• Tuberculosis and Respiratory Diseases
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• v.59 no.4
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• pp.361-367
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• 2005

Background : Differential diagnosis of lymphocytic pleural effusion is difficult even with many laboratory findings. Nitric oxide(NO) level is higher in the sputum or exhaled breath of patients with active pulmonary tuberculosis than in those without tuberculosis. In addition, there are some reports about the increased level of NO metabolites in body fluids of cancer patients. However, there is no data on the NO levels in the pleural fluid of patients with tuberculous pleurisy. Method : The serum and pleural fluid NO in the patients with acute lymphocytic pleural effusion were analyzed. Results : Of total 27 patients, there were 14 males and average age of patients was 48 years. The final diagnosis was tuberculous pleurisy in 17 cases and malignant pleural effusion in 10. The pleural fluid NO level was $540.1{\pm}116.4{\mu}mol$ in the tuberculous pleurisy patients and $383.7{\pm}71.0{\mu}mol$ in the malignant pleural effusion patients. The serum NO level was $624.7{\pm}142.0{\mu}mol$ in tuberculous pleurisy patients and $394.4{\pm}90.4{\mu}mol$ in malignant pleural effusion patients. There was no significant difference in the serum and pleural fluid NO level between the two groups. The NO level in the pleural fluid showed a significant correlations with the pleural fluid neutrophil count, the pleural fluid/serum protein ratio, and pleural fluid/serum albumin ratio (p<0.05 in each). The protein concentration, leukocyte and lymphocyte count in the pleural fluid were significantly higher in the tuberculous pleurisy patients than the malignant pleural effusion patients (p<0.05 in each). Conclusion : NO is not a suitable marker for a differential diagnosis of lymphocytic pleural effusion. However, the NO level in the pleural fluid might be associated with the neutrophil recruitment and protein leakage in the pleural space.

• Tuberculosis and Respiratory Diseases
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• v.49 no.2
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• pp.149-161
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• 2000

Background : Residual pleural thickening (RPT) develops in about 50% of tuberculous pleurisy ($PL_{TB}$). Some reports have suggested that elevated TNF-$\alpha$ and impaired fibrinolysis could be the cause of RPT, but until now, the mechanism and predictors of RPT have not been well known. TGF-$\beta$ has been known to promote fibrogenesis and is increased in tuberculous pleural fluid (PF). $PL_{TB}$ and malignant pleurisy ($PL_{MAL}$) manifest lymphocyte-dominant exudative pleural effusion, and it has clinical implications in the differentiation of the two diseases based on the findings of pleural effusion. We performed this study to compare pleural fluid TNF-$\alpha$ TGF-$\beta$, and fibrinolytic parameters between $PL_{TB}$ and $PL_{MAL}$, and to find the predictors of RPT in $PL_{TB}$. Methods : Thirty-five $PL_{TB}$ and 14 $PL_{MAL}$ patients who were admitted to the Asan Medical Center from February 1997 to August 1999 were enrolled. All $PL_{TB}$ patients were prescribed a primary, short-course, anti-tuberculosis regimen. INF-$\alpha$ tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), plasminogen, $\alpha$2-antiplasmin, and D-dimer were measured in both PF and PB. TGF-$\beta$was measured only in PF. Clinical characteristics, TNF-$\alpha$ TGF-$\beta$ and fibrinolytic parameters were compared between patients with RPT less than 2 mm and patients with more than 2 mm of the thirty patients who completed the anti-tuberculosis treatment. Results : The levels of TNF-$\alpha$ tPA, PAI-1, plasminogen, $\alpha$2-antiplasmin, and D-dimer in PF were higher than those in peripheral blood (PB) in $PL_{TB}$, whereas only plasminogen, $\alpha$2-antiplasmin, and D-dimer were higher in PF than in PB in $PL_{MAL}$. Pleural fluid TNF-$\alpha$ TGF-$\beta$, PAI-1, plasminogen, $\alpha$2-antiplasmin were increased in $PL_{TB}$ compared with $PL_{MAL}$, but these factors did not show any further advantages over ADA in differentiation between $PL_{TB}$ and $PL_{MAL}$. TNF-$\alpha$ TGF-$\beta$ and fibrinolytic parameters did not show any differences between patients with RPT less than 2 mm and patients with RPT more than 2 mm. Conclusion : Our data suggest that TNF-$\alpha$, TGF-$\beta$ and fibrinolytic parameters may play some role for the development of RPT in $PL_{TB}$, but they failed to predict the occurrence of RPT in $PL_{TB}$. Also these parameters did not seem to have any advantages over ADA in differentiating between two diseases.

