Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Effusion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed2002

Pleural effusion and serum soluble fas-ligand levels are elevated in different clinical conditions.

Fas ligand (FasL) plays an important role in the regulation of apoptosis. Soluble FasL (sFasL) is produced by a cleavage of FasL from the cell surface by metalloproteinase. Whether or not sFasL exists or is elevated in the pleural effusion of different etiologies is unknown. The present study is designed to determine pleural effusion and serum sFasL levels under different clinical conditions, and ascertain if there exists a significant difference in the levels found in different clinical conditions, and whether this difference can be used as a tool for differential diagnosis. Soluble FasL levels in the pleural effusion and serum of 103 patients, including 37 with malignant pleural effusion, 24 with uncomplicated parapneumonic effusion, 8 with bacterial empyema, 16 with tuberculous pleurisy, and 18 with transudate effusion (8 with congestive heart failure and 10 with viral liver cirrhosis), were analyzed with ELISA assays. Pleural effusion from patients with bacterial empyema (median 79.4 pg/ml) and TB pleurisy (median 31.9 pg/ml) contained significantly higher amounts of sFasL than the pleural effusion from all other conditions studied (p <0.001). Viral liver cirrhosis had a significantly higher serum sFasL level (median 53.6 pg/ml, p = 0.025, when compared with other patients). Patients with congestive heart failure had the lowest serum sFasL levels when compared with other patients (p = 0.014). There was no significant correlation between pleural effusion sFasL levels and other parameters, such as effusion LDH, cell count, neutrophil, and lymphocyte percentage. In conclusion, soluble FasL is a useful marker for the differentiation of bacterial empyema and TB pleurisy from other disease entities. In addition, the elevation of serum sFasL levels in viral liver cirrhosis can also be used to differentiate cirrhosis from congestive heart failure, in which both effusions are transudate.

Aged↗
PubMed1996

IL-8 in pleural effusion.

Interleukin-8 (IL-8) is a recently described potent chemotactic factor that may be involved in the pathogenesis of pleural effusions. To understand the actual mechanisms mediating the inflammatory response, changes in cellular components and IL-8 level in pleural fluid of different aetiologies were evaluated. Thirty-four patients (19 male, 15 female) with a mean age of 46 +/- 22 years (range 16-92) were included in the study. Of these, 13 had tuberculous pleural effusion, seven had empyema/parapneumonic pleural effusion, and 14 had malignant pleural effusion (seven adenocarcinoma, three ovarian carcinoma, two lymphoma, one chronic myeloid leukaemia, and one small cell carcinoma) with positive cytology. Differential cell counts in the pleural fluid were obtained using cytocentrifuge preparations. The concentrations of IL-8 in pleural fluid were measured by the ELISA method. Interleukin-8 was detected in all 34 pleural fluid samples. The serum IL-8 level was analysed only in the empyema/parapneumonic pleural effusion group. The mean IL-8 levels of tuberculous, empyema/parapneumonic, and malignant pleural effusions were 1420 +/- 1049 pg ml-1, 4737 +/- 2297 pg ml-1, and 1574 +/- 1079 pg ml-1, respectively. The IL-8 levels in the empyema/parapneumonic group were significantly raised over malignant and tuberculous groups (P < 0.02). The mean pleural fluid neutrophil counts in tuberculous, empyema/parapneumonic and malignant pleural effusions were 315 +/- 575 cells mm-3, 11,136 +/- 12,452 cells mm-3, and 635 +/- 847 cells mm-3, respectively (P < 0.003). There was a significant positive correlation between pleural IL-8 levels and neutrophil counts (r = 0.46, P < 0.006). The levels of IL-8 in paired samples of serum and pleural fluid in the empyema/parapneumonic effusion group were compared, and the concentration of IL-8 was higher in the pleural effusion than serum (means, 4737 +/- 2297 pg ml-1 and 130.0 +/- 62.5 pg ml-1, respectively, P < 0.03). There was a significant negative correlation between IL-8 concentrations in serum and pleural fluid (r = -0.80, P < 0.03). This data suggests that production of IL-8 in pleural effusion may play a key role in initiation and maintenance of inflammatory reactions, especially in empyema/parapneumonic pleural effusions. It may offer the basis for introduction of novel anti-inflammatory agents in treatment.

