Respiration

Download Fulltext PDF

Clinical Investigations

Free Access

The Prevalence and Diagnostic Significance of Eosinophilic Pleural Effusions: A Meta-Analysis and Systematic Review

Oba Y. · Abu-Salah T.

Author affiliations

University of Missouri, Columbia, Mo., USA

Corresponding Author

Yuji Oba, MD

University of Missouri

1 Hospital Drive

Columbia, MO 65212 (USA)

Tel. +1 573 882 8583, E-Mail obay@health.missouri.edu

Keywords: Pleural fluidPleural fluid eosinophilia

Related Articles for ""
Respiration 2012;83:198-208
https://doi.org/10.1159/000327200

Abstract

Background: Eosinophilic pleural effusion (EPE) is defined by an eosinophil count of ≧10% in the pleural fluid and often caused by air or blood in the pleural space. The diagnostic significance of EPEs is still a matter of debate. Objective: The objective of this study was to systematically review the medical literature to evaluate the diagnostic significance of EPEs. Methods: Electronic databases were searched from 1950 to April 2010 to perform a meta-analysis. Data were extracted using standardized forms, and pooled odds ratios with 95% confidence intervals were calculated. A logistic regression analysis was also performed to evaluate the association between the pleural eosinophil counts and the likelihood of underlying causes of EPEs. Results: We identified a total of 687 cases of EPE. The most common cause of EPEs was malignancy (26%) followed by idiopathic (25%) and parapneumonic (13%) effusions. The likelihood of malignancy or tuberculosis was somehow lower in EPEs than in non-EPEs, but the differences were not statistically significant. The prevalence of malignancy was significantly lower in the group of patients that required a pathologic confirmation (21 vs. 30%; p = 0.01). The likelihood of malignancy was inversely correlated with the pleural fluid eosinophil counts. The likelihood of idiopathic effusion was significantly higher in EPEs than in non-EPEs. Conclusions: Malignancy was the most common cause of EPEs. EPEs appeared to be a negative predictor of malignancy when a pleural fluid eosinophil count was extremely high. EPEs were more likely to be idiopathic as compared with non-EPEs.

© 2011 S. Karger AG, Basel

Introduction

Eosinophilic pleural effusion (EPE) is defined by an eosinophil count of ≥10% in the pleural fluid and accounts for approximately 10% of exudative pleural effusions [1]. The pathogenesis of EPEs is poorly understood and likely multifactorial. Animal and human studies suggest an important role of interleukin-5 in their pathogenetic pathways [2,3].

The causes of EPEs include but are not limited to the presence of air or blood in the pleural space, malignancy, infections (bacteria, fungi, mycobacteria, parasites and viruses), pulmonary embolism, drug reactions and asbestos exposure.

The diagnostic significance of EPEs is still a matter of debate. It was once believed that malignancy or tuberculosis was an unlike cause of EPEs [4], but recent studies argued against such a notion [5,6]. A possible explanation for such disparity was that the study population was different in each study and the varying disease spectrum of EPEs was just a reflection of the population studied.

Therefore, we hypothesized that the disease spectrum of EPEs was not different from that of non-EPEs. The objective of this study was to systematically review the medical literature to evaluate the diagnostic significance of EPEs.

Materials and Methods

Search Strategy

Two authors independently searched the National Library of Medicine's Medline database for studies in the English language published from 1950 to April 2010 by using the following headings and keywords of the Medical Subject Headings: pleural effusion or pleurisy or pleura AND eosinophils or eosinophilia. We searched the Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, Database of Abstracts of Reviews of Effects, Biologic Abstracts and Cumulative Index to Nursing and Allied Health Literature. All searches were restricted to human studies including only adults (≥19 years). Bibliographies of all selected articles and review articles that included information on EPEs were reviewed for other relevant articles.

Study Selection

Studies relevant to the prevalence and diagnostic significance of EPEs were included if the following criteria were met: (1) if at least more than 5 of the original cases of EPE, which is defined by an eosinophil count of ≥10% in the pleural fluid, were reported; (2) a clinical study with the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) score [7] of at least 5; (3) if the etiology of EPEs was described in all patients. The results from a study that used a different cutoff point (e.g., an eosinophil count of ≥5%) were modified using the 10% cutoff and included in the analysis.

Assessment of Study Quality

The quality of included studies was assessed with the STROBE criteria. Each study was given a score on a scale from 1 to 22, reflecting how many of the 22 STROBE items were complied with (with each item being given equal weighting). This score was termed ‘STROBE score'.

Data Extraction

The etiology of EPEs was classified into the following categories: malignancy, parapneumonic effusion, tuberculosis, pulmonary embolism, transudate (congestive heart failure, kidney disease and hepatic cirrhosis), collagen vascular disease (CVD), idiopathic effusion, pleural air/blood (hemothorax, post-trauma, thoracotomy, pneumothorax and previous thoracentesis), and others. Diagnostic criteria for the above disorders were extracted from the included studies and tabulated. Cases were reclassified as pleural air/blood, whenever possible, if EPE was found only on repeated thoracentesis or was associated with chest trauma or pneumothorax.

