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PubMed2002

Diagnostic value of interleukin-1alpha, interleukin-6, and tumor necrosis factor in pleural effusions.

STUDY OBJECTIVES: Interleukin (IL)-1alpha, IL-6, and tumor necrosis factor (TNF)-alpha were measured in pleural fluid from 57 patients with pleural effusion in order to evaluate the diagnostic utility of these cytokines. We studied 20 patients with malignant pleural effusion, 11 patients with parapneumonic pleural effusion, 9 patients with tuberculous pleural effusion, and 17 patients with transudative pleural effusion. Cytokines were measured by radioimmunoassay. SETTING: University tertiary hospital. RESULTS: The mean values of the three cytokines measured in pleural fluid or in serum were significantly higher in patients with exudates than with transudates (p < 0.05). The ratio of IL-6 in pleural fluid to serum was significantly higher in exudates than in transudates (p < 0.05). The level of IL-6 in pleural fluid was significantly higher in tuberculous than malignant (p < 0.007) or parapneumonic pleural effusions (p < 0.04). No significant difference between the three types of exudates was found in pleural fluid levels of IL-1alpha or TNF-alpha. CONCLUSIONS: Serum levels of IL-1alpha, TNF-alpha, and in particular IL-6 can distinguish exudates from transudates, while pleural fluid IL-6 levels could be useful as an additional marker in the differential diagnosis of tuberculous, malignant, and parapneumonic exudates. Finally, our results suggest that there is local cytokine production in exudative pleural effusions.

Adult↗
PubMed1990

[Biochemical study of the pleural fluid in exudative pleurisy].

The authors relate the data on the importance of a biochemical analysis of the pleural fluid for the differential diagnosis of pleurisy and identification of the early signs of pleural fluid suppuration. For the purposes of the differential diagnosis between transudates and exudates measurements are made of the protein content and LDH activity in the pleural fluid. The exudate protein/serum protein and exudate LDH/serum LDH ratios are computed in necessary cases. The high prothrombin index (over 100%) and the level of lysozyme (over 25 (micrograms/ml) in the pleural fluid provide evidence in favour of the tuberculous etiology of pleurisy. The low level of glucose (under 2 mmol/l), high activity of LDH (over 6.2 mmol/l) and the negative ethanol test may point to the initial signs of exudate suppuration.

Algorithms↗
PubMed1984

Restriction of C1 hemolytic function by human proline-rich salivary proteins.

Acidic proline-rich salivary proteins, PRPI, PRPII, PRPIII, PRPIV, upper Db and Statherin, were isolated from parotid saliva and tested for interaction with complement. It was determined that each of the isolated proline-rich proteins blocked C1 hemolytic activity in assay systems where C1 was rate-limiting. Further studies comparing the specific activity of the proline-rich proteins to unfractionated parotid saliva indicated that other salivary substances (sensitive to urea treatment of parotid saliva) were also interacting with the first complement component but in a time-dependent manner. Based on a series of experiments examining the effect of the sequence of addition of the proline-rich proteins in the complement assay systems, it is postulated that these salivary proteins are able to block the proper interaction of C1 with EAC4 cells (sheep erythrocytes coated with antibody and C4gp). The proline-rich salivary proteins had no effect on C1 once C1 was bound to the immune complexes on the EAC4 cells. The C1 macromolecular complex undergoes conformational changes upon interaction with immune complexes resulting in a more avid binding of the C1q-Clr-Cls subunits with one another. Thus it is speculated that the EAC4-bound C1 becomes resistant to disruption by the proline-rich salivary proteins. Although the urea-sensitive factors had the highest specific C1-fixing activity, the activity of the acidic proline-rich proteins on C1 is important because of their relatively high concern in salivary secretions. Since complement-containing serous exudates and transudates are present on inflamed mucosal tissues, salivary substances which interact with C1 may play a role in regulating the initiation of the classical complement pathway, particularly at those mucosal sites where there is a high ratio of salivary secretion to serous exudate.

Chromatography, Gel↗
PubMed2003

Pharmacodynamics, chiral pharmacokinetics and PK-PD modelling of ketoprofen in the goat.

