scholarly journals Diagnostic Value of Soluble Form of Mer Tyrosine Kinase (sMerTK) in Tuberculous Pleural Effusion and Malignant Pleural Effusion

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Han Liu ◽  
Shuai Wang ◽  
Zhenzhen Zhang ◽  
Jing Jie ◽  
Lei Song ◽  
...  
Keyword(s):  
Pleural Effusion ◽  
Tyrosine Kinase ◽  
Malignant Pleural Effusion ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Soluble Form ◽  
Tuberculous Pleural Effusion ◽  
Potential Biomarker ◽  
Tnf Α ◽  
Mer Tyrosine Kinase

Objectives. With the development of proteomics, it has been indicated that differentially expressed proteins are biological markers for the diagnosis of different types of pleural effusion (PE). The aim of our study was to explore the value of sMerTK (soluble form of Mer tyrosine kinase) in the differential diagnosis of tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE). In addition, we also wanted to explore whether MerTK was associated with IL-1β and TNF-α, which are inflammatory factors related to pleural effusion. Methods. We screened all patients who underwent thoracoscopy and had a definite diagnosis. In total, 136 patients were enrolled in this study and classified into two groups, with 64 patients in the TPE group and 72 patients in the MPE group. The concentrations of sMerTK in the TPE and MPE groups were detected by ELISA. The diagnostic accuracy was determined by generating receiver operating characteristic (ROC) curves and calculating the area under the curve (AUC). Correlations between the expression level of sMerTK and those of the inflammatory factors interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) were also studied using Pearson’s linear correlation analysis. Results. The concentrations of sMerTK were 5,278.77 ± 2,479.98   ng / L and 859.91 ± 540.45   ng / L in the TPE and MPE groups, respectively. The concentration of sMerTK in TPE was shown to be significantly higher than that in MPE ( P < 0.05 ). The area under the ROC curve for sMerTK in distinguishing TPE from MPE was 0.958, with a cutoff value of 2,122 ng/L. The sensitivity and specificity for sMerTK were 98.61% and 90.63% ( P < 0.05 ). The expression levels of sMerTK in these two groups were not correlated with those of the inflammatory factors IL-1β and TNF-α ( P > 0.05 ). Conclusions. The expression level of sMerTK in PE could be a potential biomarker for common use in the diagnosis of TPE and MPE.

Proteome analysis of malignant pleural effusion

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. e22194-e22194
Author(s):  
K. Lee ◽  
J. Bang ◽  
K. Kim
Keyword(s):  
Pleural Effusion ◽  
Malignant Pleural Effusion ◽  
False Positive Rate ◽  
Coagulation Factor ◽  
Proteome Analysis ◽  
Diagnostic Value ◽  
Complement Factor ◽  
Glycoprotein Precursor ◽  
Tuberculous Pleural Effusion ◽  
Potential Biomarker

e22194 Background: Because pleural effusion contains proteins of potential diagnostic value, a comprehensive proteomic analysis of the pleural effusion is worthy to discover a new biomarker. Malignant pleural effusion and tuberculous pleural effusion are sometimes diagnositc challenge due to their similarity like lymphocyte-dominant effusion. Herein, we tried to identify differentially expressed proteins in both effusion using proteomic anlaysis. Methods: Twenty microliters of pleural effusions(PEs) from 3 patients with non-small cell lung cancer(NSCLC) and 3 patients with tuberculous pleurisy(TBC) were used for proteome analysis. After depletion of high abundant proteins including albumin, IgG with MARS Hu-6(Agilent), proteins were separated by SDS-PAGE and subject to in-gel tryptic digestion. The resulting peptides were analyzed by liquid chromatography/tandem mass spectrometry (LC/MS/MS). The MS/MS spectra were analyzed by Spectrum Mill against normal and reversed human protein databases. Results: In the total of 6 samples, 90 proteins were identified with more than 2 peptides and less than 1% of false positive rate. Among the identified pleural proteins, 57 proteins were detected both in PEs of NSCLS and TBC, 19 and 14 proteins were identified only in the PE of NSCLC and TBC, respectively. We analysed molecular functions, molecular composition and molecular processes of identified proteins with FindGo software. Among the identified proteins, we found the biomarker candidates that significantly have different expression levels in malignant effusion; apolipoprotein B precursor, vitronectin, complement factor B, histidine-rich glycoprotein precursor, coagulation factor II precursor variant. Conclusions: We found that several pleural effusion proteins may serve as potential biomarker candidates for differential diagnosis between maligant and tuberculous pleural effusion. We'll confirm these proteins through the proteomic method(MRM) and immunological method(Western bolt). No significant financial relationships to disclose.