We performed a separate analysis examining the correlation between pleural fluid eosinophil counts and the likelihood of underlying causes of EPEs. We extracted cases of EPE from the medical literature in which a pleural fluid eosinophil count and an underlying etiology were individually reported.

Statistical Analysis

The pooled prevalence of EPEs among all pleural effusions was calculated from included studies, and it was reported along with its 95% confidence interval (CI). We examined the change in the prevalence of underlying causes over time using a cumulative meta-analysis [8]. Studies were sequentially added by year of publication to a random-effects model after excluding cases associated with pleural air/blood.

To determine the diagnostic significance of EPEs, the pooled prevalence of underlying causes of EPEs was calculated and compared with that of non-EPEs. The calculations were performed after excluding the cases of transudate and pleural air/blood. The results were expressed as odds ratios (ORs) along with their 95% CIs.

A Z test was performed to examine the overall effect. We tested heterogeneity between trials with I2 statistic, with I2 >50% indicating significant heterogeneity [9]. A random-effects model was used for the meta-analysis if significant heterogeneity was detected. A fixed effects model was used otherwise [10].

Sensitivity analyses were performed to assure the robustness of the results by excluding studies individually from the pooled analyses and using a random- or fixed-effects model, relative risks and risk differences [11].

A logistic regression analysis was performed to examine the correlation between pleural fluid eosinophil counts and the probability of underlying causes of EPEs. A receiver operator characteristic curve was constructed to summarize the sensitivity and specificity estimates. The standard χ2 test was used for the comparison of 2 data points. All reported p values are 2-sided. p values <0.05 were considered to indicate statistical significance. The data analysis was performed using meta-analysis software (StatsDirect, StatsDirect Ltd., Cheshire, UK).

Results

Studies and Cases Identified

The electronic database searches identified 411 citations. Initially, 30 studies were considered potentially relevant. After a more detailed review, an additional 15 papers did not meet the inclusion criteria and were excluded. The remaining 15 studies were reviewed [1,5,6,12,13,14,15,16,17,18,19,20,21,22,23] for duplicate publications. We did not find any duplicate publications. A non-electronic search identified 2 studies that met our inclusion criteria [24,25]. We included a total of 17 studies in our analysis (fig. 1).

Fig. 1

Flow of study selection.

http://www.karger.com/WebMaterial/ShowPic/209532

The characteristics of included studies are shown in table 1. Six hundred and ninety-two cases of EPE were extracted. Five cases, reported by Mihailescu and Micu [15], with a pleural fluid eosinophil count >5 but <10% were excluded. Then, a total of 687 cases were included in our analysis.

Table 1

Characteristics of included studies

http://www.karger.com/WebMaterial/ShowPic/209536

Eight studies reported the cases of EPE with the first thoracentesis only [5,6,14,18,19,20,23,25]. Cases of EPE on repeated thoracentesis were reclassified as pleural air/blood whenever possible. However, this reclassification was not possible in 4 studies because of lack of information [1,13,15,22].

The prevalence of EPEs in all pleural effusions was reported in 12 studies [5,13,14,15,16,17,18,19,20,22,23,24]. The pooled prevalence of EPEs was 9% (random-effects model, 95% CI 7-10). The mean age of patients (56 years, range 48-63) was reported in 6 studies [14,19,20,21,22,23]. The proportion of male patients (71%, range 45-100) was reported in 9 studies [6,12,13,14,20,21,22,23]. The mean pleural fluid eosinophil count (27%, range 21-40) was reported in 12 studies [12,14,15,16,17,18,19,20,21,22,23,24] .

The quality of included studies was variable and their quality score ranged from 5 to 17 with a median score of 13 (the maximum possible score was 22) (table 1, Appendix 1). The diagnostic criteria used in the included studies for the underlying causes of EPEs are summarized in table 2.

Table 2

Diagnostic criteria used in the included studies

http://www.karger.com/WebMaterial/ShowPic/209535

The most common cause of EPEs was malignancy (26%) followed by idiopathic (25%) and parapneumonic (13%) effusions, pleural air/blood (13%), tuberculosis (7%), transudate (7%), other (6%) and CVD (3%) (table 3). Three studies excluded cases of EPE resulting from pleural air/blood [5,18,19]. The pooled prevalence of EPEs associated with pleural air/blood was 15% when these studies were excluded. When cases of pleural air/blood were excluded from all studies, the prevalence of malignancy, idiopathic and parapneumonic effusions, tuberculosis, transudate, others and CVD was 30, 29, 14, 8, 7, 4 and 4%, respectively.