There have been few studies of the pharmacodynamics of nonsteroidal antiinflammatory drugs (NSAIDs) using PK-PD modelling, yet this approach offers the advantage of defining the whole concentration-effect relationship, as well as its time course and sensitivity. In this study, ketoprofen (KTP) was administered intravenously to goats as the racemate (3.0 mg/kg total dose) and as the single enantiomers, S(+) KTP and R(-) KTP (1.5 mg/kg of each). The pharmacokinetics and pharmacodynamics of KTP were investigated using a tissue cage model of acute inflammation. The pharmacokinetics of both KTP enantiomers was characterized by rapid clearance, short mean residence time (MRT) and low volume of distribution. The penetration of R(-) KTP into inflamed (exudate) and noninflamed (transudate) tissue cage fluids was delayed but area under the curve values were only slightly less than those in plasma, whereas MRT was much longer. The S(+) enantiomer of KTP penetrated less readily into exudate and transudate. Unidirectional inversion of R(-) to S(+) KTP occurred. Both rac-KTP and the separate enantiomers produced marked inhibition of serum thromboxane B2 (TxB2) synthesis (ex vivo) and moderate inhibition of exudate prostaglandin E2 (PGE2) synthesis (in vivo); pharmacodynamic variables for S(+) KTP were Emax (%) = 94 and 100; IC50 (microg/mL) = 0.0033 and 0.0030; N = 0.45 and 0.58, respectively, where Emax is the maximal effect, IC50 the plasma drug concentration producing 50% of Emax and N the slope of log concentration/effect relationship. The IC50 ratio, serum TxB2:exudate PGE2 was 1.10. Neither rac-KTP nor the individual enantiomers suppressed skin temperature rise at, or leucocyte infiltration into, the site of acute inflammation. These data illustrate for KTP shallow concentration-response relationships, probable nonselectivity of KTP for cyclooxygenase (COX)-1 and COX-2 inhibition and lack of measurable effect on components of inflammation.

Animals↗
PubMed1998

Clara cell protein (CC16) in pleural fluids: a marker of leakage through the visceral pleura.

Pleural fluid (PF) proteins either derive from serum by diffusion or are locally secreted within the pleural space. Another hypothetical origin is a leakage of lung secretory proteins across the visceral pleura. To test this hypothesis, we investigated the occurrence, sources, and determinants in PF of CC16, a small-size and readily diffusible protein of 16 kDa secreted by bronchiolar Clara cells. CC16 concentration was determined by a sensitive latex immunoassay in serum and PF of 117 subjects (86 exudates and 31 transudates) and, for purpose of comparison, in ascites samples from another group of 38 subjects (7 exudates and 31 transudates). CC16 was also studied in serum and PF of normal rats and in rats with pleural exudate induced by alpha-naphthyl-thiourea (ANTU). The levels of CC16 in PF and ascites were highly correlated with that in serum, suggesting a diffusional exchange across the pleural/blood and peritoneal/blood barriers. Whereas CC16 occurs at similar levels in ascites and serum, the protein was found to be more concentrated in PF than in serum in both humans (geometric mean in microg/L, 26.2 versus 14.6, p < 0.0001) and rats (213 versus 16.2, p < 0.001). A local synthesis of CC16 appeared unlikely in view of the lack of CC16-immunostaining in pleura of both species. The only plausible explanation for these findings is that CC16 in PF originates from two sources: diffusion from plasma and a leakage from the lung into the pleural space across the semipermeable visceral pleura. This interpretation is supported by a markedly increased leakage of CC16 in experimental exudates induced by ANTU and the finding of high CC16 concentrations in human transudates associated with congestive heart failure, two conditions wherein PF has been shown to arise from the interstitial spaces of the lung.

Aged↗
PubMedDate not supplied

Interleukin-6 and its relationships to acute phase proteins in serous effusion differentiation.

