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R W Light

Publications and source records attributed to R W Light.

At least 19 recordsLinked to original sources
PubMed2006

Routine use of pleural fluid cultures. Are they indicated? Limited yield, minimal impact on treatment decisions.

In pleural infection, it has been recommended that Gram stain and cultures should be obtained on a routine basis. However, this recommendation has not been tested prospectively. We evaluated the yield of microbiological studies in 259 patients with parapneumonic pleural effusion. Microbiological studies were positive on the pleural fluid of 50 patients (19.3%). In 48 of the 50 patients with positive microbiological results (96%), the need for pleural drainage was correctly predicted by pleural fluid parameters. There were no differences in hospital stay (9.5+/-2.5 days versus 9.9+/-3.2 days, P=0.68) or in mortality (2 deaths in each group, P=0.58) between the group of patients in which antibiotic treatment was changed according to microbiological results and the group of patients in which it is not. In conclusion, this study demonstrates that, at least in our institution, routine microbial investigation of pleural fluid adds very little to the standard management of parapneumonic effusions.

Adult↗
PubMed2006

D-dimer levels in pleural effusions.

INTRODUCTION: D-dimer is a degradation product of cross-linked fibrin. We hypothesized that hemorrhagic pleural effusions would have greater D-dimer levels than non-hemorrhagic pleural effusions, and that persistently bloody effusions would be distinguishable from thoracentesis-induced bloody effusions by the D-dimer level. METHODS: Forty pleural effusions were studied. D-dimer levels (measured by ELISA), red blood cell (RBC) count, white blood cell (WBC) count, lactate dehydrogenase (LDH), and protein level was measured for each effusion. Ten effusions, five non-bloody, and five bloody were studied for each of the following disease states: parapneumonic effusion, congestive heart failure, post-coronary artery bypass grafting, and lung cancer. RESULTS: No significant difference of the D-dimer level was noted between bloody and non-bloody effusions of different disease states (P=0.286). There was no significant difference in the median D-dimer levels between all the bloody and all the non-bloody effusions (P=0.88). There was no significant difference (P=0.51) in D-dimer levels between five diseases groups when the bloody and non-bloody fluids were combined. The D-dimer levels did not correlate with the RBC count (r=0.11, P=0.48), WBC count (r=0.13, P=0.53), LDH (r=0.01, P=0.93), or protein levels (r=-0.01, P=0.93) in any of the groups. CONCLUSION: Measurement of pleural fluid D-dimer levels does not distinguish persistently bloody effusions from non-bloody effusions, and does not aid in narrowing the differential diagnosis of an effusion.

Coronary Artery Bypass↗
PubMed2004

Penetration of newer quinolones in the empyema fluid.

The degree of penetration of newer quinolones into the pleural fluid has not been studied. The objective of the present study was to determine the degree to which moxifloxacin and levofloxacin penetrate into empyemic pleural fluid using a new rabbit model of empyema. An empyema was created via the intrapleural injection of turpentine (1 mL), followed 24 h later by instillation of 2 mL (1 x 10(10)) Escherichia coli bacteria (ATCC 35218) into the pleural space of New Zealand white rabbits. After an empyema was verified by thoracentesis and pleural fluid analysis, moxifloxacin and levofloxacin (25 mg.kg(-1) for both, i.v.) were administered. Antibiotic levels were determined in samples of pleural fluid and in blood collected serially over 12 h. Antibiotic levels were measured using HPLC. Each of the antibiotics penetrated well into the empyemic pleural fluid. Antibiotic penetration was the greatest for moxifloxacin (area under the curve (AUC) for pleural fluid/blood (AUCPF/AUCblood) ratio=1.37) followed by levofloxacin (ratio=1.13). The time to equilibration between the pleural fluid and blood antibiotic levels was more rapid for moxifloxacin (3.9 h) than for levofloxacin (4.4 h). With moxifloxacin, the peak pleural fluid concentration (Cmax,PF) was 2.77 microg.mL(-1) and occurred at a time to maximum pleural fluid concentration (Tmax,PF) of 6 h after infusion and decreased thereafter. The peak blood concentration (Cmax,blood) was 4.81 microg.mL(-1) at 1 h after administration. With levofloxacin, the peak pleural fluid level (Cmax,PF=1.39 microg.mL(-1)) occurred at 6 h (Tmax,PF=6 h) after infusion. The Cmax,blood was 1.88 microg.mL(-1) at 1 h after administration. In conclusion, differences were found in the degree of penetration of the two quinolones into infected pleural fluid in rabbits. The clinical significance of these differences is unknown. More studies are needed to evaluate the pharmacokinetic parameters in the pleural space in humans.