Table 3

Etiology of EPEs

http://www.karger.com/WebMaterial/ShowPic/209534

Eight studies reported the underlying causes of non-EPEs and EPEs. A total of 1,810 and 184 patients with non-EPE and EPE were reported in these studies, respectively. Cases associated with a transudate and pleural air/blood consisted of 17 and 0.2% of non-EPEs and 5 and 0.5% of EPEs, respectively. The prevalence of individual causes in non-EPEs and EPEs is shown in table 4.

Table 4

Comparison of disease spectrum between EPEs and non-EPEs

http://www.karger.com/WebMaterial/ShowPic/209533

We identified 144 cases of EPE in which an underlying cause and a pleural fluid eosinophil count were individually reported [15,17,18,24,26,27,28,29]. They consisted of 22 cases of malignancy (15%), 27 cases of parapneumonic effusion (19%), 19 cases of tuberculosis (13%), 7 cases of pulmonary embolism (5%), 6 cases of CVD (4%), 4 cases of transudate (3%), 11 cases of other causes (8%), 10 cases of pleural air/blood (7%) and 38 cases of idiopathic pleural fluid (26%). The mean ± standard deviation of the eosinophil count was 37 ± 21%.

Malignancy

The cumulative prevalence of malignancy among EPEs has gradually increased over the last 4 decades from 7% (95% CI -7 to 21) to 25% (95% CI 17-33) (fig. 2). The diagnosis of malignancy required a pathological confirmation in some studies but not in others (table 3). The prevalence of malignancy was significantly lower in the group of patients that required a pathologic confirmation (21 vs. 30%; p = 0.01).

Fig. 2

Cumulative prevalence of malignancy in cases with EPEs. Each later estimate is a pooled estimate of all previous studies. Data are ORs, with confidence limits in parentheses.

http://www.karger.com/WebMaterial/ShowPic/209531

Eight studies reported the prevalence of malignant pleural effusions in EPEs and non-EPEs [5,14,15,17,18,19]. The prevalence of malignancy was lower in EPEs than in non-EPEs except in 1 study [19] (fig. 3). The odds of malignancy in EPEs, as compared with non-EPEs, was 0.63 (95% CI 0.28-1.47; p = 0.29). The odds ratio (OR) became statistically significant when a study by Riantawan et al. [19] was excluded from the analysis (OR 0.51, 95% CI 0.32-0.78; p = 0.001).

Fig. 3

OR meta-analysis plot (random-effects model). Pooled OR for malignancy in EPEs as compared with non-EPEs. Test for heterogeneity: χ2 = 1.12 (d.f. = 1); I2 = 74.4%. Data are ORs, with confidence limits in parentheses.

http://www.karger.com/WebMaterial/ShowPic/209530

The logistic regression analysis revealed a significant correlation between the pleural fluid eosinophil counts and the likelihood of malignancy among EPEs with an area under the receiver operator characteristic curve of 0.71. The likelihood of malignancy was inversely correlated with the pleural eosinophil counts, as shown in figure 4.

Fig. 4

Correlation between the probability of malignancy and pleural fluid eosinophil counts in 144 cases with EPE.

http://www.karger.com/WebMaterial/ShowPic/209529

The estimated probability of malignancy for a particular patient with EPE was equal to y = 1/(1 + e-z), where z = -0.345953 - 0.043784 · (pleural eosinophil count), and e is the mathematical constant and base value of natural logarithms: p > ∣z∣ = 0.01 (95% CI -0.77 to -0.01). The odds of malignancy for every 1% increase in pleural eosinophil count were 0.96 (95% CI 0.91-0.99).

Based on the receiver operating characteristic curve, the highest accuracy (maximum sensitivity and specificity) was achieved when a cutoff of pleural fluid eosinophil count was 32%. The probability of malignancy was only 7% when a pleural fluid eosinophil count was ≥32%. Using this cutoff, the sensitivity, specificity and positive and negative predictive values were 77, 56, 24 and 93%, respectively.

Tuberculosis

The cumulative prevalence of tuberculosis in EPEs has been relatively stable for the last 4 decades and stayed at around 7% (fig. 5). The odds of tuberculosis in EPEs, as compared with non-EPEs, was 0.29 (95% CI 0.07-1.09; p = 0.07) (fig. 6). The OR became statistically significant when the study by Mihailescu and Micu [15] (OR 0.20, 95% CI 0.06-0.70; p < 0.05) or Kuhn et al. [17] (OR 0.22, 95% CI 0.06-0.84; p < 0.05) was excluded from the analysis. The logistic regression analysis failed to show a significant correlation between the pleural fluid eosinophil counts and the likelihood of tuberculosis among EPEs (OR 1.01, 95% CI 0.99-1.03; p = 0.42).

