Higher pleural eosinophil counts esp. Steroids has been shown to mitigate this. Pleural Effusion. NEJM Incidence and aetiology of eosinophilic pleural effusion. Eur Respir J ; — Glucose, LDH, lipase, and amylase were normal.
The pH was alkaline 7. CBC revealed a leukocytosis of Peripheral blood smear, lymph node biopsy, and bone marrow aspiration showed eosinophilia with normal morphology, lymphoid hyperplasia, and hypercellular marrow with eosinophilia, respectively. Bone marrow flow cytometry showed polytypic B cells. A diagnosis of hypereosinophilic syndrome was made by exclusion. As initial treatment of hydroxycarbamide provided no clinical benefit or reduction in the eosinophilia, prednisone was added with prompt reduction of the eosinophilia.
He had recurrent pleural effusions requiring repeated thoracentesis which continued to demonstrate persistent elevated eosinophil counts Table 1. A permanent catheter was placed in the right pleural space and accessed for thoracentesis of about two liters every three to five days along with repeated large volume paracentesis for persistent ascites. Four months after his initial presentation, he developed bilateral empyemas with methicillin resistant staphyloccus aureus as a complication of multiple thoracentesis, rapidly deteriorated in spite of aggressive management and died from multiple organ dysfunction.
Hypereosinophilic syndrome rarely presents with eosinophilic pleural effusion. If pleural effusions are present in HES, they typically result from heart failure due to cardiac eosinophilic disease [ 3 ]. However, our patient had a normal trans-thoracic echocardiography and beta natriuretic peptide. In addition, the pleural effusion of the three previously reported patients resolved rapidly with clinical improvement, using treatment recommendations for HES of normalizing the peripheral eosinophilia [ 5 — 7 ].
Despite rapid reduction of the peripheral eosinophilia in our patient, the eosinophilic pleural effusion continued to accumulate for months questioning this therapeutic recommendation. A recent review of patients with EPE reported 2 out of patients with percentage of eosinophils in peripheral blood higher than in pleural fluid. Those two patients had hematological malignancies [ 1 ]. Our patient had features of both the myeloproliferative and the lymphocytic variants of HES.
There are several chemotherapy choices depending on the variant of HES and new drugs are in clinical trials [ 3 ]. Our patient expired prior to receiving alternate treatment; however, it should be noted that the recommendation of titrating these therapies as well is normalization of the peripheral eosinophilia which had already been obtained in our patient but without clinical benefit.
Treatment of eosinophilic pleural effusions is directed toward the underlying cause, in this case hypereosinophilic syndrome.
Disease remission cannot be determined by resolution of peripheral eosinophilia alone but also by the absence of recurrence or progression of end-organ damage [ 8 ]. Pleuroscopy, thoracentesis, laboratory tests, and cytological analysis, provide further information about the aetiology of the disease and thus, are also essential [ 2 , 3 ]. There are several aetiological factors for EPE including trauma, infectious diseases, malignant tumours, asbestos exposure and several medications [ 4 , 5 , 6 , 7 , 8 ].
IEPE is likely to benefit from the use of glucocorticoids [ 7 , 8 , 9 , 10 , 11 ]. The reported prevalence of IEPE is inconsistent. In contrast, another study reported only 8. The clinical characteristics and diagnostic approach for IEPE have remained unclear to physicians.
In order to better characterize IEPE and to outline its diagnostic procedure, comprehensive clinical data of 11 consecutive patients with EPE was collected and analysed in the prospective study. Importantly, a preliminary diagnostic procedure of IEPE was introduced. Five hundred and 56 consecutive patients with PE were admitted to the First Affiliated Hospital of Guangzhou Medical University due to respiratory symptoms between January and January Past medical, surgical, traumatic infectious and drug-related histories were obtained from a total of 74 patients with EPE.
These patients also received extensive work-up to identify a definite aetiology for their EPE. After excluding EPE cases with known aetiological factors, the complete clinical data of 11 patients with IEPE were prospectively collected and analysed.