Animals↗
PubMed2003

Diagnostic value of adenosine deaminase in nontuberculous lymphocytic pleural effusions.

Adenosine deaminase (ADA) can aid in the diagnosis of tuberculous pleural effusions, but false-positive findings from lymphocytic effusions have been reported. The purpose of this study is to assess the ADA levels in nontuberculous lymphocytic pleural effusions (lymphocyte count > 50%) of different aetiologies. Altogether, 410 nontuberculous lymphocytic pleural fluid samples were consecutively selected. These included malignant effusions (n = 221), idiopathic effusions (n = 76), parapneumonic effusions (n = 35), postcoronary artery bypass graft surgery effusions (n = 6), miscellaneous exudative effusions (n = 21) and transudative effusions (n = 51). The ADA level reached the diagnostic cut-off for tuberculosis (40 U x L(-1)) in seven of the 410 cases (1.71%). The negative predictive value of ADA for the diagnosis of pleural tuberculosis was 99% (403 of 407 cases) in the group of lymphocytic pleural effusions. In five of these seven patients ADA1 and ADA2 were measured, and in all these cases (100%) ADA1/ADA(p) correctly classified these lymphocytic effusions as nontuberculous (ratio < 0.42). This prospective study provides additional evidence that adenosine deaminase levels in nontuberculous lymphocytic pleural effusions seldom exceed the cut-off set for tuberculous effusions. The pleural fluid adenosine deaminase levels were significantly higher in different types of exudative effusions than in transudates. An adenosine deaminase level < 40 IU x L(-1) virtually excluded a diagnosis of tuberculosis in lymphocytic pleural effusions. Adenosine deaminase1/adenosine deaminase(p) correctly classified all nontuberculous lymphocytic pleural effusions with high adenosine deaminase levels.

Adenosine Deaminase↗
PubMed2003

Transforming growth factor-beta induces collagen synthesis without inducing IL-8 production in mesothelial cells.

Conventional pleurodesing agents often provoke acute pleural inflammation followed by fibrosis. The inflammation frequently causes pain and fever. Transforming growth factor (TGF)-beta is a pro-fibrotic but anti-inflammatory cytokine. Intrapleural TGF-beta2 administration produces effective pleurodesis in animals, but its effects on mesothelial cells are unknown. The authors hypothesised that, unlike conventional pleurodesing agents, TGF-beta2 can induce collagen synthesis without stimulating pleural inflammation. In the in vitro studies, TGF-beta2, talc and doxycycline were administered to rabbit mesothelial cells for 24 h. These agents were also injected intrapleurally in rabbits and the induced pleural fluids collected at 24 h. TGF-beta2 was as potent as talc and doxycycline in upregulating mesothelial cell collagen expression. Talc and doxycycline both induced significant increases in interleukin (IL)-8 production from mesothelial cells in vitro and in rabbit pleural fluids in vivo. TGF-beta2, however, did not stimulate mesothelial cell IL-8 release in vitro and induced a dose-dependent suppression of pleural fluid IL-8. Pleural fluid IL-8 levels correlated significantly with leukocyte and lactate dehydrogenase concentrations in the fluids. In summary, transforming growth factor-beta was a potent inducer of mesothelial cell collagen synthesis. Unlike talc and tetracycline, which provoked pleural inflammation, transforming growth factor-beta2 suppressed pleural inflammation in vivo. Transforming growth factor-beta2 can produce effective pleural fibrosis without necessitating acute pleural inflammation.

Animals↗
PubMed2003

Prognostic features of residual pleural thickening in parapneumonic pleural effusions.