Fig. 5

Cumulative prevalence of tuberculosis in cases with EPEs. Each later estimate is a pooled estimate of all previous studies. Data are ORs, with confidence limits in parentheses.

http://www.karger.com/WebMaterial/ShowPic/209528

Fig. 6

OR meta-analysis plot (random-effects model). Pooled OR for tuberculosis in EPEs as compared with non-EPEs. Test for heterogeneity: χ2 = 3.35 (d.f. = 1); I2 = 73.9%. Data are ORs, with confidence limits in parentheses.

http://www.karger.com/WebMaterial/ShowPic/209527

Parapneumonic Effusion and Pulmonary Embolism

The prevalence of parapneumonic effusion or pulmonary embolism was not statistically different in EPEs as compared with non-EPEs (OR 1.27, fixed-effects model, 95% CI 0.83-1.95, p = 0.32; OR 2.02, fixed-effects model, 95% CI 0.57-7.22, p = 0.49, respectively). The result was unchanged when the included studies were removed individually or analyzed using a random-effects model, relative risk and risk difference. There was no significant association between the pleural fluid eosinophil counts and the likelihood of parapneumonic effusion or pulmonary embolism (p = 0.78 and 0.20, respectively).

Collagen Vascular Disease

Six studies reported the prevalence of CVD-associated pleural effusions in non-EPEs and EPEs [5,14,17,18,19,24]. The prevalence of CVD-associated pleural effusions was significantly higher in EPEs compared with non-EPEs (OR 2.84, fixed-effects model, 95% CI 1.28-6.31; p = 0.02) (fig. 7). The result was unchanged when the included studies were analyzed using a random-effects model, relative risk and risk difference. However, the OR became statistically non-significant when the study by Pettersson and Riska [14] was excluded from the analysis (OR 2.18, 95% CI 0.61-7.76; p = 0.41). There was no significant association between the pleural fluid eosinophil counts and the likelihood of CVD-associated pleural effusion (p = 0.06).

Fig. 7

OR meta-analysis plot (fixed-effects model). Pooled OR for CVD-associated pleural effusion in EPEs as compared with non-EPEs. Test for heterogeneity: χ2 = 5.61; I2 = 0%. Data are ORs, with confidence limits in parentheses.

http://www.karger.com/WebMaterial/ShowPic/209526

Idiopathic Pleural Effusion

The duration of follow-up to confirm the diagnosis of idiopathic effusions varied. Five studies described the duration of follow-up, but the rest of the studies did not (table 2). The prevalence of idiopathic pleural effusions was significantly lower in the studies that reported certain duration of follow-up (23 vs. 32%; p = 0.03).

The prevalence of idiopathic pleural effusions was significantly higher in EPEs than in non-EPEs (OR 3.20, 95% CI 1.60-6.39; p = 0.001) (fig. 8). The result was unchanged when the included studies were removed individually or analyzed using a fixed-effects model, relative risk and risk difference. There was no significant association between the pleural fluid eosinophil counts and the likelihood of idiopathic pleural effusion (p = 0.96).

Fig. 8

OR meta-analysis plot (random-effects model). Pooled OR for identical pleural effusion in EPEs as compared with non-EPEs. Test for heterogeneity: χ2 = 10.8 (d.f. = 1); I2 = 58.7%. Data are ORs, with confidence limits in parentheses.

http://www.karger.com/WebMaterial/ShowPic/209525

Other Causes

Other causes of EPEs were as follows: gastrointestinal diseases in 12 (pancreatic diseases, subdiaphragmatic abscess/inflammation), cardiovascular diseases in 5 (myocardial infarction, postcardiac injury syndrome, aortic aneurysm), eosinophilic lung diseases in 5, parasitic infections in 3 (strongyloides, paragonimiasis, hydatid cyst), occupational lung diseases in 2 (benign asbestos effusion, byssinosis), ‘serositis' in 2, atelectasis in 2, ‘hypersensitivity state' in 1, viral pleuritis in 1, actinomycosis in 1, radiation therapy in 1, and Gorham's disease in 1 case. The etiology was not specified in 4 cases which were classified as ‘other' in 1 study [1]. The prevalence of pleural effusions resulting from other causes was not statistically different in EPEs as compared with non-EPEs (OR 1.56, fixed-effects model, 95% CI 0.71-3.47; p = 0.37). The result was unchanged when the included studies were removed individually or analyzed using a random-effects model, relative risk and risk difference.

Discussion

Our systematic review of the medical literature identified a total of 687 cases of EPE. The most common cause of EPE was malignancy (26%) followed by idiopathic (25%) and parapneumonic (13%) effusions, pleural air/blood (13%), tuberculosis (7%), transudate (7%), other (6%) and CVD (3%).