The aim of the study was to assess the discriminative power of cytokine interleukin 6 (IL-6) between transudative and exudative pleural and peritoneal effusions, and to compare IL-6 with common acute phase proteins in serous effusion differentiation. One hundred and forty-five consecutive patients with pleural or peritoneal effusion underwent diagnostic parecentesis. Patients were categorized in three groups. Malignant effusion (group A) 56 patients, non-malignant effusion (group B) 46 patients and transudate (group C) 43 patients. Serum and effusion levels of IL-6, C-reactive protein (CRP), alpha2-macroglobuline (alpha2-MG), alpha1-antitrypsin (alpha1-AT) and alpha1-acid glycoprotein (alpha1-AG) were determined. Serum IL-6 levels were significantly higher in groups A and B in comparison to group C (p<0.001 and 0.001, respectively). In addition, serum IL-6 levels were higher in group A compared to group B (p<0.001), while the studied acute phase proteins were not significantly different. All the studied parameters were higher in the effusions of groups A and B compared to group C. At a cut-off value of 72.1 fmol/ml IL-6 had a sensitivity of 82.6-89.3%, specificity of 88.4-90.7% and positive predictive value of 90.7-94.6% among the three groups. Our results suggest that IL-6 at levels > or =72.1 fmol/ml, alpha1-AT at > or =170 mg/dl and alpha1-AG at > or =52.3 mg/ml give strong evidences for malignancy in exudates.

Acute-Phase Proteins↗
PubMed2001

Biochemical analysis of pleural fluid: what should we measure?

Biochemical examination of pleural fluid is usually done to try to identify the cause of a pleural effusion. The various analytes that have been suggested for this are reviewed and evaluated. Distinguishing whether the effusion is an exudate or transudate is a pragmatic first step. with further investigations dictated by the clinical features and these results. Total protein and lactate dehydrogenase were used first; Light's criteria were published in 1972 and since then additional markers including cholesterol, bilirubin and albumin gradient plus combinations of these have been proposed. Although combination testing does improve the sensitivity for diagnosis of an exudate. this is at the expense of specificity. Measurement of fluid to serum ratios appears to confer no advantage, and if a single test is required total protein performs as well as any. Additional tests may be useful in specific circumstances: pleural fluid pH may aid decisions over drainage of a parapneumonic effusion; glucose may indicate an effusion associated with rheumatoid arthritis; and adenosine deaminase may help with the diagnosis of tuberculous effusions.

Bilirubin↗
PubMed1998

Cytology of 100 samples of abdominal fluid from 100 horses with abdominal disease.

A total of 100 samples of abdominal fluid (AF) from 100 horses with abdominal disease were evaluated by cytology. Cytology results were subsequently correlated with the final outcome of the disease. The horses were classified into 4 groups: Group I, horses that were treated with conventional (nonsurgical) therapy and recovered; Group II, horses that had surgery and survived; Group III, horses that had surgery but died; and Group IV, horses that were subjected to euthanasia prior to surgery. Statistical analysis showed that both nucleated cell count and total neutrophils were significantly higher in Group III than in Group I; and that the total mesothelial cells were significantly higher in Group III than in Groups I and II. No significant differences were found for erythrocyte counts and fluid total protein levels among the 4 groups. The findings suggest that classifying AF as transudate, modified transudate and exudate, as well as grading of inflammation as mild, moderate and severe on the basis of nucleated cell count (NCC) and fluid total protein (AFTP) can be greatly misleading. Differential identification of the nucleated cells was found to be far more reliable than the NCC alone, with or without the AFTP, and rendered valuable information, which overruled many times a diagnosis of transudate or modified transudate. Bands, metamyelocytes, toxic changes, plasma cells, and neutrophils penetrating rafts or fronds of mesothelial cells, supported a diagnosis of inflammation, even when the NCC, and the AFTP (interpreted according to currently accepted values) suggested otherwise. Several morphological features were found, including some cell types for which little or no mention was found at all in 22 major studies of this fluid in horses. Among these were 'reddish neutrophils', large granular lymphocytes (LGL), plasma cells, Mott cells, blasts, and a unique hitherto undescribed granular mesothelial cell.

Animals↗
PubMed1977

Pleural effusions.

