11.52 pg/mL vs 17.77 pg/mL, U=565.5, P=0.017) was significantly lower than that in malignant pleural effusion. Furthermore, IFN-γ/IL-10 (100.07 vs 16.19, U=116.0, P<0.01) and IP-10/IL-10 (2 930.91 vs 591.18, U=75.0, P<0.01) in tuberculous pleural effusion were significantly higher than those in malignant pleural effusion. Area under the curve of receiver operating characteristic of IFN-γ, IP-10, IFN-γ/IL-10, and IP-10/IL-10 were 0.91, 0.93, 0.92 and 0.95, respectively, with the cut-off value of 483.5 pg/mL, 20 340 pg/mL, 41.11 and 1 614. For the diagnosis of tuberculous pleural effusion, the sensitivities and specificities of IFN-γ≥483.5 pg/mL, IP-10≥20 340 pg/mL, IFN-γ/IL-10≥41.11, and IP-10/IL-10≥1 614 were 0.830(95%CI: 0.702-0.920) and 0.962(95%CI: 0.804-0.999), 0.906(95%CI: 0.793-0.969) and 0.923(95%CI: 0.749-0.991), 0.811(95%CI: 0.680-0.906) and 0.923(95%CI: 0.749-0.991), 0.868(95%CI: 0.747-0.945) and 0.923(95%CI: 0.749-0.991), respectively. Conclusions The expression levels of IFN-γ, IP-10 and IL-10 in pleural effusion detected by Luminex method is convenient, rapid, noninvasive, sensitive and specific, which is helpful for the diagnosis of tuberculous pleural effusion. Key words: Cytokines; Tuberculosis, pleural; Pleural effusion, malignant; Diagnosis, differential

Pleural fluid adenosine deaminase/serum C-reactive protein ratio for the differentiation of tuberculous and parapneumonic effusions with neutrophilic predominance and high adenosine deaminase levels.

Tuberculous pleural effusion (TPE) and parapneumonic effusion (PPE) are usually distinguished by cellular predominance and pleural fluid adenosine deaminase (ADA) levels. However, both diseases may occasionally show similar neutrophilic predominance and high ADA levels. In such cases, the differential diagnosis between TPE and PPE is challenging and has been rarely investigated. A retrospective study was conducted on TPE and PPE patients with neutrophilic exudate and pleural fluid ADA levels≥40 U/L. Individual and combined parameters of routine blood and pleural fluid tests were compared between the two groups, and receiver operating characteristic (ROC) curves were constructed for identifying TPE. Thirty-six TPE and 41 PPE patients were included. White blood cell counts, serum C-reactive protein (S-CRP), and pleural fluid pH, lactate dehydrogenase, and ADA levels showed significant difference between the two groups (p<0.001). Among multiple parameters, pleural fluid ADA/S-CRP ratio, which best reflected different local and systemic characteristics between TPE and PPE, provided the highest diagnostic accuracy with an area under the ROC curve of 0.93. At a cutoff value of 5.62, ADA/S-CRP ratio had a sensitivity of 89%, specificity of 88%, positive likelihood ratio of 7.29, and negative likelihood ratio of 0.13 for identifying TPE. Additionally, more than half of TPE patients had a ratio above 15.82, while none of PPE patients showed such findings. Pleural fluid ADA/S-CRP ratio, as a simple method using routine laboratory tests, may be helpful in discriminating between TPE and PPE patients with neutrophilic predominance and ADA ≥40U/L.

The spectrum of heart disease in adults in Malawi: A review of the literature with reference to the importance of echocardiography as a diagnostic modality.

Malawi, like many developing countries, is in a state of health transition from predominately infectious diseases to predominately noncommunicable diseases (NCDs).1–3 This transition has caused many countries to have a “double burden” of disease, with high levels of both communicable and noncommunicable pathologies.4,5 The transition has coincided with increasing affluence and life expectancy among Malawians. Between 2003 and 2013, life expectancy in Malawi has increased from 37 to 53 years,6 with an adjusted life expectancy of 77 years for Malawians who survive to age 60.7 Cardiac diseases related to infection may present at any age, but those related to NCDs predominate in older age groups. The spectrum of heart disease can provide an indicator of the health transition from infectious to non-infectious diseases. Echocardiography is a noninvasive modality for gaining both structural and functional information about the heart. Echocardiography can be used to identify infection-related pathology, such as valvular heart disease following rheumatic fever or tuberculous pericardial effusion,8 and noncommunicable pathologies such as hypertensive heart disease or cor pulmonale. The information gained can lead to life-saving changes in management. This review will describe the spectrum of adult cardiac disease in Malawi, including changes over time, especially the impact of the HIV epidemic and the health transition from communicable to noncommunicable diseases. Selected studies from the sub-Saharan region will be reviewed to illustrate the usefulness of echocardiography in diagnosing heart disease when other investigations are not available.