The cumulative prevalence of malignancy among EPEs has gradually increased from 7 to 25% over the last 4 decades, while that of tuberculosis has been relatively stable and stayed at around 7% (fig. 2, 5). The likelihood of malignancy or tuberculosis was somehow lower in EPEs than in non-EPEs, but the difference was not statistically significant. We found that the likelihood of malignancy was inversely correlated with the pleural eosinophil counts (fig. 4). Such correlation was not found in tuberculosis.

The above findings could explain the difference in opinion on the diagnostic significance of EPE in the medical literature. Adelman et al. [4] reported that the prevalence of malignancy among EPEs was 4.9% and concluded that the presence of pleural fluid eosinophilia considerably reduced the probability of malignancy. However, Kuhn et al. [17] reported a much higher prevalence of malignancy (40%) among EPEs which is most likely due to the different population they studied. In addition, 2 recent studies demonstrated that the prevalence of malignancy was as frequent in EPEs as in non-EPEs - 20.5 versus 20.1% in the study by Rubins and Rubins [6] and 24.4 versus 26.8% in the study by Martinez-Garcia et al. [5].

EPEs appeared to be a very weak negative predictor of malignancy when the conventional cutoff of 10% was used (OR 0.63, 95% CI 0.28-1.47). In addition, we found that the higher a pleural fluid eosinophil count was, the lower the likelihood of malignancy (fig. 4). The probability of malignancy was only 7% when a pleural fluid eosinophil count was >32% in our analysis, which is in accordance with a study by Martensson et al. [30] who concluded that more than 30% eosinophils in the pleural fluid had the strongest negative predictability towards malignancy.

The likelihood of malignancy in a pleural effusion is affected by various factors, and the presence of pleural fluid eosinophilia by no means excludes malignancy. The clinical predictors for malignant pleural effusions include older age, a symptomatic period >1 month, absence of fever, blood-tinged pleural effusion, large or massive pleural effusion, and chest CT scan findings suggestive of malignancy [31,32,33]. Thus, it is not surprising that one of the patients with malignant pleural effusion had a pleural eosinophil count of 70% [27].

Our study has several limitations. First, the baseline characteristics between EPEs and non-EPEs are not matched and the presence of confounding factors cannot be excluded. We attempted to adjust for known confounding factors, but it was impossible because of the lack of information. The clinical heterogeneity, such as different types and degrees of confounding factors in each study, could explain the weak robustness of effect size in several analyses. A large multicenter prospective study is needed to better characterize the diagnostic significance of EPEs. However, the pooled comparison of disease spectrum between EPEs and non-EPEs may provide the most generalizable information on the diagnostic significance of EPEs in the absence of such study.

Second, the diagnostic criteria were somehow different from study to study. The prevalence of malignancy was significantly lower in studies that required a pathologic confirmation and the prevalence of idiopathic pleural effusions was significantly lower in studies that required certain duration of follow-up. The prevalence of malignancy among EPEs was likely underestimated and that of idiopathic effusions was likely overestimated in our analysis. As in exudative pleural effusions, a certain duration of follow-up would be strongly recommended in EPEs in order not to overlook malignancy when an initial work-up is unrevealing.

Third, we tried to limit the cases of EPE only with the first thoracentesis, but it was not possible in some studies [1,13,15,22]. This factor may have affected the results on the prevalence and diagnostic significance of EPEs. However, recent studies suggested that the prevalence of EPEs with a repeated thoracentesis was similar to that of EPEs with the first thoracentesis [5,23].

Fourth, the prevalence of idiopathic pleural effusion may be overestimated because there were no cases of drug-induced EPE reported among the included studies and only 1 study indicated that the possibility of drug-induced EPE was investigated [5]. At least 10 drugs are known to be associated with EPEs [1], but the prevalence of the drug-induced EPEs is poorly studied. The presence of peripheral eosinophilia may suggest parasitic or medication-induced EPE, but it is not helpful to delineate the etiology of EPE since it can be found in patients with malignancy including Hodgkin's disease, pulmonary embolism, trauma and infections [1,16,26]. In addition, there is no correlation between the number of eosinophils in the peripheral blood and the pleural fluid [6].

It was once believed that EPEs denoted a favorable prognosis, based on their association with benign diseases such as air or blood in the pleural space, benign asbestos-related pleural effusion, parasitic infection and drug effect [34]. The prevalence of the above-mentioned diagnoses was actually very low in our pooled analysis except for air or blood in the pleural space. It is possible that a significant proportion of the idiopathic pleural effusions were actually due to medications, asbestos or other unrecognized benign diseases.

Despite the limitations described above, our analysis gives an insight and explanation for the difference of opinions in the medical literature on this topic. The disease spectrum of EPEs has changed since 1960, and malignancy should no longer be considered uncommon among EPEs. Some medical textbooks still describe that EPEs militate greatly against malignancy or tuberculosis [35,36]. The readers are warned not to be misled by information from the remote past.

Financial Disclosure and Conflicts of Interest

None of the authors received financial support.