scholarly journals CEA and ADA in Pleural Fluid for Differential Malignant Pleural Effusion and Tuberculous Pleural Effusion

2021 ◽  
Author(s):  
Jianhong Yu ◽  
Qirui Cai
Keyword(s):  
Pleural Effusion ◽  
Pleural Fluid ◽  
Roc Curve ◽  
Malignant Pleural Effusion ◽  
Diagnostic Value ◽  
Diagnostic Model ◽  
Diagnostic Efficacy ◽  
Tuberculous Pleural Effusion ◽  
Diagnostic Models ◽  
Independent Risk Factors

Abstract Objective This study aimed to establish a predictive model based on the clinical manifestations and laboratory findings in pleural fluid of patients with pleural effusion for the differential diagnosis of malignant pleural effusion (MPE) and tuberculous pleural effusion (TPE). Methods Clinical data and laboratory indices of pleural fluid were collected from patients with malignant pleural effusion and tuberculous pleural effusion in Zigong First People's Hospital between January 2019 and June 2020，and were compared between the two groups. Independent risk factors or Independent protective factors for malignant pleural effusion were investigated using multivariable logistic regression analysis. Receiver operating characteristic curve (ROC) analysis was performed to assess the diagnostic performance of factors with independent effects, and combined diagnostic models were established based on two or more factors with independence effect. ROC curve was used to evaluate the diagnostic ability of each model, and the fit of the eath model was measured using Hosmer-Lemeshow goodness-of-fit test. Results Patients with MPE were older than those with TPE, the rate of fever of patients with MPE was lower than that of patients with TPE, and these differences were statistically significant (p < 0.05). Carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), cytokeratin-19 fragment antigen (CYFRA21-1), cancer antigen 125 (CA125), and glucose (GLU) levels in the pleural fluid were higher, but total protein (TP), albumin (ALB) and Adenosine deaminase (ADA) levels in the pleural fluid were lower in MPE patients than in TPE patients, and the differences were statistically significant (P<0.05). In multivariate logistic regression analysis, CEA and NSE levels in the pleural fluid were independent risk factors for MPE, whereas ADA levels in pleural fluid and fever were independent protective factors for MPE. The differential diagnostic value of pleural fluid CEA and pleural fluid ADA for MPE and TPE were higher than that of pleural fluid NSE（p<0.05） and the area under the ROC curve was 0.901, 0.892, and 0.601, respectively. Four different binary logistic diagnostic models were established based on pleural fluid CEA combined with pleural fluid NSE, pleural fluid ADA or ( and ) fever. Among them, the model established with the combination of pleural fluid CEA and pleural fluid ADA (logit (P) = 0.513 + 0.457*CEA-0.101*ADA) had the highest diagnostic value for malignant pleural effusion, and its predictive accuracy was high with an area under the ROC curve of 0.968 [95% confidence interval (0.947, 0.988)]. But the diagnostic efficacy of the diagnostic model could not be improved by adding pleural fluid NSE and fever. Conclusion The model established with the combination of CEA and ADA in the pleural fluid has a high differential diagnostic value for malignant pleural effusion and tuberculous pleural effusion, and NSE in the pleural fluid and fever cannot improve the diagnostic efficacy of the diagnostic model.

