Explore the vast range of titles available.

This review discusses the substantial advances that have been made in our understanding of pleural biology and related pathophysiology, as well as in the epidemiology and treatment of parapneumonic effusions, empyema, and malignant pleural effusions.

ObjectiveTumor-related eosinophilia may have extended survival benefits for some cancer patients. However, there has been no report on the prognosis difference between eosinophilic pleural effusion (EPE) and non-EPE in lung cancer patients. Our study aimed to investigate the prognosis difference between EPE and non-EPE due to lung cancer.Patients and methodsWe retrospectively reviewed patients diagnosed with lung cancer who presented with malignant pleural effusion (MPE) between May 2007 and September 2020 at the National Hospital Organization Kochi Hospital. EPE is defined as pleural fluid with a nucleated cell count containing 10% or more eosinophils.ResultsA total of 152 patients were included: 89 were male (59%). The median age was 74.4 years (range 37–101), and all patients were pathologically shown to have MPE. Most patients (140; 92%) had an Eastern Cooperative Oncology Group (ECOG) Performance Status (PS) of 0/1. Twenty patients had EPE. The median overall survival (OS) of all 152 lung cancer patients with MPE was 298 days. The median OS of the patients with EPE was 766 days, and the median OS of the patients with non-EPE was 252 days. Kaplan–Meier univariate analysis showed that lung cancer patients with EPE had a significantly better prognosis than patients with non-EPE (P < 0.05). Cox proportional regression analysis showed that EPE, ECOG PS, sex, and the neutrophil-to-lymphocyte ratio in the serum (sNLR) may be independent prognostic factors affecting survival in patients with MPE.ConclusionLung cancer patients with EPE have a better prognosis than those with non-EPE.

Cytological examination serves as a crucial diagnostic tool for pleural effusion, with its diagnostic efficacy influenced by variations in specimen processing and staining techniques. Cellular morphological analysis of pleural effusions was performed using Wright-Giemsa staining to assess its diagnostic accuracy and clinical utility in differentiating the various etiologies of exudative pleural effusion. A routine examination was conducted on 2305 cases of unexplained pleural effusion, followed by cellular classification and morphological analysis in 1376 cases identified as exudative effusion. Among the 479 patients with malignant tumors, cytomorphological examination identified malignant cells in 295 patients, resulting in a clinical diagnosis coincidence rate of 98.6%. Abnormal cells, including malignant and heterogeneous nuclear cells, were observed in 364 cases, yielding a detection rate of 76.0%. The proportion of positive malignant cells in the newly diagnosed patient group was significantly higher than that in the previously diagnosed group ( P  < 0.01). Cytological analysis revealed the presence of bacteria, fungi, and phagocytes in 51 out of 1376 cases. The positivity rate for multiple bacterial infections detected through cytology was significantly greater than that identified by culture ( P  < 0.01). Additionally, various special morphologies and pathogens, which are rare in clinical practice, were detected, including mixed metastasis of small cell lung carcinoma and adenocarcinoma cells, as well as concurrent infections with Talaromyces marneffei and Pneumocystis jirovecii . This method enables the rapid and comprehensive differentiation between malignant tumors, tuberculosis, pneumonia, and rare exudative pleural effusions resulting from specific clinical conditions.

Background In most cases, patients with pleural effusion require a pleural biopsy to confirm the diagnosis, due to the low diagnostic sensitivity of thoracentesis. Among the different biopsy modalities, real time computed tomography scan-guided cutting-needle pleural biopsy (CT-CNPB) ensures high sensitivity and accessibility. However, there is no study investigating the difference in the diagnostic sensitivity of CT-CNPB for lesions with variable pleural thickness in effusions of different types. Methods Of the 303 patients who underwent CT-CNPB, 218 met the eligibility criteria and were retrospectively analyzed from November 2021 to June 2024. Patients were divided into malignant pleural effusion (MPE), tuberculosis pleural effusion (TPE), and non-tuberculous benign pleural effusion (BPE) groups according to the diagnosis with a minimum follow-up of 6 months. Pleural thickness was defined as the length of the portion of the puncture needle that passes through the thickened parietal pleura or the pleural lesion (nodule/mass). In further analysis, we compare the differences in sensitivity between subgroups with different pleural thicknesses in each group. Results The overall diagnostic sensitivity is 74.3%. The sensitivity in MPE, TPE, and BPE is 75.7%, 78.6%, and 67.8%, respectively. There was a significant difference in sensitivity between the < 5 mm and ≥ 5 mm groups in MPE and BPE groups but was not observed in the TPE group. In the further analysis, there was a significant difference in sensitivity between < 3 mm and 3–5 mm groups in TPE ( p  = 0.046) and a significant difference in sensitivity between 3 and 5 mm and 5–10 mm groups in MPE ( p  = 0.017), but a significant difference was not observed in BPE group. Conclusion CT-CNPB may serve as a preferred diagnostic approach in suspected TPE with pleural thickening ≥ 3 mm and suspected MPE with thickening ≥ 5 mm on chest CT. Where MT is unavailable, CT-CNPB is a viable alternative for suspected MPE or TPE patients with pleural thickening, nodularity, or mass lesions observed on CT. However, in suspected BPE, CT-CNPB alone is often insufficient; integrated clinical, laboratory, and imaging evaluation remains essential.