• Korean Journal of Clinical Laboratory Science
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• v.48 no.1
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• pp.30-35
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• 2016

Pleurisy, an inflammation of the lining around the lungs, is associated with a common complication of several different medical conditions, the most pervasive being viral and mycobacterial infections. We evaluated the relevance of pleurisy and high blood pressure, diabetes. This study is a survey of 136 patients in whom pleural aspiration was performed to confirm the relationship with hypertension or diabetes mellitus and pleurisy. In the 136 patients, 47.8% were normal people (without hypertension and diabetes mellitus), 32.3% were hypertension patients, 7.4% were diabetes mellitus patients, and 12.5% were patients with hypertension and diabetes mellitus. Odds ratio of normal and hypertension group by pleurisy was 2.524 and the confidence interval was 1.050, 6.069, odds ratio of normal and hypertension group was 4.417 and the confidence interval was 1.101, 17.714. According to these results, hypertension and diabetes mellitus may increase the risk of pleurisy.

• Tuberculosis and Respiratory Diseases
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• v.65 no.1
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• pp.7-14
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• 2008

Background: Residual pleural thickening (RPT) is the most frequent complication of tuberculous pleurisy (TP), and this can happen despite of administering adequate anti-tuberculous (TB) therapy. Yet there was no definite relation between RPT and other variables. The aim of this study was to examine matrix metalloproteinases (MMPs) and the inhibitors of metalloproteinases (TIMPs) and to identify the factors that can predict the occurrence of RPT. Methods: The patients with newly-detected pleural effusions were prospectively enrolled in this study from January 2004 to June 2005. The levels of MMP-1, -2, -8 and -9, and TIMP-1 and -2 were determined in the serum and pleural fluid by ELISA. The residual pleural thickness was measured at the completion of treatment and at the point of the final follow-up with the chest X-ray films. Results: The study included 39 patients with pleural fluid (PF). Twenty-three had tuberculous effusion, 7 had parapneumonic effusion, 7 had malignant effusion and 2 had transudates. For the 17 patients who completed the anti-TB treatment among the 23 patients with TP, 7 (41%) had RPT and 10 (59%) did not. The level of PF TIMP-1 in the patients with RPT ($41,405.9{\pm}9,737.3ng/mL$) was significantly higher than that of those patients without RPT ($29,134.9{\pm}8,801.8$) at the completion of treatment (p=0.032). In 13 patients who were followed-up until a mean of $8{\pm}5$ months after treatment, 2 (15%) had RPT and 11 (85%) did not. The level of PF TIMP-2 in the patients with RPT ($34.4{\pm}6.5ng/mL$) was lower than that of those patients without RPT ($44.4{\pm}15.5$) at the point of the final follow-up (p=0.038). Conclusion: The residual pleural thickening in TP might be related to the TIMP-1 and TIMP-2 levels in the pleural fluid.

• Tuberculosis and Respiratory Diseases
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• v.42 no.4
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• pp.455-464
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• 1995

Background: Considering that both humoral and cell mediated immunities play an important role for human tuberculosis infection, enzyme-linked immunosorbent assay(ELISA) measurement of immunoglobulin G (IgG) antibody to mycobacterial antigens can be used for the serologic diagnosis of tuberculous pleural effusion. Method: We measured absorbance values of IgG antibodies to purified-protein-derivative (PPD) and lipoarabinomannan-B (LAM-B) in the pleural fluid (PF) and the serum in 40 tuberculous (TPE) and 19 nontuberculous pleural effusions (NTPE). Results: 1) The IgG antibodies to PPD and LAM-B were significantly (P<0.0005) higher in the PF and the serum of TPE compared to NTPE. 2) The IgG antibodies to PPD and LAM-B in the serum were higher than that in PF. 3) Significant correlations were found between pleural and serum IgG antibodies to PPD and LAM-B. 4) With a cutoff value for IgG antibody to PPD in the PF of 0.091, sensitivity was 55.0% and specificity 94.7% in the diagnosis of TPE. 5) With a cutoff value for IgG antibody to LAM-B in the PF of 0.337, sensitivity was 50.0% and specificity 94.7% in the diagnosis of TPE. 6) The seropositive rates in TPE were not related to PPD skin test status, the amount of PF and coexisting active pulmonary tuberculosis. Conclusion: The assay of IgG antibodies to PPD and LAM-B might be useful for the diagnosis of TPE. Our study suggests the mechanism of passive transfer of IgG antibodies to PPD and LAM-B from the serum to the PF through pleural tissue.