Appendix

Quality of Included Studies

http://www.karger.com/WebMaterial/ShowPic/209537


Related Articles:

References

  1. Kalomenidis I, Light RW: Eosinophilic pleural effusions. Curr Opin Pulm Med 2003;9:254-260.
    External Resources
  2. Mohamed KH, Abdelhamid AI, Lee YC, Lane KB, Conner B, Hawthorne M, et al: Pleural fluid levels of interleukin-5 and eosinophils are closely correlated. Chest 2002;122:576-580.
    External Resources
  3. Kalomenidis I, Light RW: Pathogenesis of the eosinophilic pleural effusions. Curr Opin Pulm Med 2004;10:289-293.
    External Resources
  4. Adelman M, Albelda SM, Gottlieb J, Hapo-nik EF: Diagnostic utility of pleural fluid eosinophilia. Am J Med 1984;77:915-920.
    External Resources
  5. Martinez-Garcia MA, Cases-Viedma E, Cordero-Rodriguez PJ, Hidalgo-Ramirez M, Perpina-Tordera M, Sanchis-Moret F, et al: Diagnostic utility of eosinophils in the pleural fluid. Eur Respir J 2000;15:166-169.
    External Resources
  6. Rubins JB, Rubins HB: Etiology and prognostic significance of eosinophilic pleural effusions. A prospective study. Chest 1996;110:1271-1274.
    External Resources
  7. Vandenbroucke JP, von Elm E, Altman DG, Gotzsche PC, Mulrow CD, Pocock SJ, et al: Strengthening the Reporting of Observational Studies in Epidemiology (STROBE): explanation and elaboration. PLoS Med 2007;4:e297.
    External Resources
  8. Lau J, Schmid CH, Chalmers TC: Cumulative meta-analysis of clinical trials builds evidence for exemplary medical care. J Clin Epidemiol 1995;48:45-57, discussion 59-60.
    External Resources
  9. Higgins JP, Thompson SG, Deeks JJ, Altman DG: Measuring inconsistency in meta-analyses. BMJ 2003;327:557-560.
    External Resources
  10. Normand SL: Meta-analysis: formulating, evaluating, combining, and reporting. Stat Med 1999;18:321-359.
    External Resources
  11. Egger M, Smith GD, Phillips AN: Meta-analysis: principles and procedures. BMJ 1997;315:1533-1537.
    External Resources
  12. Bower G: Eosinophilic pleural effusion. A condition with multiple causes. Am Rev Respir Dis 1967;95:746-751.
    External Resources
  13. Kokkola K, Valta R: Aetiology and findings in eosinophilic pleural effusion. Scand J Respir Dis Suppl 1974;89:159-165.
    External Resources
  14. Pettersson T, Riska H: Diagnostic value of total and differential leukocyte counts in pleural effusions. Acta Med Scand 1981;210:129-135.
    External Resources
  15. Mihailescu E, Micu D: Eosinophilia in the pleural and peritoneal effusions. Med Interne 1985;23:191-194.
    External Resources
  16. Wysenbeek AJ, Lahav M, Aelion JA, Kaufmann L: Eosinophilic pleural effusion: a review of 36 cases. Respiration 1985;48:73-76.
    External Resources
  17. Kuhn M, Fitting JW, Leuenberger P: Probability of malignancy in pleural fluid eosinophilia. Chest 1989;96:992-994.
    External Resources
  18. Lakhotia M, Mehta SR, Mathur D, Baid CS, Varma AR: Diagnostic significance of pleural fluid eosinophilia during initial thoracocentesis. Indian J Chest Dis Allied Sci 1989;31:259-264.
    External Resources
  19. Riantawan P, Bangpattanasiri K, Chaowalit P, Sangsayan P: Etiology and clinical implications of eosinophilic pleural effusions. Southeast Asian J Trop Med Public Health 1998;29:655-659.
    External Resources
  20. Matthai SM, Kini U: Diagnostic value of eosinophils in pleural effusion: a prospective study of 26 cases. Diagn Cytopathol 2003;28:96-99.
    External Resources
  21. Reechaipichitkul W, Chuesakoolvanich K: Eosinophilic pleural effusion in adults at Srinagarind Hospital. Southeast Asian J Trop Med Public Health 2003;34:374-378.
  22. Ozkara SK, Turan G, Basyigit I: Clinicopathologic significance of eosinophilic pleural effusions in a population with a high prevalence of tuberculosis and cancer. Acta Cytol 2007;51:773-781.
    External Resources
  23. Krenke R, Nasilowski J, Korczynski P, Gorska K, Przybylowski T, Chazan R, et al: Incidence and aetiology of eosinophilic pleural effusion. Eur Respir J 2009;34:1111-1117.
    External Resources
  24. Light RW, Erozan YS, Ball WC Jr: Cells in pleural fluid. Their value in differential diagnosis. Arch Intern Med 1973;132:854-860.
    External Resources
  25. Hirsch A, Ruffie P, Nebut M, Bignon J, Chretien J: Pleural effusion: laboratory tests in 300 cases. Thorax 1979;34:106-112.
    External Resources
  26. Bower G: Eosinophilic pleural effusion. A condition with multiple causes. Am Rev Respir Dis 1967;95:746-751.
    External Resources
  27. Brocard H, Broquie G, Blanchon F: The future of eosinophilic pleurisies. Ann Med Interne (Paris) 1973;124:877-882.
    External Resources
  28. Campbell GD, Webb WR: Eosinophilic pleural effusion: a review with the presentation of seven new cases. Am Rev Respir Dis 1964;90:194-201.
    External Resources
  29. Filip A, Dobre V: Eosinophilic pleurisy (a study of 27 cases). Pneumoftiziologia 1996;45:127-130.
    External Resources
  30. Martensson G, Pettersson K, Thiringer G: Differentiation between malignant and non-malignant pleural effusion. Eur J Respir Dis 1985;67:326-334.
    External Resources
  31. Maher GG, Berger HW: Massive pleural effusion: malignant and nonmalignant causes in 46 patients. Am Rev Respir Dis 1972;105:458-460.
    External Resources
  32. Ferrer J, Roldan J, Teixidor J, Pallisa E, Gich I, Morell F: Predictors of pleural malignancy in patients with pleural effusion undergoing thoracoscopy. Chest 2005;127:1017-1022.
    External Resources
  33. Porcel JM, Vives M: Etiology and pleural fluid characteristics of large and massive effusions. Chest 2003;124:978-983.
    External Resources
  34. Morelock SY, Sahn SA: Drugs and the pleura. Chest 1999;116:212-221.
    External Resources
  35. Gibson J, Geddes D, Costabel U, Sterk P, Corrin B: Respiratory Medicine, ed 3. London, Saunders, 2003.
  36. Albert RK, Spiro SG, Jett JR: Clinical Respiratory Medicine, ed 3. Philadelphia, Mosby/Elsevier, 2008.