scholarly journals Pro-cathepsin D as a diagnostic marker in differentiating malignant pleural effusion from benign pleural effusion: A retrospective cohort study

2020 ◽  
Author(s):  
Hayoung Choi ◽  
Yousang Ko ◽  
Chang Youl Lee
Keyword(s):  
Pleural Effusion ◽  
Pleural Fluid ◽  
Cathepsin D ◽  
Malignant Pleural Effusion ◽  
Operating Characteristic ◽  
Standard Procedure ◽  
Characteristic Curve ◽  
Enzyme Linked Immunosorbent Assay ◽  
Potential Biomarker ◽  
Benign Pleural Effusion

Abstract Background Malignant pleural effusion (MPE) is a common complication of lung cancer and intrathoracic spreading or metastasis of extra-thoracic malignancy. The aim of the present study was to evaluate the levels of pro-cathepsin D from plasma and pleural fluid in patients with MPE and those in patients with benign pleural effusion (BPE) including pleural tuberculosis and parapneumonic effusion.Methods This study included 81 patients with pleural effusion who underwent thoracentesis and pleural biopsy. Pleural fluid and serum were collected as a standard procedure for all individuals at the same time. The level of pro-cathepsin D was measured by the sandwich enzyme-linked immunosorbent assay method.Results Though there were no significant differences in plasma pro-cathepsin D between the two groups, the level of pleural fluid pro-cathepsin D was significantly higher in the MPE group than the BPE group (0.651 versus 0.590 pg/mL, P = 0.034) (Table 1). In addition, there were no differences in pleural fluid pro-cathepsin D level according to causative malignancy of MPE. On receiver operating characteristic curve analysis, the optimal discrimination point between the MPE group and BPE group was defined as a cut-off value of 0.5960 pg/mL for pleural fluid pro-cathepsin D (81.0% sensitivity; 53.0% specificity) and 0.4335 pg/mL for plasma pro-cathepsin D (71.4% sensitivity; 61.7% specificity).Conclusions We found that the level of pleural fluid pro-cathepsin D was significantly higher in the MPE group than the BPE group. Pro-cathepsin D could be a novel and potential biomarker to discriminate MPE from BPE.

Role of monocyte chemoattractant protein-1, tumor necrosis factor-α and interleukin-6 in the control of malignant pleural effusion and survival in patients with primary lung adenocarcinoma

2012 ◽  
Vol 27 (2) ◽  
pp. 118-124 ◽  
Author(s):  
Qian Qian ◽  
Wen-Kui Sun ◽  
Ping Zhan ◽  
Yu Zhang ◽  
Yong Song ◽  
...  
Keyword(s):  
Pleural Effusion ◽  
Lung Adenocarcinoma ◽  
Malignant Pleural Effusion ◽  
Monocyte Chemoattractant Protein 1 ◽  
Monocyte Chemoattractant ◽  
Primary Lung Adenocarcinoma ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

This study aimed at assessing the role of monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the control of pleural effusion (PE) and survival in patients with primary lung adenocarcinoma. The concentrations of the 3 cytokines were measured in PE from 79 lung adenocarcinoma patients with malignant pleural effusion (MPE) and 23 patients with tuberculosis. Data were correlated with the efficacy of MPE control and patient survival. The level of MCP-1 in PE was significantly higher in patients with lung adenocarcinoma than those with tuberculosis. By contrast, the levels of TNF-α and IL-6 were significantly lower in patients with lung adenocarcinoma than those with tuberculosis. An MCP-1 level greater than 3,187 pg/mL (which was used as a cutoff point) indicated failure to control MPE (odds ratio [OR]=2.82, 95% confidence interval [CI]=1.02–7.82, p=0.04). In multivariate analysis, MCP-1 was confirmed as an independent prognostic factor for progression-free survival (hazard ratio [HR]=2.02, 95% CI=1.24–3.30, p=0.01). The level of MCP-1 in PE appears to be a reliable surrogate marker for evaluating the therapeutic efficacy in the control of MPE and predicting survival in lung adenocarcinoma patients with MPE.