Adolescent↗
PubMed1997

Diagnostic value of ferritin, haptoglobin, alpha 1-antitrypsin, lactate dehydrogenase and complement factors C3 and C4 in pleural effusion differentiation.

Searching to define diagnostic criteria for malignant and non-malignant pleural effusions, the differential diagnostic value of ferritin (FRT), haptoglobin (Hp), alpha 1-antitrypsin (alpha 1-AT), lactate dehydrogenase (LDH) and complement factors C3 and C4 were investigated prospectively in 100 consecutive patients with pleural effusions of various aetiologies. Pleural effusion FRT, C3 and C4 concentrations were found to be useful in differentiating exudates from transudates, so that transudates practically could be excluded in pleural effusion: serum FRT ratio lower than 0.5 and/or in pleural effusion values for C3 and C4 higher than 300 mg dl-1 and 70 mg dl-1, respectively. A pleural effusion: serum C3 ratio greater than 2 is seen only in malignant effusions. No discriminative pleural: serum ratio could be found in FRT and C4 values capable of differentiating malignant from non-malignant effusions. Pleural effusion alpha 1-AT and LDH values were elevated in exudates, as compared with transudates, and had an excellent sensitivity and predictive value, but low specificity, in differentiating malignant from non-malignant effusions. Finally, the sensitivity, specificity and positive predictive value of pleural effusion Hp concentrations were lower than those of FRT and complement factors C3 and C4, respectively.

Adult↗
PubMed2004

Sensitive detection of tumour cells in effusions by combining cytology and fluorescence in situ hybridisation (FISH).

Diagnosis of malignant cells in effusions is important for staging procedures and resulting therapeutic decisions. Cytodiagnostics in effusions is sometimes difficult since reactive mesothelial cells can mimic malignant cells. We used fluorescence in situ hybridisation (FISH) in single-colour or if appropriate in dual-colour evaluation to detect chromosomal aberrations in effusion cells as markers of malignancy, to raise the diagnostic yield. Cytologic and FISH evaluations--by using probes representing several chromosomes always including chromosomes 11 and 17--were performed in 358 effusion fluids. Cytology was positive for malignancy in 44.4% of all effusions, whereas FISH was positive in 53.9% (P=0.0001). The combination of cytology and FISH was diagnostic for malignancy in 60.9% of effusions. Diagnostic superiority of FISH was demonstrated in effusions from breast cancer, lung cancer, pancreatic cancer, and in effusions from the entire group of gynaecological and gastrointestinal carcinomas. In transudates (effusion protein <2.5 g dl(-1)), malignant cells were detectable by cytology, FISH, and combined use of both methods in 18.6, 30, and 37.1% of effusions, respectively, suggesting that cytologic and molecular analysis should be performed also with transudates. In conclusion, FISH in combination with conventional cytology is a highly sensitive and specific diagnostic tool for detecting malignant cells in effusions.

Aneuploidy↗
PubMed1994

Comparison of nucleolar organiser regions and DNA flow cytometry in the evaluation of pleural effusion.

BACKGROUND: In conventional cytological diagnosis of pleural effusions the assessment of morphological features plays an important part. However, false negative and false positive results may occur. In this study conventional cytology was compared with flow cytometric DNA analysis and the argyrophil staining technique for nucleolar organiser regions (AgNOR) to characterise benign and malignant effusions. METHODS: Pleural effusions from 71 patients (38 with benign lung disease, 33 with proven adenocarcinoma of lung) were studied by conventional cytology, flow cytometric DNA analysis, and the AgNOR technique. Tumour cell ploidy was determined by flow cytometry. In an attempt to detect the cell proliferative state, flow cytometric S phase fraction and the AgNOR technique were used. The correlations among conventional cytology, flow cytometric DNA ploidy, S phase fraction analysis, and nucleolar organiser regions were investigated. RESULTS: All the 38 benign pleural effusions were diploid. There were 17 (52%) aneuploid and 16 (48%) diploid malignant pleural effusions. Based on these results this type of DNA analysis had a sensitivity of 52% and a specificity of 100%. The mean (SD) numbers of flow cytometric S phase fractions of benign and malignant cases were 5.32 (1.67)% and 12.45 (3.93)% respectively. The mean numbers of S phase fractions of diploid malignant cases were higher than diploid benign cases. In each case the number of AgNORs was counted in 100 cells. The mean number of AgNOR dots per nucleus was 12.57 (3.64) for malignant pleural effusion cells and 3.96 (1.39) for benign pleural effusion cells. The mean number of AgNOR dots was 14.45 (3.36) for aneuploid malignant pleural effusion cells and 10.57 (2.82) for diploid malignant pleural effusion cells. The AgNOR numbers were higher in diploid malignant cells than in diploid benign cells. There was a significant correlation between the S phase fraction determined by flow cytometry and the mean number of AgNORs per nucleus in malignant cases. CONCLUSIONS: Both flow cytometry and the AgNOR methods provide comparable measurements in the diagnosis of pleural effusion. The study also indicates that the AgNOR method, which is rapid and easy to perform, may be a useful adjunct to flow cytometry, S phase fraction analysis and conventional cytology in the routine diagnosis of malignant pleural effusion.