• Tuberculosis and Respiratory Diseases
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• v.61 no.6
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• pp.526-532
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• 2006

Backgroud: Traditionally, tuberculous pleurisy has been known to largely develop as primary tuberculosis. However, as the incidence of tuberculosis decrease, recent studies have shown reactivation tuberculosis has become the main cause of tuberculous pleurisy. Methods: 141 cases of tuberculous pleurisy, between January 2003 and February 2006, at the Dankook university hospital. were retrospectively studied. The patients were divided into primary and reactivation tuberculosis. based on the history and radiological characteristics, and the clinical, radiological characteristics at the time of diagnosis and residual pleural thickening after 6 month of chemotherapy were compared between the two groups. Results: 1. Of the 141 tuberculous pleurisy cases, in 135 it was possible to differentiate between primary and reactivation tuberculosis. 2. Of the 135 tuberculous pleurisy cases, 38 (28%) showed a primary tuberculosis pattern, and 98 (72%) showed a reactivation tuberculosis pattern. 3. There were no significant differences between primary and reactivation tuberculosis in relation to age, sex, duration of symptom, amount of pleural effusion, pleural fluid WBC, lymphocyte count, and level of protein, LDH and ADA at the time of diagnosis 4. 124 patients were followed for 6 months after diagnosis of tuberculous pleurisy, and there was no significant difference in the residual pleural thickening between primary and reactivation tuberculosis. Conclusion: In South Korea, a reactivation disease is currently a more common cause of tuberculous pleurisy than a primary disease. There was no difference in the clinical characteristics between primary and reactivation tuberculosis.

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.280-289
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• 1998

Background: It is sometimes difficult to differentiate tuberculous pleural effusion from malignant pleural effusion by clinical symptoms, signs, by routine tests of pleural fluid, and by pathologic studies. And recently, it was discovered that cytokines such as IL-2, IFN-$\gamma$, TNF-$\alpha$ are elevated in tuberculous pleural fluid, and there have been several attempts to diagnose tuberculous pleural effusion by using these immunological mediators. There are several studies regarding the diagnostic value of IFN-$\gamma$, and there are two studies in Korea. But the diagnostic values of IFN-$\gamma$ in these studies were slightly lower than those in other countries. To compare the diagnostic value of IFN-$\gamma$ with those of CEA and ADA, and to determine the sensitivity and specificity of IFN-$\gamma$ in Korean, we mesured IFN-$\gamma$, CEA level and ADA activity in pleural effusions. Methods: ADA activity, IFN-$\gamma$ level and CEA level as well as cell count, differential count, and biochemical assays such as protein content and lactate dehydrogenase were measured in 40 cases of tuberculous pleuritis and 42 cases of malignant pleural effusion. Results: Tuberculous pleural fluid showed higher levels of IFN-$\gamma$ and ADA ($832.6{\pm}357.2$ pg/ml and $82.5{\pm}25.9$ U/L, respectively) than those of malignant pleural effusion ($2.6{\pm}8.0$ pg/ml and $19.2{\pm}10.9$ U/L, respectively) (p<0.01). Malignant pleural effusions showed higher median value (102.2 ng/ml) than tubercalous pleural effusions (1.8 ng/ml) (p<0.01). The sensitivities of IFN-$\gamma$, ADA, CEA were 0.97, 0.87, 0.67 and the specificities of IFN-$\gamma$, ADA, CEA were 1.0, 0.97, 1.0, respectively. There was no significant correlation between ADA activity and IFN-$\gamma$ level. Conclusion: This study showed that IFN-$\gamma$ test would be a very useful clinical test for differential diagnosis of tuberculous pleuritis and malignant pleural effusion because it is very sensitive and specific, although it is an expensive test.