The objective of the study was the identification of predictive factors for the development of residual pleural thickening (RPT) in patients with parapneumonic effusion. The design of the prospective study involved investigating patients with parapneumonic pleural effusions diagnosed between March 1991 and December 2000 in the respiratory department of Hospital Ramón y Cajal (Madrid, Spain) which is a 1,500 tertiary-care hospital. The clinical and radiological characteristics and measurements of microbiological and biochemical variables in the pleural fluid taken from the patients were studied. RPT was defined in a posteroanterior chest radiograph as pleural thickening of > or = 10 mm measured at the lateral chest wall at the level of an imaginary line, tangent to the diaphragmatic dome. A total of 48 of the 348 patients studied (13.79%) were found to have RPT. Among the factors studied, only presence of pus in the pleural space, Fine classes IV and V, temperature > or = 38 degrees C and delayed resolution of pleural effusions after diagnosis (> 15 days) were independently associated with the risk of RPT. This study showed that significant residual pleural thickening was not a common complication of parapneumonic pleural effusions. There are certain risk factors for the development of residual pleural thickening. However, this complication was not associated with long-term functional repercussions in the series of patients involved in this study.

Adult↗
PubMed2002

Determining the optimal number of specimens to obtain with needle biopsy of the pleura.

The aim of this study was to define the number of pleural biopsy samples necessary for optimum diagnostic performance and determine to what extent they are complementary. Eighty-four closed pleural biopsies were performed in our department between June 1996 and January 1998 on 55 males and 29 females with an average age of 64.4 +/- 16.7 years. The study of the pleural fluid included: pH, biochemical testing of pleura/serum (proteins, lactate dehydrogenase, glucose, cholesterol, triglycerides, albumin and adenosine deaminase), haemogram, cytology and microbiological testing (Gram-staining, aerobes, anaerobes and mycobacteriae cultures). The biopsies were performed using a Cope needle, with a total of five biopsies for each patient: four for pathological examination (taken numerically in the order in which they were performed: D1, D2, D3 and D4) and one for microbiological testing. In those cases in which the diagnosis was uncertain or effusion persisted, a thoracoscopy or thoracotomy was performed. There were no significant differences in the diagnostic yield of each individual sample (D1, D2, D3 and D4), but there were differences in the sum of the samples, depending on the number of biopsies performed.This was true for total group and the group with carcinomas, but not for the group with tuberculosis. The increase in diagnostic yield with the number of biopsies was more remarkable in the carcinoma cases, where it increased by 35% when four biopsies were performed (54% with one biopsy versus 89% with four biopsies, P < 0.002). In conclusion, the diagnostic yield increased with the number of biopsy samples in the total group and the group with malignancy but not in the group with tuberculous effusions. The best diagnostic performance for malignant pathology was obtained with four samples. In pleural tuberculosis, the diagnostic yield did not increase with more biopsy samples. One high quality sample should be enough to obtain a diagnosis.

Aged↗
PubMed2001

Routine measurement of pleural fluid amylase is not indicated.

BACKGROUND: The routine measurement of pleural fluid amylase is frequently recommended, but the cost-effectiveness of this procedure is unknown. METHODS: To assess the utility of routine measurement of pleural fluid amylase in evaluating pleural effusions, we measured amylase, glucose, lactate dehydrogenase, and protein levels and blood cell counts in 379 patients undergoing thoracentesis during a 22-month period from 1997 to 1999. Of these, 199 had effusions after cardiac surgery; 61, malignant; 48, transudative; 28, parapneumonic; 2, chylous; 2, rheumatoid; 1, tuberculous; and 1, from chronic pleuritis. There were 37 exudates of unknown origin. RESULTS: Measurement of pleural fluid amylase levels did not assist in determining the origin of the effusion in any of the patients. Amylase levels greater than 100 U/L (normal serum level in our laboratory is 30-110 U/L) were found in 5 (1.3%) of 379 patients: 1 patient with congestive heart failure (amylase, 173 U/L), 2 with post-cardiac surgery effusions (144 U/L and 130 U/L), 1 with pneumonia (109 U/L), and 1 with lung cancer (105 U/L). CONCLUSIONS: The routine measurement of pleural fluid amylase levels is neither clinically indicated nor cost-effective. We suggest that pleural fluid serum amylase levels be measured only if there is a pretest suspicion of acute pancreatitis, chronic pancreatic disease, or esophageal rupture.