Author Contacts

Yuji Oba, MD

University of Missouri

1 Hospital Drive

Columbia, MO 65212 (USA)

Tel. +1 573 882 8583, E-Mail obay@health.missouri.edu

Article / Publication Details

First-Page Preview
Abstract of Clinical Investigations

Received: December 08, 2010
Accepted: March 01, 2011
Published online: May 11, 2011
Issue release date: February 2012

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 4

ISSN: 0025-7931 (Print)
eISSN: 1423-0356 (Online)

For additional information: https://www.karger.com/RES

Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

References

  1. Kalomenidis I, Light RW: Eosinophilic pleural effusions. Curr Opin Pulm Med 2003;9:254-260.
    External Resources
  2. Mohamed KH, Abdelhamid AI, Lee YC, Lane KB, Conner B, Hawthorne M, et al: Pleural fluid levels of interleukin-5 and eosinophils are closely correlated. Chest 2002;122:576-580.
    External Resources
  3. Kalomenidis I, Light RW: Pathogenesis of the eosinophilic pleural effusions. Curr Opin Pulm Med 2004;10:289-293.
    External Resources
  4. Adelman M, Albelda SM, Gottlieb J, Hapo-nik EF: Diagnostic utility of pleural fluid eosinophilia. Am J Med 1984;77:915-920.
    External Resources
  5. Martinez-Garcia MA, Cases-Viedma E, Cordero-Rodriguez PJ, Hidalgo-Ramirez M, Perpina-Tordera M, Sanchis-Moret F, et al: Diagnostic utility of eosinophils in the pleural fluid. Eur Respir J 2000;15:166-169.
    External Resources
  6. Rubins JB, Rubins HB: Etiology and prognostic significance of eosinophilic pleural effusions. A prospective study. Chest 1996;110:1271-1274.
    External Resources
  7. Vandenbroucke JP, von Elm E, Altman DG, Gotzsche PC, Mulrow CD, Pocock SJ, et al: Strengthening the Reporting of Observational Studies in Epidemiology (STROBE): explanation and elaboration. PLoS Med 2007;4:e297.
    External Resources
  8. Lau J, Schmid CH, Chalmers TC: Cumulative meta-analysis of clinical trials builds evidence for exemplary medical care. J Clin Epidemiol 1995;48:45-57, discussion 59-60.
    External Resources
  9. Higgins JP, Thompson SG, Deeks JJ, Altman DG: Measuring inconsistency in meta-analyses. BMJ 2003;327:557-560.
    External Resources
  10. Normand SL: Meta-analysis: formulating, evaluating, combining, and reporting. Stat Med 1999;18:321-359.
    External Resources
  11. Egger M, Smith GD, Phillips AN: Meta-analysis: principles and procedures. BMJ 1997;315:1533-1537.
    External Resources
  12. Bower G: Eosinophilic pleural effusion. A condition with multiple causes. Am Rev Respir Dis 1967;95:746-751.
    External Resources
  13. Kokkola K, Valta R: Aetiology and findings in eosinophilic pleural effusion. Scand J Respir Dis Suppl 1974;89:159-165.
    External Resources
  14. Pettersson T, Riska H: Diagnostic value of total and differential leukocyte counts in pleural effusions. Acta Med Scand 1981;210:129-135.
    External Resources
  15. Mihailescu E, Micu D: Eosinophilia in the pleural and peritoneal effusions. Med Interne 1985;23:191-194.
    External Resources
  16. Wysenbeek AJ, Lahav M, Aelion JA, Kaufmann L: Eosinophilic pleural effusion: a review of 36 cases. Respiration 1985;48:73-76.
    External Resources
  17. Kuhn M, Fitting JW, Leuenberger P: Probability of malignancy in pleural fluid eosinophilia. Chest 1989;96:992-994.
    External Resources