Purpose The aim of this study is to determine the diagnostic performances of pleural procedures in undiagnosed exudative pleural effusions and to evaluate factors suggestive of benign or malignant pleural effusions in tertiary care centers. Methods This was a multicenter prospective observational study conducted between January 1 and December 31, 2018. A total of 777 patients with undiagnosed exudative pleural effusion after the initial work-up were evaluated. The results of diagnostic procedures and the patients' diagnoses were prospectively recorded. Sensitivity, specificity, and accuracy estimates with 95% confidence intervals were used to examine the performance of pleural procedures to detect malignancy. Results The mean age ± SD of the 777 patients was 62.0 ± 16.0 years, and 68.3% of them were male. The most common cause was malignancy (38.3%). Lung cancer was the leading cause of malignant pleural effusions (20.2%). The diagnostic sensitivity and accuracy of cytology were 59.5% and 84.3%, respectively. The diagnostic sensitivity of image-guided pleural biopsy was 86.4%. The addition of image-guided pleural biopsy to cytology increased diagnostic sensitivity to more than 90%. Thoracoscopic biopsy provided the highest diagnostic sensitivity (94.3%). The highest diagnostic sensitivity of cytology was determined in metastatic pleural effusion from breast cancer (86.7%). Conclusion The diagnostic performance increases considerably when cytology is combined with image-guided pleural biopsy in malignant pleural effusions. However, to avoid unnecessary interventions and complications, the development of criteria to distinguish patients with benign pleural effusions is as important as the identification of patients with malignant pleural effusions.

Malignant pleural effusion (MPE) is indicative of terminal malignancy with a uniformly fatal prognosis. Often, two distinct compartments of tumour microenvironment, the effusion and disseminated pleural tumours, co-exist in the pleural cavity, presenting a major challenge for therapeutic interventions and drug delivery. Clinical evidence suggests that MPE comprises abundant tumour-associated myeloid cells with the tumour-promoting phenotype, impairing antitumour immunity. Here we developed a liposomal nanoparticle loaded with cyclic dinucleotide (LNP-CDN) for targeted activation of stimulators of interferon genes signalling in macrophages and dendritic cells and showed that, on intrapleural administration, they induce drastic changes in the transcriptional landscape in MPE, mitigating the immune cold MPE in both effusion and pleural tumours. Moreover, combination immunotherapy with blockade of programmed death ligand 1 potently reduced MPE volume and inhibited tumour growth not only in the pleural cavity but also in the lung parenchyma, conferring significantly prolonged survival of MPE-bearing mice. Furthermore, the LNP-CDN-induced immunological effects were also observed with clinical MPE samples, suggesting the potential of intrapleural LNP-CDN for clinical MPE immunotherapy.Malignant pleural effusion (MPE) is the terminal stage of cancer and the current standard of care for MPE is largely palliative. Here the authors design a liposomal nanoparticle loaded with cyclic dinucleotide for targeted activation of STING signalling in macrophages and dendritic cells and show that, on intrapleural administration, the nanoparticle effectively mitigates the immune cold MPE and significantly augments the checkpoint blockade immunotherapy in a mouse MPE model and clinical patients’ samples.