Informed consent was obtained from all patients for the use of identified personal data extracted from their medical records for research purposes only. Additionally, it is important to review of any drug intake, occupational and infectious disease exposure and comorbid conditions to rule out the common causes of EPE. Pleural samples were acquired by combined ultrasound-guided cutting needle biopsy and standard pleural biopsy [ 17 ].
Biochemical analysis total protein, lactate dehydrogenase , bacterial, fungal and mycobacterial culture, Gram stain, and cytological examinations were performed for all PE samples. Meanwhile, total protein and lactate dehydrogenase in the serum were measured by standard methods.
The diagnostic approach for PPI was as previously described by the authors [ 18 ]. Stool examinations for the detection of parasite eggs were performed in all patients. In total, complete clinical data sets of 11 patients with IEPE were collected and analysed in this study.
The clinical characteristics of 11 cases are summarized in Table 1. Three were 5 men and 6 women, with a median age of Pulmonary physical examination revealed remarkably decreased breath sounds with dullness to percussion on the lateral or bilateral chests, without other significantly positive signs. Among the 11 patients, 2 presented with left PE, 2 others presented with right PE, and the remaining 7 had bilateral PE. The diagnosis was similar to PPE in 3 cases.
Five cases were initially misdiagnosed with TPE. PBC analysis was conducted in all patients Table 2. Antinuclear antibody, rheumatoid factor antibody, proteinase 3, myeloperoxidase and anticyclic citrullinated peptide antibody were not detected. Sputum smears and cultures for fungi, acid-fast bacilli and other bacteria were also negative. In addition, the test for parasite-specific IgG antibody was negative, and parasite eggs were not found in any stool samples.
After thoracentesis and pleura biopsy, pleural effusions were collected for further analysis. Bloody effusions due to thoracic trauma or surgery and effusions associated with air in the pleural space were not found in this study. Bilateral effusions were seen in 7 patients. Four cases had intrapulmonary involvement and intrapulmonary lesions presented as consolidation or infiltration. Bronchoscopy and transbroncial lung biopsy TBLB were performed in these patients, but eosinophilic infiltration was not found, and there was no evidence of tuberculosis or malignancy.
Furthermore, two cases developed pericardial effusion as detected by chest CT Fig. Chest CT a, b scans showed bilateral PE and consolidation in the lower right lung, pericardial effusion.
Eosinophilic count ranged from Eosinophilic infiltration, lymphocyte infiltration, granulocytic infiltration and noncaseating granulomas were found in the pleural samples, but no evidence of either tuberculosis or malignancy was found in any of these patients. Moreover, comprehensive haematological detection was performed in cases 2 and Smear and biopsy of bone marrow showed no evidence of hypereosinophilia or infiltration indicative of lymphoproliferative malignancy.
The median follow-up was All the patients showed total regression of the pleural effusion, without re-occurrence. These patients remained stable during follow-up and did not receive any additional therapy. Figure 2 shows the follow-up chest CT of a patient case 3. Follow-up chest CT scan of case 3. Total regression of PE, consolidation in the lower right lung and pericardial effusion with no recurrences. Complete medical and surgical histories should be obtained from patients with EPE of unknown aetiology.
It is recommended the patients should be followed up after receiving glucocorticoid, until the effusion resolves or a known cause becomes apparent. However, well-documented cases are limited [ 12 , 13 , 14 , 15 , 16 ]. In this study, we tried to analyse the clinical characteristics of IEPE and to clarify the diagnostic procedure.
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SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact. SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. However, these theories have fallen by the wayside in the light of recent publications.. To determine the incidence and etiology of EPE and to observe whether the eosinophils in the pleural liquid PL increase in successive thoracocenteses..
We analyzed PL samples from patients hospitalized between January and December We identified 55 samples with EPE from 50 patients 8. There were no significant differences in the incidence of neoplasms between the non-eosinophilic pleural effusions non-EPE One hundred patients Out of the 91 with non-EPE in the first thoracocentesis, 8 8. An EPE cannot be considered an indicator of benignancy; therefore it should be studied like any other pleural effusion.
