BACKGROUND/AIMS: Pleuropulmonary paragonimiasis produces no specific symptoms or radiologic findings, allowing for the possibility of misdiagnosis. We evaluated the specific clinical and pleural fluid features of pleuropulmonary paragonimiasis masquerading as pleural tuberculosis. METHODS: We retrospectively analyzed the clinical and radiologic characteristics of 20 patients diagnosed with pleuropulmonary paragonimiasis between 2001 and 2011. RESULTS: In total, 17 patients presented with respiratory symptoms, including dyspnea (30%), hemoptysis (20%), cough (20%), and pleuritic chest pain (15%). Chest radiographs revealed intrapulmonary parenchymal lesions, including air-space consolidation (30%), nodular opacities (20%), cystic lesions (15%), ground-glass opacities (10%), and pneumothorax (5%). A pleural f luid examination revealed eosinophilia, low glucose levels, and high lactate dehydrogenase (LDH) levels in 87%, 76%, and 88% of the patients, respectively. These traits helped to distinguish pleuropulmonary paragonimiasis from other pleural diseases such as parapneumonic effusion, malignancy, and pleural tuberculosis. CONCLUSIONS: Pleuropulmonary paragonimiasis is often initially misdiagnosed as other pleural diseases. Therefore, it is important to establish the correct diagnosis. In patients with unexplained pleural effusion living in paragonimiasis-endemic areas, pleural fluid obtained by thoracentesis should be examined to distinguish pleuropulmonary paragonimiasis. When marked eosinophilia, high LDH levels, and low glucose levels are identified in pleural fluid, physicians could consider a diagnosis of pleuropulmonary paragonimiasis.
Adolescent ; Adult ; Aged ; Animals ; Biological Markers/analysis ; Child ; Child, Preschool ; Diagnosis, Differential ; Enzyme-Linked Immunosorbent Assay ; Eosinophilia/diagnosis/parasitology ; Female ; Glucose/analysis ; Humans ; L-Lactate Dehydrogenase/analysis ; Lung Diseases, Parasitic/*diagnosis/metabolism/parasitology/radiography ; Male ; Middle Aged ; Paracentesis ; Paragonimiasis/*diagnosis/metabolism/parasitology/radiography ; Paragonimus westermani/*isolation & purification ; Pleural Effusion/*diagnosis/metabolism/parasitology/radiography ; Predictive Value of Tests ; Retrospective Studies ; Tomography, X-Ray Computed ; Tuberculosis, Pleural/*diagnosis ; Young Adult

OBJECTIVE: To investigate the clinical characteristics of fetal hydrops and to find the antenatal ultrasound findings predictive of adverse perinatal outcome. METHODS: This is a retrospective study of 42 women with fetal hydrops who delivered in a tertiary-referral center from 2005 to 2013. Fetal hydrops was defined as the presence of fluid collection in > or =2 body cavities: ascites, pleural effusion, pericardial effusion, and skin edema. Predictor variables recorded included: maternal characteristics, gestational age at diagnosis, ultrasound findings, and identifiable causes. Primary outcome variables analyzed were fetal death and neonatal death. RESULTS: The mean gestational age at diagnosis was 29.3+/-5.4 weeks (range, 18 to 39 weeks). The most common identifiable causes were cardiac abnormality (10), followed by syndrome (4), aneuploidy (3), congenital infection (3), twin-to-twin transfusion syndrome (3), non-cardiac anormaly (2), chorioangioma (2), inborn errors of metabolism (1), and immune hydrops by anti-E antibody isoimmunization (1). Thirteen cases had no definite identifiable causes. Three women elected termination of pregnancy. Fetal death occurred in 4 cases. Among the 35 live-born babies, only 16 survived (54.0% neonatal mortality rate). Fetal death and neonatal mortality rate was not significantly associated with Doppler velocimetry indices or location of fluid collection, but increasing numbers of fluid collection site was significantly associated with a higher risk of neonatal death. CONCLUSION: The incidence of fetal hydrops in our retrospective study was 24.4 per 10,000 deliveries and the perinatal mortality rate was 61.9% (26/42). The number of fluid collection sites was the significant antenatal risk factor to predict neonatal death.
Aneuploidy ; Ascites ; Diagnosis ; Edema ; Female ; Fetal Death ; Fetofetal Transfusion ; Gestational Age ; Hemangioma ; Humans ; Hydrops Fetalis* ; Incidence ; Infant ; Infant Mortality ; Metabolism, Inborn Errors ; Pericardial Effusion ; Perinatal Mortality ; Pleural Effusion ; Pregnancy ; Retrospective Studies ; Rheology ; Risk Factors ; Skin ; Ultrasonography