Amylases↗
PubMed2001

Comparing transforming growth factor beta-2 and fibronectin as pleurodesing agents.

BACKGROUND: We have recently demonstrated that transforming growth factor beta-2 (TGF-beta2) can produce effective pleurodesis. Whether this effect can be reproduced by the use of its downstream proteins is not known. This study compared the effectiveness of TGF-beta2 and fibronectin in inducing pleurodesis in rabbits. METHODOLOGY: New Zealand white rabbits (1.5-2.0 kg) were given 1.7 microg of TGF-beta2 (n=5) or 2.0 mg of cellular fibronectin (n=4) intrapleurally via a chest tube. The induced pleural fluid was collected and analyzed. The rabbits were sacrificed after 14 days. The pleurodesis was graded macroscopically from 1 (none) to 8 (symphysis > 50%). RESULTS: All rabbits in the TGF-beta2 group developed effective pleurodesis while none in the fibronectin group had scores > 2 (pleurodesis scores 7.0 +/- 0.6 vs 1.3 +/- 0.3, P < 0.001). Rabbits that received TGF-beta2 produced large amounts of pleural fluid initially (< 4 days). Microscopically, the pleura of rabbits in the TGF-beta2 group showed prominent spindle cell proliferation and collagen deposition, but no significant inflammation or mesothelial proliferation. Pleural tissues of rabbits in the fibronectin group had occasional thin collagen deposits only. The intrapleural administration of 2.0 mg of fibronectin, a downstream product of TGF-beta, did not induce effective pleurodesis, as did the intrapleural administration of TGF-beta2. CONCLUSIONS: The present study suggests that the mechanism by which TGF-beta2 induces pleurodesis is not predominantly dependent on the production of fibronectin.

Animals↗
PubMed2001

Pleural effusions following cardiac injury and coronary artery bypass graft surgery.

This article discusses the pleural effusions that occur with the post-cardiac injury (Dressler's) syndrome (PCIS) and those that occur after coronary artery bypass graft (CABG) surgery. The PCIS can occur after any type of cardiac injury and is thought to be due to anti-myocardial antibodies. The primary symptoms are fever and chest pain, and pericarditis is frequently present. Pleural effusions are common with PCIS. The primary treatment for PCIS is a nonsteroidal anti-inflammatory agent or corticosteroids. Following CABG surgery, most patients will have a small unilateral left-sided pleural effusion, and approximately 10% of patients will have a larger effusion. These large effusions can be separated into early effusions occurring within the first 30 days of surgery that are bloody exudates with a high percentage of eosinophils, and late effusions occurring more than 30 days after surgery that are clear yellow lymphocytic exudates. The primary symptom of a patient with a pleural effusion post-CABG surgery is dyspnea; chest pain and fever are uncommon. Most patients with large pleural effusions postCABG surgery are managed successfully with one to three therapeutic thoracenteses.

Journal Article↗
PubMed2001

Pleural effusion due to pulmonary emboli.

Pulmonary embolism is the fourth leading cause of pleural effusion. The possibility of pulmonary embolus should be evaluated for all patients who have undiagnosed pleural effusion. The mechanism of pleural effusion caused by pulmonary embolus is usually increased interstitial fluid in the lungs as a result of ischemia or the release of vasoactive cytokines. Approximately 75% of patients with pulmonary emboli and pleural effusion have pleuritic chest pain. The most common cause of pleuritic chest pain and pleural effusion in patients under 40 years old is pulmonary emboli. Pleural effusion resulting from a pulmonary embolus usually occupies less than one-third of the hemithorax. Dyspnea is frequently out of proportion to the size of the pleural effusion. Pleural fluid caused by pulmonary emboli is usually exudative but is occasionally transudative. d-Dimer testing is a good screen for pulmonary emboli. If d-dimer results are positive, then a spiral computed tomograph should be obtained to confirm the diagnosis. Low-molecular-weight-heparin has become the initial treatment of choice for patients with pulmonary emboli and pleural effusion.