• 보건세계
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• v.38 no.12 s.424
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• pp.4-5
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• 1991

• Tuberculosis and Respiratory Diseases
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• v.45 no.2
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• pp.301-310
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• 1998

Background: Cell mediated immune response mediated by interaction between CD4+ T lymphocytes and macrophagies is thought to play an important role in tuberculous pleurisy. This interaction is dependent on the interplay of various cytokines. The immunologic response of tuberculous pleurisy is thought to depend on the balance between helper T cell(Th1) cytokine Interleukin-12, Interferon gamma and Th2 cytokine IL-4, IL-10. To understand immunologic mechanism in tuberculous pleurisy and evaluate diagnostic value of these cytokines, the concentrations of Th1 cytokine IL-12, IFN -$\gamma$ and Th2 cytokine IL-10 were measured in tuberculous pleurisy and malignant pleural effusion group. Material and Methods: The concentrations of IL-10, IL-12 and IFN-$\gamma$ were measured by ELISA method in pleural fluids and serums of 20 patients with tuberculous pleurisy and 20 patients with malignant pleural effusion ADA activities were measured by spetrophotomery in pleural fluids of both groups. Results: In tuberculous pleurisy, the mean concentrations of IL-10, IL-12 and IFN-$\gamma$ of pleural fluids showed $121.3{\pm}83.7$ pg/mL, $571.4{\pm}472.7$ pg/mL and $420.4{\pm}285.9$ pg/mL. These were significantly higher than that of serum, $21.2{\pm}60.9$ pg/mL, 194.5 pg/mL, $30.1{\pm}18.3$ pg/mL respectively(p< 0.01). In malignant pleural effusion, the mean concentrations of IL-10, IL-12 and IFN-$\gamma$ of pleural fluids showed $88.4{\pm}40.4$ pg/mL, $306.5{\pm}271.1$ pg/mL and $30.5{\pm}54.8$ pg/mL respectively. Compared with that of serum ($43.4{\pm}67.2$ pg/mL, $206.8{\pm}160.6$ pg/mL, $14.6{\pm}3.3$ pg/mL), only IL-10 was significantly higher (p<0.001), but IL-12, IFN-$\gamma$ were not significant. In tuberculous pleural effusion compared with malignant pleural effusion, the concentration of IL-12, IFN-$\gamma$, ADA were significantly higher (p=value 0.046, <0.001, <0.001), but IL-10 was not significant. For differential diagnosis of tuberculous pleurisy from malignant pleural effusion, using cut-off value of IL-12, IFN-$\gamma$, ADA as 300 pg/mL. 100 pg/mL, 45 U/L, the sensitivity/specificity were 60%/70%, 90%/87.5%, 85%/90% respectively. Conclusion: In tuberculous pleurisy, IL-10, IL-12 and IFN-$\gamma$ were selectively concentrated highly in pleural space than serum. Compared with malignant pleural effusion, IL-12 and IFN-$\gamma$ were significantly higher, but IL-10 were not in tuberculous pleural effusion. The results suggest that Th1 pathway contributes to immune resistant mechanism in tuberculous pleurisy. IFN-$\gamma$ and ADA revealed useful methods of differential diagnosis in tuberculous pleurisy from malignant pleural effusion.

• Tuberculosis and Respiratory Diseases
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• v.50 no.5
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• pp.607-614
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• 2001

Background : Residual pleural thickening is frequently seen following treatment for tuberculous pleurisy, and pleural decortication is performed occasionally in patients with severe residual pleural thickening. However, predictive factors for the development of residual pleural thickening are uncertain at the initial diagnosis of the tuberculous pleurisy. Therefore, the purpose of this study was to identify the associated factors for residual pleural thickening at initial diagnosis. Methods : We separated 63 patients diagnosed as tuberculous pleurisy into two groups; group 1 consisted of patients without residual pleural thickening and group 2 comprised patients with residual pleural thickening at the end of tuberculous pleurisy treatment. We analyzed the clinical characteristics, radiological findings, pleural biopsy and characteristics of pleural fluid between group 1 and group 2. Results : The study population and clinical symptoms of the two groups were not significantly different and the duration of symptoms before treatment and the peripheral WBC were similar between the two groups. The presence of pulmonary tuberculosis, pleural fluid loculation or the amount of pleural effusion sid not differ significantly between the two groups. The incidence of positive AFB staining(group 1 : 8%, group 2 : 38%) and granuloma(group 1 : 30%, group 2: 62%)on pleural biopsy specimens was significantly higher in group 2 than in group 1. Pleural fluid WBC and differential count, adenosine deaminase level, pH, protein level or glucose level did not differ between the two groups. However, group 2 had higher LDH levels ($1370{\pm}208mg/dL$) than group 1 ($860{\pm}71mg/dL$, p<0.05). Conclusion : In tuberculous pleurisy, patients with residual pleural thickening following treatment demonstrated a higher incidence of positive AFB staining and granuloma on the pleural biopsy specimens or higher LDH level in the pleural fluid than patients without residual pleural thickening From these results, we speculate that the amount of tuberculous bacilli and granuloma are probably correlated with residual pleural thickening in the tuberculous pleurisy.