OBJECTIVETo investigate the value of detecting thyroid transcription factor 1 (TTF-1) and Noval aspartic proteinase of pepsin family A (napsin A) in pleural fluid cell blocks in cytopathologic diagnosis of pulmonary adenocarcinoma.

METHODSConventional cell smears of pleural effusions were obtained from 48 patients with a history of lung adenocarcinoma for cytological analysis. The cell blocks were prepared using the cytological specimens and examined with immunohistochemistry for TTF-1 and napsin A. The rates of a positive diagnosis of pulmonary adenocarcinoma were compared between the two methods, and the diagnositic value of TTF-1 and napsin A in pleural fluid cell blocks was evaluated.

RESULTSImmuno- histochemistry of the cell block sections yielded a significantly higher positive rate of diagnosis than cytological analysis of conventional cell smear (84.44% vs 55.56%, P<0.05). Most of the pleural fluid cell blocks showed positive expressions of TTF-1 (36/38, 94.74%) and napsin A (30/38, 78.95%), and none of samples showed TTF-1 or napsin A expression in the mesothelial cells (P<0.05). The combination detection of TTF-1 and napsin A in pleural fluid cell blocks had a high diagnosis value with a diagnostic sensitivity of 97.37% and a specificity of 100% for pulmonary adenocarcinoma.

CONCLUSIONSThe combined detection of TTF-1 and napsin A in pleural fluid cell blocks facilitates cytopathologic diagnosis of pulmonary adenocarcinoma.

Adenocarcinoma ; diagnosis ; metabolism ; Aspartic Acid Endopeptidases ; metabolism ; Biomarkers, Tumor ; metabolism ; Humans ; Immunohistochemistry ; Lung Neoplasms ; diagnosis ; metabolism ; Nuclear Proteins ; metabolism ; Pleural Effusion ; Sensitivity and Specificity ; Thyroid Nuclear Factor 1 ; Transcription Factors ; metabolism

BACKGROUNDInterleukin (IL)-27 has been reported to have anti-proliferate and anti-angiogenic activities on cancer cells. However, the involvement of IL-27 in malignant pleural effusion (MPE) remains unknown. Thus, in this research, we compared the immune functions of IL-27, interferon (IFN)-γ, and IL-17 on lung cancer cells and revealed the regulatory mechanism of IL-27 in MPE.

METHODSThe distribution of IL-27 in both MPE and blood was evaluated by enzyme-linked immunosorbent assay and flow cytometry. The expressions of cytokine receptors and the levels of the phosphorylated signal transducer and activator of transcription (STAT) signalings were detected by flow cytometry. As well as the effects of proliferation, apoptosis, migration, and adherent activity of IL-27, IFN-γ, and IL-17 on lung cancer cells were also explored.

RESULTSThe expression of IL-27 was increased in MPE when compared with blood (147.3 ± 25.1 pg/ml vs. 100.3 ± 13.9 pg/ml, P = 0.04). IL-27 was noted to suppress both proliferation (18.33 ± 0.21 vs. 27.77 ± 0.88, P = 0.0005) and migration (1.82 ± 0.44 vs. 3.13 ± 0.07, P = 0.04) of A549 cells, but obviously promoted apoptosis of A549 cells (9.47 ± 1.14 vs. 4.96 ± 0.17, P = 0.02) by activating STAT1 signaling. Interestingly, IL-27 played totally opposite effects on A549 cells by activating STAT3 pathway. Moreover, IL-27 exerted different intercellular adherent activities of A549 cells to pleural mesothelial cell monolayer by activating different STAT signalings.

CONCLUSIONSIL-27 might exert an important immune regulation on lung cancer cells in human pleural malignant environment.