  18. Lakhotia M, Mehta SR, Mathur D, Baid CS, Varma AR: Diagnostic significance of pleural fluid eosinophilia during initial thoracocentesis. Indian J Chest Dis Allied Sci 1989;31:259-264.
    External Resources
  19. Riantawan P, Bangpattanasiri K, Chaowalit P, Sangsayan P: Etiology and clinical implications of eosinophilic pleural effusions. Southeast Asian J Trop Med Public Health 1998;29:655-659.
    External Resources
  20. Matthai SM, Kini U: Diagnostic value of eosinophils in pleural effusion: a prospective study of 26 cases. Diagn Cytopathol 2003;28:96-99.
    External Resources
  21. Reechaipichitkul W, Chuesakoolvanich K: Eosinophilic pleural effusion in adults at Srinagarind Hospital. Southeast Asian J Trop Med Public Health 2003;34:374-378.
  22. Ozkara SK, Turan G, Basyigit I: Clinicopathologic significance of eosinophilic pleural effusions in a population with a high prevalence of tuberculosis and cancer. Acta Cytol 2007;51:773-781.
    External Resources
  23. Krenke R, Nasilowski J, Korczynski P, Gorska K, Przybylowski T, Chazan R, et al: Incidence and aetiology of eosinophilic pleural effusion. Eur Respir J 2009;34:1111-1117.
    External Resources
  24. Light RW, Erozan YS, Ball WC Jr: Cells in pleural fluid. Their value in differential diagnosis. Arch Intern Med 1973;132:854-860.
    External Resources
  25. Hirsch A, Ruffie P, Nebut M, Bignon J, Chretien J: Pleural effusion: laboratory tests in 300 cases. Thorax 1979;34:106-112.
    External Resources
  26. Bower G: Eosinophilic pleural effusion. A condition with multiple causes. Am Rev Respir Dis 1967;95:746-751.
    External Resources
  27. Brocard H, Broquie G, Blanchon F: The future of eosinophilic pleurisies. Ann Med Interne (Paris) 1973;124:877-882.
    External Resources
  28. Campbell GD, Webb WR: Eosinophilic pleural effusion: a review with the presentation of seven new cases. Am Rev Respir Dis 1964;90:194-201.
    External Resources
  29. Filip A, Dobre V: Eosinophilic pleurisy (a study of 27 cases). Pneumoftiziologia 1996;45:127-130.
    External Resources
  30. Martensson G, Pettersson K, Thiringer G: Differentiation between malignant and non-malignant pleural effusion. Eur J Respir Dis 1985;67:326-334.
    External Resources
  31. Maher GG, Berger HW: Massive pleural effusion: malignant and nonmalignant causes in 46 patients. Am Rev Respir Dis 1972;105:458-460.
    External Resources
  32. Ferrer J, Roldan J, Teixidor J, Pallisa E, Gich I, Morell F: Predictors of pleural malignancy in patients with pleural effusion undergoing thoracoscopy. Chest 2005;127:1017-1022.
    External Resources
  33. Porcel JM, Vives M: Etiology and pleural fluid characteristics of large and massive effusions. Chest 2003;124:978-983.
    External Resources
  34. Morelock SY, Sahn SA: Drugs and the pleura. Chest 1999;116:212-221.
    External Resources
  35. Gibson J, Geddes D, Costabel U, Sterk P, Corrin B: Respiratory Medicine, ed 3. London, Saunders, 2003.
  36. Albert RK, Spiro SG, Jett JR: Clinical Respiratory Medicine, ed 3. Philadelphia, Mosby/Elsevier, 2008.
ppt logo Download Figures (.pptx)

Figures
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Thumbnail
Tables
Thumbnail
Thumbnail
Thumbnail
Thumbnail

Article Tools
Article Details

2012, Vol.83, No. 3

February 2012

Article

Recommend This
TOP