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At least 19 recordsLinked to original sources
PubMed2006

Pleural tuberculosis.

Pleural effusions in tuberculosis are commonly seen in young adults as an immunological phenomenon occurring soon after primary infection. However, the epidemiology and demographics of tuberculous pleurisy are changing due to the impact of HIV co-infection and the increasing number of pleural effusions seen as part of re-activation disease. Pleural biopsy for histology and culture is the mainstay of diagnosis with closed needle biopsy adequate in the majority of cases. Techniques such as PCR of biopsy specimens and the role of pleural fluid ADA are still being evaluated as a diagnostic aid. Tuberculous empyema is less commonly seen in the western world and the diagnostic yield from pleural fluid here is greater than in "primary" effusions. Treatment with appropriate antituberculous chemotherapy is generally successful though there is currently insufficient evidence to recommend the routine use of corticosteroids in this condition.

AIDS-Related Opportunistic Infections↗
PubMed2001

HIV-1-related pleural tuberculosis: elevated production of IFN-gamma, but failure of immunity to Mycobacterium tuberculosis.

BACKGROUND: Pleural tuberculosis can resolve spontaneously, suggesting that the inflammatory process may represent a protective immune response. However, pleural tuberculosis is strongly associated with HIV infection. It has been suggested that cell-mediated immune responses may be reduced, and direct bacterial invasion may have a role in pathogenesis, in HIV-positive cases. To test this hypothesis, we compared production of the pro-inflammatory cytokines, interferon (IFN)-gamma and tumour necrosis factor(TNF)-alpha, production of the immunosuppressive cytokine, interleukin (IL)-10, and mycobacterial culture positivity, in HIV-negative and HIV-positive patients with pleural tuberculosis. METHODS: Cytokine levels were measured in serum and pleural fluid, and in supernatants of blood and pleural fluid stimulated in vitro using mycobacterial antigens. Intracellular IFN-gamma and TNF-alpha production was measured after stimulation with phorbol myristate acetate and ionomycin in vitro. RESULTS: IFN-gamma was strikingly elevated in serum and pleural fluid in HIV-positive, compared to HIV-negative subjects (P < or = 0.02). TNF-alpha was elevated, but this was not statistically significant. IL-10 levels were higher in serum (P < 0.001), but similar in pleural fluid. IFN-gamma responses to soluble mycobacterial antigen in vitro were reduced in peripheral blood (P = 0.006), but not pleural fluid, of HIV-positive subjects. Intracellular cytokine staining suggested that CD8+ T cells were a major source of IFN-gamma in HIV-positive subjects. The proportion of subjects with a positive culture for Mycobacterium tuberculosis from pleural fluid was higher in the HIV-positive group. CONCLUSIONS: HIV-positive patients with pleural tuberculosis show elevated production of IFN-gamma, for which CD8+ T cells may be a major source. Mycobacterium tuberculosis can proliferate despite high levels of pro-inflammatory cytokines.

Adult↗
PubMed1999

ADA1/ADAp ratio in pleural tuberculosis: an excellent diagnostic parameter in pleural fluid.

We analysed the efficacy of pleural adenosine deaminase (ADAp) and the ADA1/ADAp ratio in the diagnosis of pleural tuberculosis in 103 pleural effusions, 27 of which were tuberculosis (TB) and 76 other diagnoses (non-TB). Smears, cultures and pleural biopsies were carried out in all cases, and were used for final diagnosis. The diagnostic yield of the parameters under study were as follows: smears/cultures of mycobacteria in fluid 11.1%/33.3%; biopsy 33.3%/51.8% and tuberculosis granulomas 85.1%. The levels of ADAp and ADA1/ADAp ratio in TB and non-TB groups showed very significant differences (P < 0.00001); in the TB group: ADAp 54.7 +/- 23.5 IU and ADA1/ADAp 0.27 +/- 0.08; in the non-TB group: ADAp 18.3 +/- 43.2 IU and ADA1/ADAp 0.64 +/- 0.14. The assay established ADA levels in pleural fluid > or = 40 IU and an ADA1/ADAp ratio < or = 0.42 as cut-off levels to identify individuals in the TB group, with a sensitivity of 88.8%/100%, a specificity of 92%/98.6%, a positive predictive value (PPV) of 80%/96.4%, a negative predictive value (NPV) of 95.8%/100% and an accuracy of 91.2%/99.02%. The ADAp levels in 27 patients with TB, showed close correlation with the number of monocyte macrophages (P = 0.001), but not with the number of lymphocytes (P = n.s.). The ADA1/ADAp ratio overcomes the limitations of ADAp (false positives and negatives), and is the most useful parameter for diagnosis on account of a high diagnostic yield, low cost and speed of the assay for identifying a pleural tuberculosis diagnosis, when compared with traditional methods.