Adenocarcinoma↗
PubMedDate not supplied

Etiology of exudative pleural effusions in adults in North Lebanon.

OBJECTIVE: To establish the clinical pattern and etiology of exudative pleural effusions in adults in North Lebanon. MATERIALS AND METHODS: All patients aged 21 years and older who were admitted with exudative pleural effusions to the Husseini Hospital, Tripoli, North Lebanon, between 1997 and 1999 were studied prospectively. RESULTS: Of 165 patients with exudative pleural effusions, 114 (69.1%) were men and 51 (30.9%) were women. The most frequent cause of exudative pleural effusions was tuberculosis (43.7%), followed by malignancy (32.1%). The majority (88.7%) of malignant pleural effusions were due to lung cancer. Tuberculous effusions were more frequent in the first five decades of life (66.7%) and were the most common type of pleural effusion, accounting for 68.6% of patients younger than 50 years of age. Malignant effusions were more frequent among the older age groups, with 73.6% of patients with malignant effusions being older than 50 years of age. Most types of exudative pleural effusions showed a preference for the right side of the thorax. Of the diagnostic procedures used in the present study, the most useful were histological examination and culture of pleural biopsies. CONCLUSIONS: In North Lebanon, the clinical pattern and etiology of exudative pleural effusions are similar to those in the developing countries; the most frequent cause of pleural exudates is tuberculosis, followed by malignancy, particularly malignancy due to lung cancer.

Adult↗
PubMed1993

The incidence of pleural effusion in a well-defined region. Epidemiologic study in central Bohemia.

Pleural effusion may complicate various diseases. To facilitate the differential diagnosis of pleural effusion, the authors conducted an epidemiologic study of incidence and etiology of different types of pleural effusions in a well-defined region in central Bohemia. During a 1-year period, the authors worked with the general practitioners and other physicians from the local hospital to identify patients with pleural effusion either while the patient was alive or at autopsy. During this period, 142 individuals (93 living and 49 at autopsy) with pleural effusion were identified among a population of 44,000 (incidence = 0.32 percent). The most common etiologies of the effusions were congestive heart failure (65, 46 percent), malignant effusions (31, 22 percent), parapneumonic effusions (24, 17 percent), and pulmonary emboli (8, 5.6 percent). Other etiologies for the effusions included pulmonary hemothorax (6), intra-abdominal processes (4), uremia (2), myxedema (1), and rheumatoid pleuritis (1). We conclude that pleural effusions are relatively common and if these figures are extrapolated to the United States and Czechoslovakia respectively, one could expect at least 800,000 cases in the United States and 48,000 in Czechoslovakia annually. Over 90 percent of the pleural effusions will be due to congestive heart failure, malignancy, pneumonia, or pulmonary emboli.

Aged↗
PubMed2003

Etiology and pleural fluid characteristics of large and massive effusions.