Many different conditions result in the accumulation of pleural fluid. A diagnostic thoracentesis should be performed on all patients with pleural effusion from whom pleural fluid can be easily obtained. Empirically we have found that when the pleural effusion is more than 10 mm thick on the lateral decubitus roentgenogram, pleural fluid is easily obtained. At least 30 cc fluid should be obtained and distributed to the various laboratories as outlined in Table 2. The results of these tests will show whether the fluid is a transudate or an exudate. If the fluid is a transudate, no further diagnostic procedures need be directed towards the pleura. If the fluid is an exudate, the diagnosis will frequently be made by these original tests and therapy for the pleural disease can be instituted. If the diagnosis has not been made, the results of these tests should lead to a rational diagnostic attack.

Amylases↗
PubMed2001

Pharmacodynamics and pharmacokinetics of ketoprofen enantiomers in sheep.

OBJECTIVE: To establish pharmacokinetic and pharmacodynamic properties of a racemic mixture and individual R(-) and S(+) enantiomeric forms of ketoprofen (KTP) in sheep and determine pharmacodynamic variables of KTP by pharmacokinetic-pharmacodynamic modeling. ANIMALS: 8 female Dorset crossbred sheep. PROCEDURE: A tissue cage model of inflammation was used. Carrageenan was administered into tissue cages. Time course of cyclooxygenase (COX)-2 inhibition was determined in vivo by measurement of exudate prostaglandin E2 (PGE2) concentrations. Time course of COX-1 inhibition was determined ex vivo by measurement of serum thromboxane B2 (TXB2) concentrations. In addition, plasma concentration-time course and penetration of KTP enantiomers into inflammatory exudate and transudate (noninflamed tissue cage fluid) were investigated. Four treatments were compared: placebo, racemic mixture (rac-KTP [3 mg/kg of body weight, IV]), S(+) KTP (1.5 mg/kg, IV),and R(-) KTP (1.5 mg/kg, IV). RESULTS: Both KTP enantiomers had elimination half-life and mean residence time measurements that were short and volume of the central compartment and steady state volume of distribution that were low. Clearance was rapid, particularly for R(-) KTP Elimination of both enantiomers from exudate was > 10 times slower than from plasma. Both rac-KTP and the individual enantiomers significantly inhibited serum TXB2 concentrations for 12 hours. Rac-KTP and S(+) KTP, but not R(-) KTP, also significantly inhibited PGE2 synthesis in exudate for 12 hours. CONCLUSIONS AND CLINICAL RELEVANCE: Inhibition of serum TXB2 concentration and exudate PGE2 synthesis for similar time courses after S(+) KTP administration indicates that it is a nonselective inhibitor of COX in sheep.

Animals↗
PubMed1986

Pleural effusions. 2. Definitive evaluation of the exudate.

Based on the current literature, the following steps seem reasonable in evaluating a pleural effusion: document the presence, location, and approximate volume of pleural fluid; decide clinically on the likelihood of an exudative effusion; if clinical evaluation suggests an exudative effusion, perform a thoracentesis and obtain fluid for diagnostic evaluation; perform the necessary tests to characterize the effusion as a transudate or an exudate; if a transudate exists, normally do not perform further tests on the effusion; if an exudate exists, perform selected tests to narrow the differential diagnosis; if this evaluation is undiagnostic, consider closed pleural biopsy; if the diagnosis remains unclear after two closed biopsies, consider pleuroscopy with biopsy or open pleural biopsy at the time of a thoracotomy.

Amylases↗
PubMed1995

Pharmacokinetics and pharmacodynamics of ketoprofen in calves applying PK/PD modelling.