Adult ; Aged ; Aged, 80 and over ; Cell Line ; Cell Movement ; genetics ; physiology ; Cell Proliferation ; genetics ; physiology ; Enzyme-Linked Immunosorbent Assay ; Female ; Humans ; Interleukins ; metabolism ; Lung Neoplasms ; metabolism ; Male ; Middle Aged ; Pleural Effusion, Malignant ; metabolism ; Signal Transduction

BACKGROUND/AIMS: The clinical outcomes of some patients with pleural infection may be favorable with medical treatment alone, but in others, the disease progresses and requires additional surgical treatment. However, little is known about the factors affecting this difference. The aim of this study was to investigate the factors predictive of failure of medical treatment in patients with pleural infection. METHODS: A cohort of 127 consecutive patients who were admitted to the hospital with pleural infection was studied. Clinical manifestations and laboratory findings in patients in whom medical treatment succeeded or failed were reviewed. RESULTS: In univariate analysis, the significant factors associated with medical treatment outcome were age, smoking history, duration of chief complaint, serum albumin level, and pleural fluid glucose and lactate dehydrogenase levels (p < 0.05). Multivariate logistic regression analysis identified age and duration of chief complaint as independent predictive factors for failure of medical treatment, with odds ratios of 0.871 (p = 0.013) and 0.797 (p = 0.026), respectively. Receiver operating characteristic curve analysis determined cutoff values of 50.5 years for age and 4.5 days for duration of chief complaint. CONCLUSIONS: We demonstrated that a younger age < 50.5 years and shorter duration of chief complaint < 4.5 days were independent predictive factors for the failure of medical treatment in patients with pleural infection. This suggests their role as evaluative criteria in setting indications for the optimal treatment in patients with pleural infection. A larger, prospective study is required to confirm these findings.
Adult ; Aged ; Anti-Bacterial Agents/therapeutic use ; Cohort Studies ; Drainage ; Empyema, Pleural/metabolism/*therapy ; Female ; Glucose/metabolism ; Humans ; L-Lactate Dehydrogenase/metabolism ; Male ; Pleural Effusion/metabolism/*therapy ; Serum Albumin/metabolism ; Thoracic Surgery, Video-Assisted ; Treatment Failure

No abstract available.
Aged ; Amylases/blood/*metabolism/urine ; Bone Marrow/pathology ; Electrophoresis, Agar Gel ; Gene Rearrangement ; Humans ; Immunohistochemistry ; Isoenzymes/blood/metabolism/urine ; Male ; Multiple Myeloma/*diagnosis/metabolism/pathology ; Plasmacytoma/pathology ; Pleural Effusion, Malignant/pathology

OBJECTIVETo compare the CC-chemokine ligand 18 (CCL18) expression in the serum and malignant pleural effusion (MPE) of NSCLC patients and explore its regulatory effect on differentiation of monocyte-derived dendritic cells (Mo-DC).

METHODSCCL18 levels in the serum and MPE from 62 NSCLC patients were quantitated by immunoassay. CCL18 in sera from 26 healthy individuals, 28 exudative pleural effusions from inflammatory pulmonary diseases and 17 transudative pleural effusions from non-inflammatory diseases were used as control. Mo-DC was generated by culturing NSCLC-derived monocytes with GM-CSF and IL-4 in the presence or absence of CCL18. The mean fluorescent intensity (MFI) of CD14, CD80, CD83, CD86 and HLA-DR were analyzed by flow cytometry (FCM). Mo-DC was then co-cultured with purified T cells and the percence of CD25(+)FoxP3(+) cells was assayed by FCM.