STUDY OBJECTIVE: To report the etiology of large and massive pleural effusions, and to compare their biochemical fluid characteristics with those of smaller size, and between malignant and nonmalignant conditions. DESIGN: Retrospective chart review of all patients undergoing thoracentesis at an academic medical center in Lleida, Spain, during a 10-year period. PATIENTS: Posteroanterior chest radiographs were available in 766 patients during the study period. Large pleural effusions (ie, two thirds or more of the hemithorax without its complete obliteration) were identified in 70 patients (9%), and massive pleural effusions (ie, hemithorax was completely opacified) were identified in 93 patients (12%). RESULTS: A similar etiologic spectrum between large and massive pleural effusions was observed. The most frequent cause of these pleural effusions was malignancy (89 patients; 55%), followed by complicated parapneumonic or empyema (36 patients; 22%), and tuberculosis (19 patients; 12%). Compared with nonmalignant pleural effusions, patients with large or massive malignant pleural effusions were more likely to have pleural fluids with higher RBC counts (18.0 x 10(9) cells/L vs 2.7 x 10(9) cells/L, respectively; p < 0.001) and lower adenosine deaminase (ADA) activity (11.5 vs 31.5 U/L, respectively; p < 0.001), which were the two parameters that were selected by a stepwise logistic-regression model as independent predictors of malignancy. In addition, large/massive malignant pleural effusions showed higher median RBC counts (18.0 x 10(9) cells/L vs 4.3 x 10(9) cells/L, respectively; p < 0.001), higher lactate dehydrogenase levels (641 vs 409 U/L, respectively; p = 0.001), lower pH (7.39 vs 7.42, respectively; p = 0.006) content, but similar cytologic yield (63% vs 53%, respectively; p = 0.171) than smaller malignant pleural effusions. CONCLUSIONS: The presence of a large or massive pleural effusion enables the clinician to narrow the differential diagnosis of pleurisy, since most effusions are secondary to malignancy or infections (either bacterial or mycobacterial). Bloody pleural fluid with low ADA content favors a malignant condition.

Adenosine Deaminase↗
PubMed2004

Echogenic swirling pattern as a predictor of malignant pleural effusions in patients with malignancies.

OBJECTIVES: Chest ultrasonography is a useful diagnostic tool for the detection of pleural effusions of different etiologies. Our purpose was to determine whether the echogenic swirling pattern identifiable on real-time chest ultrasonographic images is a predictor of malignant pleural effusions in patients with malignancies. DESIGN: Medical records of patients undergoing chest ultrasonography in the Tri-Service General Hospital (Taiwan) between January 2000 and December 2002 were reviewed retrospectively. Patients with an echogenic swirling pattern in the pleural effusion, or with malignant diseases associated with pleural effusions, whose pleural fluids had been examined cytologically or whose pleural tissues had been examined pathologically, were enrolled in this study (n = 140). Malignant pleural effusions were defined by the presence of malignant cells in the pleural fluid identified by thoracentesis or by pleural biopsy. The echogenic swirling pattern was defined as numerous echogenic floating particles within the pleural effusion, which swirled in response to respiratory movement or heartbeat. Correlation between malignant pleural effusions and the echogenic swirling pattern was compared in patients with an underlying malignant disease. RESULTS: In patients with underlying malignancies, malignant pleural effusions were diagnosed in 81.8% of patients with a positive echogenic swirling pattern and in 48% of those with no echogenic swirling pattern. The presence of echogenic swirling was significantly more predictive of malignant pleural effusions than was the absence of echogenic swirling (p < 0.01). CONCLUSIONS: The echogenic swirling pattern is a useful predictor of possible malignant pleural effusions, and may be a good marker for malignant pleural effusions in patients with underlying malignancies.

Adult↗
PubMed1982

Diagnostic value of tumoral markers in serous effusions: carcinoembryonic antigen, alpha1-acidglycoprotein, alpha-fetoprotein, phosphohexose isomerase, and beta 2-microglobulin.

In order to discriminate between benign and malignant effusions, the value of carcinoembryonic antigen (CEA), alpha 1-acidglycoprotein (AGP), alpha-fetoprotein (AFP), phosphohexose isomerase (PHI), and beta 2-microglobulin (B2M) has been estimated in serous effusions in a group of 106 patients, 30 with a malignant and 76 with a benign effusion. Mean CEA and AGP levels in malignant effusions were significantly higher than in benign effusions; no significant differences of mean PHI, AFP and B2M levels of benign and malignant effusions were found. CEA level estimations were useful for confirming malignancy in 27% of malignant effusions but in only 7.5% of all effusions, and AGP and PHI for excluding it in 37.5 and 36.0% of all effusions, respectively. With the combination of CEA with AGP or PHI, a correct diagnosis was achieved in only 45 and 44% of all effusions, respectively. The combination of AFP or B2M with CEA, AGP or PHI did not improve the discriminative value for differentiating malignant and benign effusions.