The pharmacokinetics (PK) and pharmacodynamics (PD) of ketoprofen (KTP) were studied in calves following intravenous administration of the drug racemate at a dose rate of 3 mg/kg. To evaluate the anti-inflammatory properties of KTP, a model of acute inflammation, consisting of surgically implanted subcutaneous tissue cages stimulated by intracaveal injection of carrageenan, was used. No differences were observed between disposition curves of KTP enantiomers in plasma, exudate or transudate. This indicates that in calves KTP pharmacokinetics is not enantioselective. S(+)- and R(-)- KTP each had a short elimination half-life (t1/2 beta) of 0.42 +/- 0.08 h and 0.42 +/- 0.09 h, respectively. The volume of distribution (Vd) was low, values of 0.20 +/- 0.06 L/kg and 0.22 +/- 0.06 L/kg being obtained for R(-) and S(+)KTP, respectively. Body clearance (ClB) was high, correlating with the short elimination half-life, 0.33 +/- 0.03 L/kg/h [R(-)KTP] and 0.32 +/- 0.04 L/kg/h [S(+)-KTP]. KTP pharmacodynamics was evaluated by determining the effects on serum thromboxane (TxB2), exudate prostaglandin (PGE2), leukotriene (LTB4) and beta-glucuronidase (beta-glu) and bradykinin (BK)-induced oedematous swelling. Effect-concentration inter-relationships were analysed by PK/PD modelling. KTP did not affect exudate LTB4, but inhibition of the other variables was statistically significant. The mean EC50 values for inhibition of serum TxB2, exudate PGE2 and beta-glu and BK-induced swelling were 0.118, 0.086, 0.06 and 0.00029 microgram/mL, respectively. These data indicate that KTP exerted an inhibitory action, not only as expected, on eicosanoid (TxB2 and PGE2) synthesis but also on exudate beta-glu and BK-induced oedema. The EC50 values for these actions indicate that they are likely to contribute to the overall anti-inflammatory effects of KTP in calves. However, claims that KTP inhibits 5-lipoxygenase and thereby blocks the production of inflammatory mediators such as LTB4 were not substantiated. PK/PD modelling has proved to be a useful tool for analysing the in vivo pharmacodynamics of KTP and for providing new approaches to elucidating its mechanism(s) of action.

Animals↗
PubMed1999

[Clinical thinking and decision-making in practice. A child with dyspnea and excess pleural fluid].

Pleural fluid was diagnosed on an X-ray in a 9-month-old boy with acute dyspnoea without fever. Thoracentesis showed exudate and the patient was diagnosed as having empyema and was treated with continuous chest tube drainage and antibiotics. The culture of the pleural fluid was negative. A month after discharge the boy developed recurrent pleural effusion with dyspnoea. A mass in the right hemithorax was found upon additional diagnostic evaluation. Microscopic evaluation of tumour biopsy specimen showed a malignancy. Infantile fibromatosis was diagnosed in a surgical specimen. The patient died after having developed a recurrent tumour. Infectious causes are not likely in a child with pleural fluid without fever. Pleural fluid has to be analysed in transudate or exudate. Exudate requires a complete diagnostic evaluation.

Anti-Bacterial Agents↗
PubMed1997

MMP and TIMP expression pattern in pleural effusions of different origins.

The matrix metalloproteinases (MMP) are proteolytic enzymes that are essentially involved in the turnover of the extracellular matrix (ECM). Their activity is counterbalanced by specific antagonists, the tissue inhibitors of metalloproteinases (TIMP). In this study, we sought to analyze the expression of MMP and TIMP isoforms in pleural effusions from 88 patients. We compared MMP and TIMP isoform expression in transudates (n = 21) and exudates (n = 67), the latter divided into exudates of paraneoplastic (n = 46) or parainfectious (n = 21) origin. Zymographic and Western blot analyses revealed constant expression of interstitial collagenase (MMP-1), gelatinase-A (MMP-2), and TIMP-1 in all 88 samples. In contrast, analyses of gelatinase-B (MMP-9) demonstrated a specific expression pattern, with high expression in exudates and lack of expression in transudates. Neutrophil collagenase (MMP-8) was detected in trace amounts, and correlated with the number of neutrophils in the effusion. Low levels of TIMP-2 were detected only in exudates and not in transudates. Quantitative analysis of the expression ratio of gelatinase-B to gelatinase-A revealed statistically significant differences between effusions of different origin. The ratio was highest in exudates of paraneoplastic origin and lowest in transudates. Our data thus suggest that interstitial collagenase, gelatinase-A, and TIMP-1 play a role in homeostasis of the pleural space in vivo as constitutively expressed proteins, whereas gelatinase-B and TIMP-2 expression are induced in specific disease states. These observations contribute to the understanding of the pathophysiology of pleural effusions, and may help to characterize and possibly distinguish effusions of different origin.