Interleukin-20 and interleukin-22 in pleural effusion

To investigate the concentrations and clinical significance of interleukin (IL)-20 and IL-22 in pleural effusion with various etiologies. Pleural effusion (PE) and corresponding serum samples were obtained from 88 patients from Wuhan Tuberculosis Prevention and Control Institute from June 2011 to June 2013. There were 27 cases with malignant pleural effusion, 24 with tuberculous pleural effusion, 17 with bacterial pleural effusion and 20 with transudativeeffusion. The pleural and serum levels of IL-20 and IL-22 were determined by sandwich enzyme-linked immunosorbent assays (ELISA). (1) Except for transudativeeffusion, the concentration of IL-20 in malignant pleural effusion (36.8±5.1) ng/L, tuberculous pleural effusion (34.8±6) ng/L, bacterial pleural effusion (41.7±20.2) ng/L, were significantly higher than that of the corresponding serum concentration (29.7±5.97) ng/L, (27.3 ±6.7) ng/L, (25.6±4.7) ng/L (t=5.044, 3.804, 3.452, P<0.05). However, the concentration of IL-20 in pleural effusions of different causes showed no significant difference; malignant (36.8±5.1) ng/L, tuberculous(34.8±6.0) ng/L, bacterial (41.7±20.2) ng/L, transudate (34.1±7.3) ng/L (P>0.05). The concentration of IL-22 (median, quartiles) in tuberculouseffusion was 146.1 (39.8) ng/L and bacterial effusion 59.6 (484.3) ng/L was significantly higher than those in the corresponding serum concentrations 18.7 (9.8) ng/L, 15.7 (17.2) ng/L (Z value respectively -3.971, -3.290, P<0.05). The concentration of IL-22 in tuberculous pleural effusion, bacterial pleural effusion, transudative pleural effusion was significant higher than those in malignant pleural effusion respectively (all P<0.001). (2)The concentrations of IL-22 in malignant pleural effusion was correlated positively with those in serum (r=0.729, P<0.001). (3) With a cut-off value of 19.7 ng/L, pleural IL-22 exhibited a high sensitivity and specificity of 95.1% (39/41) and 88.9%(24/27) respectively, when used for distinguishing infectious pleural effusion (including tuberculous and bacterial effusion) from malignant pleural effusion (P<0.001). Higher levels of IL-22 in tuberculous and bacterial pleural effusion were found when compared with corresponding serum levels and might be involved in the pathogenesis of infectious pleural effusion. Pleural IL-22 measurement provided reliable diagnostic efficiency for distinguishing infectious from malignant pleural effusion.

Development and Validation of the COMPLES Score for Differentiating Between Tuberculous Effusions with Low Pleural pH or Glucose and Complicated Parapneumonic Effusions.

The frequency of "complicated" pleural effusions (CPE) (i.e., pleural fluid pH≤7.2 and/or glucose ≤60mg/dL) of tuberculous origin (CTPE) is not well reported. This study aims to quantify their prevalence, and develop a score to differentiate CTPE from complicated parapneumonic effusions (CPPE). Retrospective analysis of databases from three Spanish hospitals which included patients with CTPE and CPPE. Forty percent of the study population served to generate a scoring system (COMPLES, COMplicated PLeural Effusion Score) that was further validated in the remaining 60%. During the study period (1992-2015) 549 patients were diagnosed with tuberculous effusions and 434 parapneumonic effusions, of whom 25 and 64%, respectively, had CPE. COMPLES was based on the combination of pleural fluid adenosine deaminase (ADA), the percentage of mononuclear cells (MNC%), pH, and age. The cutoff values and assigned scores were: ADA (<46IU/L [0 points], 46-100IU/L [4 points], ≥100IU/L [6 points]), MNC% (<10% [0 points], 10-50 [3 points], >50 [8 points]), pH (<7.07 [0 points], 7.07-7.20 [3 points], >7.20 [5 points]), and age (≥30 [0 points], <30years [3 points]). A sum of 12 or more points had 97% sensitivity, 92% specificity, likelihood ratio positive 12.3, likelihood ratio negative 0.03, and area under the curve of 0.947 for identifying CTPE versus CPPE in the validation set. CPE is not an unusual presentation of tuberculosis. A simple new scoring system provides a reliable tool for differentiating between CTPE and CPPE.