Ascites↗
PubMed1988

Etiology and prognostic implications of a large pericardial effusion in men.

To assess the etiology and prognosis of a large pericardial effusion, we reviewed 25 consecutive patients who presented with a large pericardial effusion and underwent a drainage procedure. Large pericardial effusion was defined as: (1) an echo-free space greater than or equal to 10 mm anteriorly and posteriorly by M-mode echocardiography and (2) removal of greater than or equal to 350 ml of fluid at pericardial drainage. The etiologies of large pericardial effusion were: neoplastic (36%), idiopathic (32%), uremic (20%), postmyocardial infarction (8%), and acute rheumatic fever (4%). Of our patients, 44% presented with cardiac tamponade, while 25% of patients with idiopathic pericarditis had hemorrhage effusion and cardiac tamponade. At follow-up, 37 +/- 17 months after pericardial drainage, 68% had died from complications of their underlying disease. There were no deaths attributed to pericardial disease. While 88% of patients with idiopathic large pericardial effusion were alive at follow-up, none of the neoplastic large pericardial effusion patients survived longer than 5 months after initial pericardial drainage (p less than 0.001). Additionally, the survival of patients with uremic large pericardial effusion was better than patients with neoplastic large pericardial effusion (p less than 0.05). We conclude: (1) neoplastic, idiopathic, and uremic pericarditis are the most common causes of large pericardial effusion in men, (2) idiopathic pericarditis can be hemorrhagic and cause cardiac tamponade, and (3) the prognosis of large pericardial effusion is related to patients' underlying disease.

Adult↗
PubMed2004

Significance of pleural effusion at diagnosis of Wilms tumor.

BACKGROUND: Pleural effusion is uncommon at diagnosis of Wilms tumor. Because the clinical significance of this finding has not been reported, a retrospective review of this entity was conducted. PROCEDURE: The radiology reports and medical records of 233 patients with Wilms tumor who were treated at St. Jude Children's Research Hospital between 1985 and 2001 were reviewed. RESULTS: Ten of the 233 patients (4.3%) had pleural effusions detected on pre-nephrectomy imaging studies. Computed tomography (CT) scans were more sensitive than chest X-rays in identifying pleural effusions. All of the patients with pleural effusions had tumors of favorable histology. Two patients had stage II disease, five had stage III disease, two had stage IV disease, and one had stage V (bilateral) disease. All of the effusions occurred on the same side as the primary kidney tumors and six effusions were associated with ascites. The two effusions that were tapped were negative for tumor cells. All 10 patients in our series were alive without recurrence with a median follow-up duration of 68 months, yet only two patients were treated with lung irradiation. CONCLUSION: Pleural effusion at presentation of Wilms tumor is uncommon and not associated with adverse prognosis. We recommend that pleural effusions be tapped whenever feasible if the results will change therapy. Patients with pleural effusions that are small and difficult to tap may be treated according to their local stage without pulmonary irradiation. Further analysis of pleural effusions in a larger group of patients is necessary to confirm our preliminary observations.

Follow-Up Studies↗
PubMed1995

Tumor-associated lymphocytes (TAL) are competent to produce higher levels of cytokines in neoplastic pleural and peritoneal effusions than those found in sera and are able to release into culture higher levels of IL-2 and IL-6 than those released by PBMC.