Adenosine Deaminase↗
PubMed1989

[Pleural tuberculosis: yield of thoracoscopy].

34 tuberculosis with pleural affectation were diagnosed after examining 292 pleural effusions. 19 cases studied were diagnosed by pleuroscopy. The mean age of patients was 38 years old. The cytology, being mainly limphocytes, cultures and bacyloscopy, were all negative. The cultures of the biopsies was positive in 36.7% of the cases. The pathology report was positive in 88% of them. There was macroscopic suspicion of the disease in 73.6% with good macro-microscopic correlation this being the reason of the early treatment applied. We concluded that pleuroscopy is a good technique to diagnose pleural tuberculosis, reducing the hospital admission time.

Adult↗
PubMed1997

Pleural tuberculosis.

Tuberculous pleural effusions occur in up to 30% of patients with tuberculosis. It appears that the percentage of patients with pleural effusion is comparable in human immunodeficiency virus (HIV)-positive and HIV-negative individuals, although there is some evidence that HIV-positive patients with CD4+ counts <200 cells x mL(-1) are less likely to have a tuberculous pleural effusion. There has recently been a considerable amount of research dealing with the immunology of tuberculous pleurisy. At present, we have more evidence that activated cells produce cytokines in a complex pleural response to mycobacteria. Intramacrophage elimination of mycobacterial antigens, granuloma formation, direct neutralization of mycobacteria and fibrosis are the main facets of this reaction. With respect to diagnosis, adenosine deaminase and interferon gamma in pleural fluid have proved to be useful tests. Detection of mycobacterial deoxyribonucleic acid (DNA) by the polymerase chain reaction is an interesting test, but its usefulness in the diagnosis of tuberculous pleurisy needs further confirmation. The recommended treatment for tuberculous pleurisy is a 6 month regimen of isoniazid and rifampicin, with the addition of pyrazinamide in the first 2 months. HIV patients may require a longer treatment. The general use of corticosteroids is not recommended at this time, but they can be used in individuals who are markedly symptomatic.

Adenosine Deaminase↗
PubMed2000

Evaluation of polymerase chain reaction, adenosine deaminase, and interferon-gamma in pleural fluid for the differential diagnosis of pleural tuberculosis.

STUDY OBJECTIVES: Pleural tuberculosis (TB) is a diagnostic challenge because of its nonspecific clinical presentation and paucibacillary nature. The inefficiency of conventional laboratory methods and the reliance on pleural biopsy have motivated the evaluation of alternative diagnostic strategies. We have evaluated polymerase chain reaction (PCR) directed to the IS6110 sequence of Mycobacterium tuberculosis, the determination of adenosine deaminase (ADA) activity, and measurement of interferon (IFN)-gamma levels in pleural fluid in the diagnosis of pleural TB. PATIENTS: ADA activity, IFN-gamma levels, and PCR were evaluated in 140 cases of pleural effusion, 42 with confirmed pleural TB, 19 with probable pleural TB, 70 with a nontuberculous etiology, and 9 having an undetermined etiology. RESULTS: ADA activity, IFN-gamma levels, and PCR were 88%, 85.7%, and 73.8% sensitive, respectively, and 85.7%, 97.1%, and 90% specific, respectively, for pleural TB that had been confirmed by either culture or pleural biopsy specimens. The combination of PCR, IFN-gamma measurement, and ADA activity determination allowed the selective increase of sensitivity and specificity for probable and confirmed cases compared to individual methods. Positive and negative predictive values for these individual or combined methods were maintained over a wide range of prevalence of pleural TB in the patient population presenting with pleural effusions. Fever and younger age were associated with tuberculous pleural effusion (p < 0. 0001), while blood in sputum and older age were associated with malignant etiology (p < 0.008). CONCLUSIONS: These clinical variables together with the use of ADA activity determination, PCR, and measurement of IFN-gamma levels provide the basis for the rapid and efficient diagnosis of pleural TB in different clinical settings.

Adenosine Deaminase↗
PubMed2026

Exploratory proteomic and metabolomic profiling of pleural effusions identifies histone H4 and alanine as promising complementary markers for pleural tuberculosis.