Humans↗
PubMed2001

Transforming growth factor beta2 induced pleurodesis is not inhibited by corticosteroids.

BACKGROUND: Talc and tetracyclines induce pleurodesis by directly injuring the pleura. The injury results in intense inflammation which subsequently leads to fibrosis. Corticosteroids can inhibit talc pleurodesis by reducing the inflammatory process. We hypothesised that transforming growth factor beta2 (TGFbeta2), a fibrogenic cytokine with immunomodulatory functions, could induce effective pleurodesis without generating significant pleural inflammation and therefore remain effective despite co-administration of corticosteroids. METHODS: Thirty rabbits were divided into two groups. Rabbits in the steroid group received weekly intramuscular injections of triamcinolone diacetate (0.8 mg/kg). Ten rabbits in each group were given 5.0 microg TGFbeta2 intrapleurally via a chest tube while the remaining five received 1.7 microg TGFbeta2. Pleurodesis was graded macroscopically after 14 days from 1 (none) to 8 (>50% symphysis). RESULTS: TGFbeta2 produced excellent pleurodesis at both 5.0 microg and 1.7 microg doses. The pleural effusions produced after the injection were low in all inflammatory markers. No significant differences were seen between the steroid group and controls in macroscopic pleurodesis scores (7.2 (1.3) v 7.1 (1.2)), levels of inflammatory markers in the pleural fluids (leucocyte 1107 (387)/mm(3) v 1376 (581)/mm(3); protein 3.1 (0.3) mg/dl v 2.9 (0.3) mg/dl, and LDH 478 (232) IU/l v 502 (123) IU/l), and the degree of microscopic pleural fibrosis and pleural inflammation. CONCLUSIONS: TGFbeta2 can induce effective pleurodesis and remains effective in the presence of high dose parenteral corticosteroids.

Animals↗
PubMed2001

Transforming growth factor-beta2 induces pleurodesis significantly faster than talc.

Transforming growth factor-beta2 (TGF-beta2) has recently been shown to produce effective pleurodesis in rabbits. Conventional pleurodesing agents such as talc act by inducing pleural injury, which results in acute inflammation and fibrosis. TGF-beta2 is a profibrotic cytokine capable of producing fibrosis without inducing significant pleural inflammation. We hypothesize that intrapleural administration of TGF-beta2 would (1) produce an effective pleurodesis faster; (2) stimulate more collagen deposition, and (3) induce less inflammation when compared with intrapleural injection of talc. Thirty rabbits were divided into two groups and given either TGF-beta(2) (1.7 microg) or talc slurry (400 mg/kg) via a chest tube. Five rabbits from each group were killed at Days 1, 4, and 7. Gross pleurodesis was graded from 1 (none) to 8 (complete symphysis). The microscopic pleural inflammation and fibrosis were graded from 0 to 4. Pleural thickening and the total area of collagen deposition were compared. Intrapleural injection of TGF-beta2 produced effective pleurodesis within 7 d (median pleurodesis score = 7 at Day 7). At Day 7, TGF-beta2 induced significantly more collagen deposition (19.4 +/- 19.6% versus 4.6 +/- 2.9% of total area of pleura at Day 7), higher pleural fibrosis score (3.0 +/- 1.0 versus 1.8 +/- 0.5), and pleural thickness (286 +/- 191 versus 85 +/- 37 microm) than did talc. There was no difference in the degree of pleural inflammation between the two groups at Day 7 (2.6 +/- 0.9 for TGF-beta2 versus 2.4 +/- 0.6 for talc) or at any other time points. In conclusion, the intrapleural administration of TGF-beta2 produced excellent pleurodesis in rabbits at a rate faster than talc slurry and all other pleurodesing agents investigated before. TGF-beta2 stimulated more collagen deposition without inducing excess inflammation when compared with talc slurry. TGF-beta2 may have advantages over talc slurry in the management of recurrent pleural effusion and pneumothorax.