scholarly journals Diagnostic Significance of TNF-α in Tuberculous and Non-Tuberculous Pleural Effusion

1997 ◽  
Vol 44 (3) ◽  
pp. 611
Author(s):  
Hyun Joo Na ◽  
Seog Chea Park ◽  
Kwang Won Kang ◽  
Hyeong Kwan Park ◽  
Young Chul Kim ◽  
...  
Keyword(s):  
Pleural Effusion ◽  
Diagnostic Significance ◽  
Tuberculous Pleural Effusion ◽  
Tnf Α

scholarly journals Differential diagnosis between lymphoma-associated malignant pleural effusion and tuberculous pleural effusion

2019 ◽  
Vol 7 (16) ◽  
pp. 373-373 ◽  
Author(s):  
Chang Ho Kim ◽  
Hong Geun Oh ◽  
Sang Yub Lee ◽  
Jae Kwang Lim ◽  
Yong Hoon Lee ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Pleural Effusion ◽  
Malignant Pleural Effusion ◽  
Tuberculous Pleural Effusion

Pcsk9 Knockout Aggravated Experimental Apical Periodontitis via LDLR

2021 ◽  
pp. 002203452110151
Author(s):  
L. Huang ◽  
H. Wu ◽  
Y. Wu ◽  
F. Song ◽  
L. Zhang ◽  
...  
Keyword(s):  
Osteoclast Differentiation ◽  
Apical Periodontitis ◽  
Cholesterol Homeostasis ◽  
Expression Level ◽  
Inflammatory Factors ◽  
Tartrate Resistant Acid Phosphatase ◽  
Dependent Manner ◽  
Lps Challenge ◽  
Tnf Α ◽  
Computed Tomography Scanning

Apical periodontitis (AP), an inflammatory lesion around the apex of tooth roots, is mostly caused by dental pulp infection. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a vital role in regulating cholesterol homeostasis by targeting low-density lipoprotein receptor (LDLR) and participates in bacterium-induced chronic periodontitis. However, the roles of PCSK9 in AP are unknown. Here, we investigated its role in AP by using Pcsk9−/− mice. Micro–computed tomography scanning and histological staining revealed that the periapical bone loss of Pcsk9−/− mice was greater than that of wild-type (WT) mice, and increased expression of inflammation-related factors tumor necrosis factor α (TNF-α) and interleukin (IL)–6 was also observed. Immunofluorescence staining and quantitative real-time polymerase chain reaction showed PCSK9 expression in bone marrow macrophages (BMMs) was increased after treatment with lipopolysaccharide (LPS). This finding was consistent with the in vivo results that the expression level of PCSK9 in exposed WT mice increased compared with that in unexposed WT mice. After LPS challenge, the expression levels of TNF-α, IL-1β, and IL-6 in BMMs were increased, and Pcsk9 knockout aggravated the expression of these inflammatory factors. The number of osteoclasts positive for tartrate-resistant acid phosphatase staining around the apical lesion in Pcsk9−/− mice was higher than that in WT mice. Then BMMs underwent the osteoclast differentiation. Pcsk9 knockout BMMs induced increased and larger osteoclasts. While this effect of Pcsk9 knockout was abolished by the addition of Ldlr small interfering RNA, revealing that Pcsk9 knockout increased osteoclastogenesis was dependent on the LDLR. Immunohistochemistry staining showed increased expression level of LDLR in exposed Pcsk9−/− periapical areas. In vitro experiments showed that LPS promoted the expression level of LDLR in Pcsk9−/− BMMs and increased osteoclast formation ability, indicating that LPS promoted the elevation of osteoclasteogenesis caused by the Pcsk9 knockout. In conclusion, Pcsk9 deficiency aggravated the inflammatory response and promoted the osteoclastogenesis in an LDLR-dependent manner in AP experimental mice.

Sign in / Sign up

Export Citation Format

Share Document