RESULTSCCL18 levels in the sera of NSCLC patients and healthy individuals were (132.70 ± 15.52) ng/ml and (18.44 ± 0.99) ng/ml, respectively (P < 0.001). The levels of CCL18 in MPE, exudative PE and transudative PE were (155.6 ± 13.58) ng/ml, (190.4 ± 22.33) ng/ml and (20.89 ± 3.03) ng/ml, respectively. CCL18 in the MPE was significantly higher than that in transudates (P < 0.001), however, no significant difference was observed between CCL18 expression in exudative PE and MPE (P = 0.172). Of note, a moderate positive correlation (r = 0.421, P < 0.01) was observed between CCL18 levels in the paired MPE and serum of NSCLC. In the healthy control group, Mo-DC cultured in the presence of CCL18 showed 31.4 ± 15.8 (MFI) of CD14 expression, which was significantly higher than that in Mo-DC cultured in the absence of CCL18 (18.5 ± 8.9, P < 0.05). In contrast, the expressions of MFI of CD80, CD83, CD86 and HLA-DR were significantly decreased upon CCL18 induction (P < 0.05). In the NSCLC group, GM-CSF+IL-4+CCL18 induced a MFI of 45.2 ± 13.8 of CD14 expression in Mo-DC, which was also significantly higher than that of GM-CSF+ IL-4 induction (22.6 ± 10.5, P < 0.01). Similarly, the expressions of MFI of CD80, CD83, CD86 and HLA-DR were significantly decreased in the presence of CCL18 (P < 0.05). Furthermore, the MFI of CD14, CD83, CD86 and HLA-DR had significant differences between GM-CSF/IL-4/CCL18-induced Mo-DC derived from NSCLC patients and healthy control (P < 0.05). Finally, CD4(+) T cells co-cultured with NSCLC-derived, GM-CSF/IL-4/CCL18-treated Mo-DC had significantly higher percent of CD25(+)FoxP3(+) cells compared with that of CD4(+) T cells stimulated with Mo-DC induced by GM-CSF/IL-4(P < 0.01).

CONCLUSIONSCCL18 is present at a high level in MPE and serum of NSCLC patients complicated with pleural effusion and a moderate positive correlation exists between CCL18 levels in the two fluids. CCL18 inhibits maturation of Mo-DC, which consequently stimulates T cells to differentiate into CD25(+)FoxP3(+) regulatory T cells.

Carcinoma, Non-Small-Cell Lung ; metabolism ; Cell Differentiation ; Chemokines ; Chemokines, CC ; metabolism ; Coculture Techniques ; Dendritic Cells ; metabolism ; Flow Cytometry ; Granulocyte-Macrophage Colony-Stimulating Factor ; metabolism ; Humans ; Interleukin-4 ; metabolism ; Ligands ; Lung Neoplasms ; Monocytes ; physiology ; Pleural Effusion ; T-Lymphocytes, Regulatory

BACKGROUND: Interferon-gamma (IFN-gamma) plays a crucial role in Mycobacterium tuberculosis induced pleural responses. Interleukin (IL)-33 up-regulates the production of IFN-gamma. We aimed to identify whether an association between pleural IL-33 levels and tuberculous pleurisy exists and determine its diagnostic value. METHODS: Pleural IL-33, ST2 (a receptor of IL-33), adenosine deaminase (ADA), and IFN-gamma, as well as serum IL-33 and ST2 were measured in 220 patients with pleural effusions (PEs). Patients with malignant (MPEs), parapneumonic (PPEs), tuberculous (TPEs), and cardiogenic (CPEs) pleural effusions were included. RESULTS: Pleural and serum IL-33 levels were highest or tended to be higher in patients with TPEs than in those with other types of PEs. The median pleural fluid-to-serum IL-33 ratio was higher in TPE cases (> or = 0.91) than in other PE cases (< or = 0.56). Pleural IL-33 levels correlated with those of pleural ADA and IFN-gamma. However, the diagnostic accuracies of pleural IL-33 (0.74) and pleural fluid-to-serum IL-33 ratio (0.75) were lower than that of ADA (0.95) or IFN-gamma (0.97). Pleural ST2 levels in patients with MPEs were higher than in patients with TPEs. Serum ST2 levels did not differ among the groups. CONCLUSIONS: We identified an association between elevated pleural IL-33 levels and tuberculous pleurisy. However, we recommend conventional pleural markers (ADA or IFN-gamma) as diagnostic markers of TPE.
Adenosine Deaminase/analysis ; Adult ; Aged ; Aged, 80 and over ; Area Under Curve ; Case-Control Studies ; Cross-Sectional Studies ; Female ; Humans ; Interferon-gamma/analysis ; Interleukins/*analysis/blood ; Male ; Middle Aged ; Pleural Cavity/*metabolism ; Pleural Effusion/diagnosis/metabolism ; Pleural Effusion, Malignant/diagnosis/metabolism ; ROC Curve ; Receptors, Cell Surface/analysis/blood ; Tuberculosis, Pleural/*diagnosis/metabolism

BACKGROUNDPrevious studies reported interleukin-27 (IL-27), interferon-γ (IFN-γ), or adenosine deaminase (ADA) alone plays a helpful role in diagnosing tuberculous pleural effusion (TPE). The present study aims at comparing the diagnostic accuracy of pleural IL-27, IFN-γ, and ADA, and investigate the diagnostic accuracy of the combination of IL-27, IFN-γ, or/and ADA for differentiating TPE from pleural effusions with the other etiologies.