The diagnostic utility and tendency of the soluble receptor for advanced glycation end products (sRAGE) in exudative pleural effusion.

The soluble receptor for advanced glycation end products (sRAGE) may have an inflammatory or homeostatic function in lung tissue. The aim of this study was to assess the usefulness of sRAGE as a diagnostic marker for exudative pleural effusions, which are common manifestations of a variety of diseases. Patients with an undiagnosed pleural effusion were prospectively enrolled between January 2013 and January 2015. Samples of blood and pleural fluid were centrifuged and the supernatant stored at -70 °C. The levels of sRAGE in serum and pleural fluid were determined using a commercially available enzyme-linked immunosorbent assay (ELISA) kit. In total 47 patients, 21 patients were diagnosed with a tuberculous effusion, and the groups diagnosed with parapneumonic or malignant effusions comprised 13 patients each. The serum sRAGE levels for tuberculosis were significantly elevated [median, 1,291 pg/mL; interquartile range (IQR), 948-1,711 pg/mL] when compared with those for both pneumonia (median, 794 pg/mL; IQR, 700-1,255 pg/mL) and lung cancer (median, 886 pg/mL; IQR, 722-1,285 pg/mL) (P=0.029). The pleural sRAGE levels for pneumonia (median, 1,763 pg/mL; IQR, 1,262-4,431 pg/mL) were lower than those for both tuberculosis (median, 5,081 pg/mL; IQR, 3,300-6,004 pg/mL) and lung cancer (median, 4,936 pg/mL; IQR, 3,282-7,018 pg/mL) (P=0.009) The receiver operating characteristic (ROC) curve analysis selected 896 pg/mL as the best cutoff value in the sRAGE serum level for tuberculosis [sensitivity, 86%; specificity 58%; area under the curve (AUC) =0.727, P=0.008]. For the pleural effusion sRAGE level, the ROC curve analysis selected 2,231 pg/mL as the best cutoff value for pneumonia (sensitivity, 91%; specificity, 62%, AUC =0.792, P=0.002). Among patients with exudative effusion, pleural and serum sRAGE measurements may be useful supportive diagnostic tools in the evaluation of ambiguous pleural effusion. Furthermore, the behavior of sRAGE in the serum and pleural fluid of various pulmonary diseases suggests that sRAGE may be linked to the chronic process of lung damage and inflammation rather than acute bacterial infection.

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The role of tumor necrosis factor alpha in differentiation between malignant and non malignant pleural effusion

BackgroundDespite the fact that Light’s criteria remain the gold standard approach in differentiating exudates from transudates, several fluid markers have been introduced for establishing the cause of pleural effusion to differentiate types of pleural exudate. AimThe aim of this study was to explore means of discriminating between malignant and non malignant pleural effusions. MethodsThe study conducted on 45 patients (28-males and 17 females) with pleural effusions of different etiologies. They were classified according to their final diagnosis into four groups: Group I: 10 cases (6 males and 4 females) with tuberculous pleural effusions. Group II: 15 cases (8 males and 7 females) with malignant pleural effusions. Group III: 10 cases (7 males and 3 females) with para-pneumonic effusion. Group IV: 10 cases (7 males and 3 females) with transudative pleural effusions included as a control group. The complete biochemical analysis of pleural fluid, pleural fluid culture, and pathological examination of pleural fluid and tissue was performed. Moreover, quantitative measurement of TNF-α in serum and pleural fluid using ELISA was performed. ResultsLevels of TNF-α were significantly higher in the pleural fluid of exudative nature compared to transudative type. There was a significant increase in pleural fluid TNF-α level in non malignant effusions (tuberculous and parapneumonic) compared with malignant effusion. Also there was a significant increase in pleural fluid TNF-α level in tuberculous effusion versus malignant effusion. These results indicate that TNF-α may be considered a sensitive marker in differentiation between malignant and non malignant pleural effusions. ConclusionPleural fluid level of TNF-α can be used in differentiating malignant from non malignant effusion. Also levels of TNF-α in the serum and pleural fluid could be useful as a complementary marker in the differential diagnosis of two most common types of exudates (tuberculous and malignant).