This work was designed to study the proliferative response of tumor-associated lymphocytes (TAL) from neoplastic effusions against autologous tumor cells and the immunophenotype pattern of TAL from neoplastic effusions and that of PBMC of the same patients. We also compared the serum levels of the cytokines interleukin (IL) 1 beta, 2 and 6, tumor necrosis factor-alpha (TNF alpha) and soluble IL-2 receptor (sIL-2R) with those present in neoplastic effusions of the same patients. Moreover, we examined the ability of TAL and peripheral blood mononuclear cells (PBMC) to produce and release the cytokines and sIL-2R and to express membrane CD25 following their stimulation with phytohemagglutinin (PHA) in vitro. Finally, we compared the cytokines/sIL-2R production and membrane CD25 expression by PHA-stimulated PBMC of the patients with neoplastic effusions with a series of 90 cancer patients without neoplastic effusions and 20 normal healthy subjects. Thirteen neoplastic pleural and eight peritoneal effusions were collected from 11 patients with primary lung cancer, 7 with primary epithelial ovarian cancer, 1 with breast cancer, 1 with pleural mesothelioma, and 1 with pancreatic cancer. The proliferative response of TAL from neoplastic effusions against autologous tumor cells was lower than the response to PHA, IL-2, and anti-CD3, but significant. The percentage distribution of CD3+ and CD8+ lymphocyte subpopulations was higher in peritoneal than in pleural effusions, while the CD16+ subset was higher in pleural than in peritoneal effusions. The percentage distribution of CD16+ was significantly lower in pleural effusions than in PBMC of patients with pleural effusions.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed2006

Pericardial effusion following pulmonary resection.

OBJECTIVE: Postoperative pericardial effusion commonly occurs after open heart surgery. However, after general thoracotomy such as pulmonary resection, there have been few reports of pericardial effusion. The purpose of this study is to investigate patients with pericardial effusion following pulmonary resection. METHODS: Among 2,385 patients with pulmonary resection for lung neoplasm in our institute, eight patients, whose pericardium had never been opened during the operation, developed pericardial effusion. The clinical characteristics of the eight patients were analyzed. RESULTS: Pericardial effusion after pulmonary resection was divided into two subtypes: pericardial effusion in three patients with left thoracotomy occurring within 30 days postoperatively, and pericardial effusion in the remaining five patients with right thoracotomy occurring more than 30 days postoperatively. Pericardiotomy or pericardiocentesis was performed in three symptomatic patients, and the remaining five asymptomatic patients were treated with diuretics. Pericardial effusion disappeared in three of the five patients about 1-3 months after the conservative treatment, while, in the remaining patients, because pericardial effusion had increased gradually, pericardiocentesis was performed. CONCLUSION: From our experience, the treatment strategy of drainage for early pericardial effusion and diuretics for late pericardial effusion seems to be appropriate.

Adult↗
PubMed2003

High incidence and spontaneous resolution of mastoid effusion after craniotomy on early postoperative magnetic resonance images.

Mastoid effusion is a poorly understood complication after craniotomy. The incidence and severity of postoperative mastoid effusion were retrospectively examined on postoperative magnetic resonance (MR) images to assess any association with craniotomy procedures, time course, and neuro-otological complications. We evaluated the early postoperative MR images (within 4 days of craniotomy) and medical records of 74 patients who underwent 77 operations for the treatment of various intracranial diseases from January 2000 to December 2001. Mastoid effusion was classified into four grades: none, partial, moderate, and severe diffuse effusion in the mastoid air cells. Thirty-three follow-up MR images from 26 patients were also reviewed. Postoperative mastoid effusion occurred ipsilateral to the craniotomy site in 62 cases and contralateral in 56 cases. Mastoid effusion was significantly more severe ipsilateral than contralateral to craniotomy with exposure of the mastoid air cells ( P<0.0001). There was no significant difference in severity between the contralateral and ipsilateral sides after craniotomy without mastoid air cell opening ( P=0.437). Mastoid effusion following craniotomy without exposure of mastoid air cells resolved within 3 months. However, otitis media with effusion developed in six patients with severe mastoid effusion ipsilateral to craniotomy with exposure of the mastoid air cells. Mastoid effusion frequently developed on both sides. Any grade of mastoid effusion on the ipsilateral side to craniotomy without exposure of mastoid air cells, or on the contralateral side, was asymptomatic or had a benign course, and disappeared within 3 months.

Brain Neoplasms↗
PubMedDate not supplied

Endostatin levels in exudative pleural effusions.