The diagnosis of pleural tuberculosis (Pl-TB) remains challenging. Histopathological analysis and pathogen detection in pleural biopsies are informative but limited. We investigated differentially expressed proteins and metabolites in pleural effusions from patients with Pl-TB, malignancies, and other pathologies. A proteomic analysis of pooled pleural effusions identified 45 proteins exclusively detected or upregulated in Pl-TB samples, many linked to infectious processes. Conversely, 18 proteins were uniquely found or upregulated in malignant pleural effusions, mainly associated with detoxification and hemostasis. To validate these findings, we employed targeted proteomics in individual samples. Eight proteins were validated: S100-A9, histone H4, insulin-like growth factor-binding protein 2, fibrinogen beta chain, ficolin-3, immunoglobulin heavy constant alpha 1, sulfhydryl oxidase 1, and histidine-rich glycoprotein. Additionally, NMR-based metabolomics identified 13 metabolites with differential abundance between Pl-TB and non-TB samples. Notably, N-acetyl-glycoprotein and the branched-chain amino acids, alanine and lysine differed between groups. Proteomic and metabolomic analyses revealed distinct molecular profiles between Pl-TB and non-TB patients, despite intra-group variability. To address this, we applied classification models. Histone H4 and alanine consistently emerged as discriminative features. Overall, this study provides novel insights into the molecular landscape of Pl-TB. The combined quantification of proteins and metabolites may improve differential diagnosis, although should be further validated in larger, independent cohorts before clinical application.

Humans↗
PubMed1991

The relationship between pleural fluid findings and the development of pleural thickening in patients with pleural tuberculosis.

The objective of the study was to determine if residual pleural thickening after treatment for pleural tuberculosis could be predicted from the pleural fluid findings at the time of the initial thoracentesis. Forty-four patients initially diagnosed as having pleural tuberculosis between January 1986 and January 1988 were separated into two groups: the 23 patients in group 1 had residual pleural disease, while the 21 patients in group 2 had no residual pleural disease after treatment for their pleural tuberculosis was completed. The clinical characteristics of the two different groups did not differ significantly, but the patients in group 1 tended to be a little sicker in that the duration of their symptoms was longer, their hemoglobin values were lower, and weight loss and cough were more frequent. There were no significant differences in the pleural fluid findings in the two different groups. The mean pleural fluid protein level was 5.40 +/- 0.58 g/dl for group 1 and 5.17 +/- 0.80 g/dl for group 2, while the mean pleural fluid glucose level was 78.6 +/- 19.5 mg/dl for group 1 and 79.5 +/- 20.1 mg/dl for group 2. The mean pleural fluid lactate dehydrogenase (LDH) level in group 1 was 593 +/- 498 IU/L, while the mean level for group 2 was 491 +/- 198 IU/L. The presence of residual pleural thickening was not related to the chemotherapeutic regimen or the performance of a therapeutic thoracentesis. From this study we conclude that approximately 50 percent of patients with pleural tuberculosis will have residual pleural thickening when their therapy is completed, but that one cannot predict which patients will have residual pleural thickening from either their clinical characteristics or their pleural fluid findings.

Adult↗
PubMed1999

Complicated pleural tuberculosis in children: CT evaluation.

PURPOSE: To describe the CT features of complicated pleural tuberculosis in children and to define the use of CT in children with pleural tuberculosis. MATERIALS AND METHODS: The CT findings in 11 children with complicated pleural tuberculosis were retrospectively analysed. CT was performed to evaluate persistent pleural thickening (n = 6) or a mass-like lesion (n = 5) detected on plain radiographs. Chest radiographs and medical records were reviewed to determine whether additional information provided by CT had altered clinical management. RESULTS: On CT, more than one location was involved in five patients (45%) and in two patients (18%) the entire pleural spaces were involved. Pleural thickening was seen in all 11 patients and enhancement after administration of contrast medium occurred in ten patients (91%). Low-density fluid collections were seen in nine patients (82%) and in two, CT revealed fluid collections within calcified pleural lesions. In five patients with mass-like lesions on plain radiographs, CT showed a low-density pleural mass with peripheral enhancement in four and a calcified pleural mass with fluid collection in one. CT demonstrated parenchymal abnormalities on the same side as pleural lesions in all 11 patients and hilar or mediastinal adenopathy in four. Four patients (36%) underwent surgery because of fluid within a calcified fibrothorax (n = 3) and chest wall tuberculosis (n = 1) that were seen only on CT. CONCLUSIONS: The CT features of complicated pleural tuberculosis in children were pleural thickening, enhancement and fluid collection with associated parenchymal abnormalities and lymphadenopathy. In the evaluation of children with pleural tuberculosis, CT can be useful for demonstrating fluid within a calcified fibrothorax or chest wall involvement, which usually requires surgical intervention.

Adolescent↗