Identifying Thoracic Malignancies Through Pleural Fluid Biomarkers: A Predictive Multivariate Model.

The diagnosis of malignant pleural effusions may be challenging when cytological examination of aspirated pleural fluid is equivocal or noncontributory. The purpose of this study was to identify protein candidate biomarkers differentially expressed in the pleural fluid of patients with mesothelioma, lung adenocarcinoma, lymphoma, and tuberculosis (TB).A multiplex protein biochip comprising 120 biomarkers was used to determine the pleural fluid protein profile of 29 mesotheliomas, 29 lung adenocarcinomas, 12 lymphomas, and 35 tuberculosis. The relative abundance of these predetermined biomarkers among groups served to establish the differential diagnosis of: malignant versus benign (TB) effusions, lung adenocarcinoma versus mesothelioma, and lymphoma versus TB. The selected putative markers were validated using widely available commercial techniques in an independent sample of 102 patients.Significant differences were found in the protein expressions of metalloproteinase-9 (MMP-9), cathepsin-B, C-reactive protein, and chondroitin sulfate between malignant and TB effusions. When integrated into a scoring model, these proteins yielded 85% sensitivity, 100% specificity, and an area under the curve (AUC) of 0.98 for labeling malignancy in the verification sample. For lung adenocarcinoma-mesothelioma discrimination, combining CA19-9, CA15-3, and kallikrein-12 had maximal discriminatory capacity (65% sensitivity, 100% specificity, AUC 0.94); figures which also refer to the validation set. Last, cathepsin-B in isolation was only moderately useful (sensitivity 89%, specificity 62%, AUC 0.75) in separating lymphomatous and TB effusions. However, this last differentiation improved significantly when cathepsin-B was used with respect to the patient's age (sensitivity 72%, specificity 100%, AUC 0.94).In conclusion, panels of 4 (i.e., MMP-9, cathepsin-B, C-reactive protein, chondroitin sulfate), or 3 (i.e., CA19-9, CA15-3, kallikrein-12) different protein biomarkers on pleural fluid samples are highly discriminative for signaling a malignant versus tuberculous effusion, or lung adenocarcinoma versus mesothelioma, respectively. Cathepsin-B could also be helpful in establishing the presence of a lymphomatous effusion versus that of TB, if the patient's age is simultaneously taken into consideration.

Estimation of Adenosine deaminase and proteinase inhibitory activity and their correlation with tuberculous effusion and other pleural effusion cases

Introduction: Diagnosis of tuberculous effusion is difficult with the conventional, bacteriological, cytological and histopathological methods in our country. Adenosine deaminase, serum proteins, phospholipids show marked variation in tuberculous exudates. Material and Methods: Twenty cases of pulmonary tuberculosis, 10 cases of malignant effusions and 8 cases of other para-pneumonic effusions visiting a tertiary care hospital were included in this study. After collecting blood and pleural fluid samples, Adenosine deaminase, Alpha-1 antitrypsin l, proteinase inhibitor activity, total lipid levels, phospholipid and Lipase activity were estimated. Observation and results: Serum ADA levels in tuberculous effusion was 21.8+ 9.8 U/L(10-45.08) P