The number of eosinophils does not seem to increase with the repetition of thoracocentesis and, lastly, the presence of blood in the PL could explain the existence of EPE.. Analizamos muestras de LP correspondientes a pacientes ingresados entre enero y diciembre Un DPE no puede considerarse un indicador de benignidad por lo que debe ser estudiado como cualquier derrame pleural. The total nucleated cell count in the pleural liquid PL usually provides useful information.
In addition to the nature of the pleural lesion that is produced, one of the factors that influences the type of existing cell population is the evolution time of the effusion.
Thus, pleural effusions with a predominance of neutrophils are usually observed in acute responses after infections, immunological or inflammatory processes such as bacterial pneumonia, pulmonary embolism or acute pancreatitis. Meanwhile, a predominance of lymphocytes is more frequent in effusions evolving over more than 2 weeks, such as in tuberculosis, lymphomas, rheumatoid pleuritis or chylothorax.
The objectives of our study are to know the incidence and etiology of EPE in our population, to evaluate whether these effusions are associated with malignancy with less frequency than non-EPE and to verify whether successive thoracocenteses cause an increase in eosinophils in the PL. We have consecutively included all the patients with pleural effusion admitted between January and December to the Pneumology Department of our hospital.
Fasting blood and PL samples were obtained the same day. The following biochemical determinations were carried out: total protein, lactate dehydrogenase LDH , glucose, cholesterol, red blood cell count and total count and percentage of nucleated cells in PL as well as in plasma P.
In addition, PL samples were sent for pathological and microbiologic anatomy studies. The pleural biopsies were taken with either Cope or Abrams needles, indiscriminately. In the cases of carrying out 2 or more thoracocentesis in the same patient and more than one sample of pleural liquid met the criteria for EPE, we only took into account the results of the first.
Those patients who underwent thoracocentesis in the Emergency Department in order to rule out empyema and did not completely follow the study protocol were also excluded. The pleural effusions were classified as transudates or exudates using Light's and pleural cholesterol criteria. The etiology of the pleural transudates congestive heart failure, chronic hepatopathy and nephrotic syndrome was based on the clinical and laboratory data as well as the negative microbiology and cytology of the pleural liquid.
Tuberculous pleural effusion: culture for Mycobacterium tuberculosis in pleural liquid or biopsy, or respiratory signs sputum, bronchial aspiration or bronchoalveolar lavage , or rather granulomas in the pleural biopsy. Post-traumatic pleural effusion: those that develop after chest trauma with no other cause that could explain it. Pleural effusions due to connective tissue diseases: patients with one of these diseases, after the exclusion of other causes of the pleural effusion. Pleural effusions of unknown origin: when all the diagnostic procedures were not able to identify the etiology of the effusion.
These patients were followed in order to make sure that the pleural effusion did not re-occur. The data are expressed as mean and interquartile range. For the comparison between the study groups, we used Pearson's chi-squared test for the qualitative variables and the non-parametric Mann—Whitney test for the quantitative variables. For the comparison of the continuous variables in the same individual, the Wilcoxon test for paired data was used. Distribution of the eosinophilic pleural effusions according to the percentage of eosinophils.
In the non-EPE, the percentage of lymphocytes is significantly higher than in the EPE, both in the totality of the effusions and in the exudates. The etiology of the patients with EPE is indicated in Table 2. Lastly, the percentage of effusions due to heart failure and parapneumonia was significantly higher in the non-EPE than in the EPE. Etiology of the Eosinophilic Pleural Effusions.
The comparative analysis of the patients with an EPE that was either malignant or non-malignant is indicated in Table 3. The diagnostic capacity of the percentage of eosinophils in PL for differentiating the malignant from the non-malignant effusions in the EPE group is discrete area under the curve 0.
We carried out a follow-up of the 18 EPE of unknown origin. Two patients were lost to follow up and did not attend scheduled office visits. In 15 of the 16 cases Two of the 15 patients in whom the pleural effusion disappeared later died, both due to respiratory infections.
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