Adult↗
PubMed2001

Assaying of tumor necrosis factor alpha, complement factors, and alpha-1-antitrypsin in the diagnosis of malignant serous effusions.

The objective of this study was to measure the concentrations of tumor necrosis factor-alpha (TNFalpha) in pleural and peritoneal effusions of different causes and to verify whether TNFalpha, alpha-1-antitrypsin (alpha1AT), and complement factors C3 and C4 can be used in the differential diagnosis of serous effusion. One hundred forty-five serous effusions of various origins were analyzed. TNFalpha, alpha1AT, and complement factors C3 and C4 concentrations were measured simultaneously in blood and serous effusion using commercially available methods. Serous effusions were classified as follows: 102 exudates and 43 transudates. All variables were found to have good diagnostic value in the differential diagnosis of serous effusion. In the stepwise discriminant analysis, four variables were selected, producing a significant discriminant function (p < 0.001). Their order of selection was alpha1AT effusion, C4 serum, TNFalpha-effusion, and C3 effusion. Combined use of these variables increased remarkably the diagnostic value (in diagnosing exudates versus transudates) giving sensitivity = 93.14%; specificity = 90.70%; positive predictive value = 95.96%; negative predictive value = 84.78%. Determination of TNFalpha, complement factors C3 and C4, and alpha1AT may be a significant parameter in the differential diagnosis of serous effusions, particularly in those patients with malignant disease. Moreover, the combination of them significantly increased their diagnostic power.

Ascitic Fluid↗
PubMed1995

Validation of the determination of the activity of adenosine deaminase in the body effusions of cats.

In order to identify parameters differentiating exudative from transudative effusions, it was postulated that the activity of adenosine deaminase (AD) (EC 3.5.4.4) might be highly correlated with granulomatous inflammatory processes of the serosa, and the activity of the enzyme in body effusions and serum from cats was examined. The method of Slaats et al (1985) for the determination of the enzyme was evaluated by using an Hitachi 705 autoanalyser, and its activity was measured in body cavity effusions of 174 cats. The activity of AD was high in effusions from cats with infectious serositis and bacterial or feline infectious peritonitis (FIP). In cases of FIP the activity of AD was very significantly different from all other cases of thoracic (P = 0.004) and abdominal (P < 0.0001) effusions. The determination of AD in the serum of cats did not contribute to the aetiological differentiation of hydrops. The increases in the activity of AD appeared to originate from the body effusion, because the ratio of the activity of the enzyme in the effusion to its activity in serum was relatively high in cases of FIP.

Adenosine Deaminase↗
PubMed2003

Cytology and fluid analysis of the acute abdomen.

In patients with acute abdominal pain, abdominal paracentesis and diagnostic peritoneal lavage often yield fluid samples for cytologic and biochemical evaluation. Cytology of the effusion from a patient with acute abdominal disease can be a crucial tool for the rapid diagnosis necessary for initiation of timely and appropriate therapy. Appropriate sample collection, handling, and preparation are essential to obtain an accurate diagnosis. Analysis of the fluid sample should include gross examination of the effusion, measurement of total nucleated cell count, packed red blood cell volume, and protein concentration, as well as examination for the presence of other cells, bacteria, food particles, or plant material. Biochemical evaluation should proceed based on the clinician's index of suspicion for a particular disease process. Abdominal effusions are generally classified as transudate, modified transudate, or exudate, depending on the total nucleated cell count and protein concentration. Cytology of all fluids collected should be performed systematically, utilizing progressively higher magnifications with a microscope. Specific diseases with associated abdominal effusions include septic peritonitis, nonseptic peritonitis, hemoabdomen, uroabdomen, pancreatitis, bile peritonitis, chylous effusion, and neoplasia. A complete description of sample preparation and evaluation is reviewed.

Abdomen, Acute↗