Study of 100 cases of pleural effusion with reference to diagnostic approach

Background: Collection of an abnormal quality and quantity of fluid in the pleural cavity is called pleural effusion. In this study an attempt has been made to arrive at the etiological diagnosis of pleural effusion by analysis of history, clinical presentation, biochemical, radiological, cytological and bacteriological methods. Methods: This study was carried out in the Department of Pulmonary Medicine, B.J. Medical College, Ahmedabad, Gujarat, India. In this study total 100 indoor patients of adult age and either sex were taken. Patients with pleural effusion as determined by clinical and or radiological means, thoracocentesis on who yield a minimum amount of fluid enough to carry out routine test were included in the study. Patients with pleural effusion with non aspirable fluid quantity decided clinically or radiologically, were excluded. Results: Most of the patients were between the age group of 31-40 years and males (68%). Most of the patients of tuberculous effusion were from younger age group between 21-50 years. Most common symptom was chest pain (72%) followed by fever (62%). Most of cases were tuberculous (62%) followed by malignant (18%). There were 15 patients with undiagnosed pleural effusion, in which, thoracoscopic pleural biopsy was done, among them 9 patients had malignancy and 5 patients had tuberculous pleural effusion. Conclusions: Most of etiologies for pleural effusion were tuberculosis among young’s and malignancy in older age. Right sided pleural effusion was more common in exudative effusion while bilateral pleural effusion was more common in patients with transudative. Thoracocentesis followed by pleural fluid analysis is the best method to diagnose the underlying etiology. Thoracoscopic pleural biopsy also has good role in undiagnosed pleural effusions.

Redefining Effusive-Constrictive Pericarditis with Echocardiography.

BackgroundEffusive-constrictive pericarditis (ECP) is traditionally diagnosed by using the expensive and invasive technique of direct pressure measurements in the pericardial space and the right atrium. The aim of this study was to assess the diagnostic role of echocardiography in tuberculous ECP.MethodsIntrapericardial and right atrial pressures were measured pre- and post-pericardiocentesis, and right ventricular and left ventricular pressures were measured post-pericardiocentesis in patients with tuberculous pericardial effusions. Echocardiography was performed post-pericardiocentesis. Traditional, pressure-based diagnostic criteria were compared with post-pericardiocentesis systolic discordance and echocardiographic evidence of constriction.ResultsThirty-two patients with tuberculous pericardial disease were included. Sixteen had ventricular discordance (invasively measured), 16 had ECP as measured by intrapericardial and right atrial invasive pressure measurements and 17 had ECP determined echocardiographically. The sensitivity and specificity of pressure-guided measurements (compared with discordance) for the diagnosis of ECP were both 56%. The positive and negative predictive values were both 56%. The sensitivity of echocardiography (compared with discordance) for the diagnosis of ECP was 81% and the specificity 75%, while the positive and the negative predictive values were 76% and 80%, respectively.ConclusionEchocardiography shows a better diagnostic performance than invasive, pressure-based measurements for the diagnosis of ECP when both these techniques are compared with the gold standard of invasively measured systolic discordance.

The Effects of Angiotensin Converting Enzyme Inhibitors (ACE-I) on Human N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) Levels: A Systematic Review and Meta-Analysis.

BackgroundTuberculous pericardial effusion is a pro-fibrotic condition that is complicated by constrictive pericarditis in 4% to 8% of cases. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a ubiquitous tetrapeptide with anti-fibrotic properties that is low in tuberculous pericardial effusion, thus providing a potential mechanism for the heightened fibrotic state. Angiotensin-converting enzyme inhibitors (ACE-I), which increase Ac-SDKP levels with anti-fibrotic effects in animal models, are candidate drugs for preventing constrictive pericarditis if they can be shown to have similar effects on Ac-SDKP and fibrosis in human tissues.ObjectiveTo systematically review the effects of ACE-Is on Ac-SDKP levels in human tissues.MethodsWe searched five electronic databases (1996 to 2014) and conference abstracts with no language restrictions. Two reviewers independently selected studies, extracted data and assessed methodological quality. The protocol was registered in PROSPERO.ResultsFour studies with a total of 206 participants met the inclusion criteria. Three studies (106 participants) assessed the change in plasma levels of Ac-SDKP following ACE-I administration in healthy humans. The administration of an ACE-I was associated with an increase in Ac-SDKP levels (mean difference (MD) 5.07 pmol/ml (95% confidence intervals (CI) 0.64 pmol/ml to 9.51 pmol/ml)). Two studies with 100 participants further assessed the change in Ac-SDKP level in humans with renal failure using ACE-I. The administration of an ACE-I was associated with a significant increase in Ac-SDKP levels (MD 8.94 pmol/ml; 95% CI 2.55 to 15.33; I2 = 44%).ConclusionACE-I increased Ac-SDKP levels in human plasma. These findings provide the rationale for testing the impact of ACE-I on Ac-SDKP levels and fibrosis in tuberculous pericarditis.