METHODSThe concentrations of IL-27, IFN-γ and ADA were simultaneously determined in pleural fluids and sera from 40 patients with TPE; 26 with malignant pleural effusion, seven with infectious pleural effusion, and eight with transudative pleural effusion by enzyme linked immunosorbent assay and colorimetric method. The corresponding biochemical indexs were also simultaneously determined.

RESULTSThe concentrations of pleural IL-27 and IFN-γ in the tuberculous group were significantly higher than those in the malignant, infectious, and transudative groups. The concentrations of ADA in TPE were significantly higher than those in MPE or transudative effusions, while much lower than those in infectious effusions. Among these three biomarkers, IL-27 was the most effective for TPE diagnosis, with the cut off value of 900.8 ng/L. IL-27 had a high sensitivity of 95% and specificity of 97.6% for differential diagnosis of TPE from non-TPEs. Combinations of IL-27, IFN-γ and ADA measurements further increased the sensitivity or specificity up to 100%.

CONCLUSIONSCompared to non-TPEs, IL-27, IFN-γ and ADA all simultaneously increased in TPE; and among these three rapid detection methods, IL-27 appeared to be the best for distinguishing tuberculous from non-TPEs, especially from MPE. Combinations of the three markers (IL-27, IFN-γ and ADA) yielded the highest sensitivity and specificity. These findings suggest that the applications of a new biomarker, IL-27, alone or with IFN-γ and ADA, may contribute to more efficient diagnosis strategies in the management of tuberculous pleurisy.

Adenosine Deaminase ; blood ; metabolism ; Aged ; Female ; Humans ; Interferon-gamma ; blood ; metabolism ; Interleukin-27 ; blood ; metabolism ; Male ; Middle Aged ; Pleural Effusion ; blood ; metabolism ; Tuberculosis, Pleural ; blood ; diagnosis ; metabolism

PURPOSE: C-reactive protein (CRP) has been implicated in various inflammatory and advanced malignant states. Increased serum CRP (s-CRP) levels have been shown to be associated with independent prognostic factors for survival in patients with advanced lung cancer. However, only few studies have focused on the role of CRP in pleural effusions. This study aimed to evaluate the diagnostic and prognostic value of pleural CRP (p-CRP) in lung cancer patients with malignant pleural effusion (MPE). MATERIALS AND METHODS: Pleural effusion (PE) samples were collected from patients with MPE (68 lung cancers; 12 extrathoracic tumors), and from 68 patients with various benign conditions (31 with pneumonia; 37 with tuberculosis). Concentrations of p- and s-CRP were measured by enzyme-linked immunosorbent assay. CRP level in pleural fluid and its association with survival were examined. RESULTS: p-CRP levels correlated with s-CRP levels (r=0.82, p<0.0001). For the differential diagnosis of MPE and benign PE, the area under the receiver operating characteristic curve was greater for p-CRP (0.86) than for s-CRP (0.77). High p-CRP expression significantly correlated with shorter overall survival (p=0.006). P-CRP was independent prognostic factor significantly associated with overall survival on multivariated analysis (p=0.0001). The relative risk of death for lung cancer patients with high p-CRP levels was 3.909 (95% confidence interval, 2.000-7.639). CONCLUSION: P-CRP is superior to s-CRP in determining pleural fluid etiology. Quantitative measurement of p-CRP might be a useful complementary diagnostic and prognostic test for lung cancer patients with MPE.
C-Reactive Protein/*metabolism ; Enzyme-Linked Immunosorbent Assay ; Humans ; Lung Neoplasms/*diagnosis/metabolism/pathology ; Multivariate Analysis ; Pleural Effusion, Malignant/*diagnosis/metabolism/pathology ; Predictive Value of Tests ; Prognosis ; Survival Analysis