Endostatin is an angiogenesis inhibitor that is an endogenously produced proteolytic fragment of type XVIII collagen. Although serum levels of endostatin have extensively been studied in patients with malignant diseases, endostatin in pleural effusion has not been fully evaluated. In order to determine whether endostatin is present in pleural effusion, and to determine whether endostatin levels vary in pleural effusion of different etiology, we measured levels of endostatin in 38 malignant pleural effusion due to lung cancer patients and 29 patients with non-malignant disease using an ELISA kit. Free form of endostatin was measurable (> 11.2 pg/ml) in 26 of 38 malignant and 13 of 29 non-malignant pleural effusion. Endostatin levels in the 38 malignant pleural effusion were significantly higher than those in patients with the 29 patients with non-malignant diseases ( p = 0.0131). However, there was not statistically significant difference between the patients with pleuropneumonia and those with tuberculous pleurisy ( p = 0.2194). In malignant pleural effusion due to lung cancer, the pleural effusion endostatin levels did not differ when the histological types of lung cancer were considered ( p = 0.0674). Endostatin was present in both malignant and non-malignant pleural effusion, and elevated levels of endostatin were observed in malignant pleural effusion. Although the mechanisms are unclear, elevated levels of endostatin in pleural effusion may represent the local productions of endostatin in pleural space.

Adenocarcinoma↗
PubMed2002

Soluble HLA class I molecules in malignant pleural and peritoneal effusions and its possible role on NK and LAK cytotoxicity.

PURPOSE: To examine the amount of sHLA-I in malignant pleural and peritoneal effusions and its possible role in natural immune defense. METHODS: Three groups of patients (75 patients with malignancy, 21 with infection, and 27 with other diseases) were studied for sHLA-I value using an ELISA method. Cytolytic activity of freshly isolated pleural and peritoneal effusion-associated lymphoid (EAL) cells from 14 of cases with malignancy were examined and compared to that of ten non-cancerous patients. EAL cells were co-cultured with the autologous cell-free effusions immediately after collection and 3 days after incubation with IL-2. RESULTS: The mean value of sHLA-I in effusions was 1.01+/-1.36 micro g/ml, 0.97+/-1.20 micro g/ml, and 0.49+/-0.45 micro g/ml, respectively. Despite higher mean sHLA-I levels in malignant and infected patients, no significant difference between these groups was observed ( P >0.05). Generally, the amount of sHLA-I in peritoneal effusions was higher than that for pleural effusions, but the difference was not significant. There were also no statistical differences in the sHLA-I levels between sub-groups of patients with malignancy. EAL cells' killing activity in malignant and infected effusions was 68.15+/-11.73 and 78.28+/-14.41, respectively ( P=0.08). No correlation between sHLA-I level and NK activity of EAL cells from the patients was found. Almost all malignant cases after exposure to cell-free effusions displayed an increase in NK activity (from 68.66+/-11.13 to 74.2+/-12.39, P=0.042) and a decrease in LAK activity (74.5+/-18.30 vs 67.72+/-16.46, P=0.040). Whereas, the same experiment performed for non-malignant effusions showed a decrease in both NK activity and LAK activity. Changes in NK and LAK activity were not correlated with the amount of sHLA-I in the effusions. CONCLUSION: The presence of sHLA-I, particularly in malignant effusions, suggests a role for these molecules in tumor immunity in the peritoneal or plural environment; however, at least with these group of patients, sHLA-I appears not to be a unique determining factor on EAL cells' killing activity.

Ascitic Fluid↗
PubMed1985

Pleural effusions after endoscopic variceal sclerotherapy.

The prevalence of pleural effusions after endoscopic variceal sclerotherapy was reviewed in 30 patients undergoing 65 sclerotherapy sessions. Pleural effusions were identified radiographically after 31 of the 65 (48%) sclerotherapy sessions. Eleven of the effusions were right-sided, 10 were left-sided, and 10 were bilateral. Most of the effusions (20 of 31, 65%) were small. Significant postsclerotherapy chest pain was found more commonly in those patients who developed pleural effusions (11 of 31, 35%) compared with those who did not (4 of 34, 12%) (p less than 0.05). The total sclerosant volume injected was significantly greater in those who developed effusions (13.2 +/- 5.8 ml) (mean +/- SD) than in those who did not (8.5 +/- 4.5 ml) (p less than 0.001). Twelve effusions were analyzed biochemically after thoracentesis. Eleven effusions met one or more of three criteria commonly used to identify exudative effusions. We conclude that pleural effusions develop frequently after sclerotherapy. The effusions are predominantly exudative in character and presumably arise from inflammation of the mediastinal parietal pleura.

Adult↗