Animals↗
PubMed2001

Relationship between pleural fluid and serum cholesterol levels.

INTRODUCTION: Since the criteria of Light and colleagues for differentiating transudates and exudates were described, other tests, including the pleural fluid (PF) cholesterol test, have been proposed for the same purpose. However, the factors influencing PF cholesterol levels have not been clearly delineated. PURPOSE: To analyze the relationships among total cholesterol (CHOL), low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides (TRIG) in serum (S) and PF. METHODS: PF and S from 99 patients (transudates, 13 patients; exudates, 86 patients) were analyzed for CHOL, HDL, LDL, TRIG, apolipoprotein AI, apolipoprotein B, and protein. The relationship between the PF and S level for each of these measurements was analyzed with linear regression and multiple regression using the ratio of PF to S protein for that measurement as a second independent variable. RESULTS: This study demonstrated that CHOL levels in PF are related to S cholesterol levels and to the permeability of the pleura (r = 0.88; p < 0.001). However, the percentage of CHOL associated with LDL and HDL (56%) in the PF was much lower than that associated with LDL and HDL in S (93%), suggesting that lipoproteins are modified once they enter the pleural space. The PF TRIG was not closely related to its S level or to the PF/S protein ratio (r = 0.49). CONCLUSION: PF cholesterol levels can be closely predicted from the S cholesterol levels and the permeability of the pleura, as reflected by the ratio of PF protein to S protein. Therefore, the CHOL ratio should not provide additional information to that provided by the protein ratio when trying to differentiate transudates from exudates. PF lipoproteins (LDL and HDL) undergo metabolic alterations once they enter the pleural space. PF TRIG levels are not closely related to S levels or to the permeability of the pleura.

Apolipoprotein A-I↗
PubMed2001

BAL neopterin : a novel marker for cell-mediated immunity in patients with pulmonary tuberculosis and lung cancer.

BACKGROUND: Neopterin is derived from guanosine triphosphate and is produced by stimulated macrophages under the influence of gamma-interferon of lymphocyte origin. It has been suggested that it is an excellent marker for the activation of the monocyte/macrophage axis in some clinical situations. However, to our knowledge, the relationship of BAL neopterin levels to disease states has not been studied. AIM: To assess the usefulness of BAL neopterin levels as an index of disease activity in patients with pulmonary tuberculosis and lung cancer. METHODS: BAL and serum neopterin levels were evaluated in 20 patients with pulmonary tuberculosis, 20 patients with bronchogenic carcinoma, and 10 healthy individuals. The concentration of neopterin was evaluated by radioimmunoassay technique. The BAL level of neopterin was standardized using the BAL urea level. RESULTS: The neopterin levels (mean +/- SD) in the BAL and serum of tuberculous patients (88.6 +/- 27.4 nmol/L epithelial lining fluid [ELF], 61.3 +/- 29.4 nmol/L, respectively) were significantly higher when compared with those in lung cancer patients (40.7 +/- 16.6 nmol/L ELF, 26.8 +/- 6.58 nmol/L, respectively, p < 0.001) and when compared with those in control subjects (26.3 +/- 11.3 nmol/L ELF, 6.8 +/- 2.7 nmol/L, respectively, p < 0.001). In the tuberculous group, BAL and serum neopterin levels in patients with far-advanced disease were significantly higher when compared with those in patients with moderately and minimally advanced diseases (p < 0.001). BAL and serum neopterin levels were significantly higher in patients with small cell carcinoma than in those with adenocarcinoma (p < 0.05). BAL neopterin levels were significantly (p < 0.001) higher than serum levels in all patients and control groups. In addition, there were significant positive correlations between BAL and serum neopterin levels in tuberculous (r = 0.92, p < 0.001), lung cancer (r = 0.62, p < 0.001), and control groups (r = 0.93, p < 0.001). CONCLUSIONS: The levels of neopterin in BAL fluid may reflect the degree of disease activity in pulmonary tuberculous patients. In addition, BAL neopterin levels are elevated in patients with lung cancer, especially the small-cell carcinoma type.

Adult↗