Introduction This multi‐centre retrospective cohort study aimed to determine whether the cause of an undiagnosed pleural effusion differed depending on if a patient presented as an outpatient or inpatient. Methods A total of 1080 adult patients (556 inpatients and 524 outpatients) presenting primarily with an undiagnosed pleural effusion from 1 January 2021 to 31 December 2022 from four UK hospitals were included. Results We found malignant effusions were more common in outpatients compared to inpatients (48.3% vs. 36.0% p < 0.0001). Infection was common in inpatients but uncommon in outpatients (36.2% vs. 5.0% p < 0.0001). Other causes in all patients included heart and/or renal failure (13.1%) and non‐specific pleuritis (5.6%). No diagnosis was possible in 11.8% of patients referred. Conclusion Investigative pathways should vary depending on whether patients present as an inpatient or outpatient. Our experience suggests that the underlying cause of a pleural effusion differs based on whether the patient presents as an emergency or if they present as an outpatient. In this large multi‐centre retrospective study, about half of outpatients had a malignant effusion with infection being rare, compared to about a third of inpatients having malignancy and infection being equally common.

The use of biomarkers on pleural fluid (PF) specimens may assist the decision-making process and enhance clinical diagnostic pathways. Three paradigmatic examples are heart failure, tuberculosis and, particularly, malignancy. An elevated PF concentration of the amino-terminal fragment of probrain natriuretic peptide (>1500 pg/ml) is a hallmark of acute decompensated heart failure. Adenosine deaminase, interferon-γ and interleukin-27 are three valuable biomarkers for diagnosing tuberculous pleurisy, yet only the first has been firmly established in clinical practice. Diagnostic PF biomarkers for malignancy can be classified as soluble-protein based, immunocytochemical and nucleic-acid based. Soluble markers (e.g. carcinoembryonic antigen (CEA), carbohydrate antigen 15–3, mesothelin) are only indicative of cancer, but not confirmatory. Immunocytochemical studies on PF cell blocks allow: (a) to distinguish mesothelioma from reactive mesothelial proliferations (e.g. loss of BAP1 nuclear expression, complemented by the demonstration of p16 deletion using fluorescence in situ hybridization, indicate mesothelioma); (b) to separate mesothelioma from adenocarcinoma (e.g. calretinin, CK 5/6, WT-1 and D2-40 are markers of mesothelioma, whereas CEA, EPCAM, TTF-1, napsin A, and claudin 4 are markers of carcinoma); and (c) to reveal tumor origin in pleural metastases of an unknown primary site (e.g. TTF-1 and napsin A for lung adenocarcinoma, p40 for squamous lung cancer, GATA3 and mammaglobin for breast cancer, or synaptophysin and chromogranin A for neuroendocrine tumors). Finally, PF may provide an adequate sample for analysis of molecular markers to guide patients with non-small cell lung cancer to appropriate targeted therapies. Molecular testing must include, at least, mutations of epidermal growth-factor receptor and BRAF V600E, translocations of rat osteosarcoma and anaplastic lymphoma kinase, and expression of programmed death ligand 1.

Malignant pleural effusion (MPE), the presence of malignant cells in pleural fluid, is often the first sign of many cancers and occurs in patients with metastatic malignancies. Accurate detection of tumor cells in pleural fluid is crucial because the presence of MPE denotes an advanced stage of disease and directs a switch in clinical managements. Cytology, as a traditional diagnostic tool, has limited sensitivity especially when tumor cells are not abundant, and may be confounded by reactive mesothelial cells in the pleural fluid. We describe a highly sensitive approach for rapid detection of metabolically active tumor cells in MPE via exploiting the altered glucose metabolism of tumor cells relative to benign cells. Metabolically active tumor cells with high glucose uptake, as evaluated by a fluorescent glucose analog (2-NBDG), are identified by high-throughput fluorescence screening within a chip containing 200,000 addressable microwells and collected for malignancy confirmation via single-cell sequencing. We demonstrate the utility of this approach through analyzing MPE from a cohort of lung cancer patients. Most candidate tumor cells identified are confirmed to harbor the same driver oncogenes as their primary lesions. In some patients, emergence of secondary mutations that mediate acquired resistance to ongoing targeted therapies is also detected before resistance is manifested in the clinical imaging. The detection scheme can be extended to analyze peripheral blood samples. Our approach may serve as a valuable complement to cytology in MPE diagnosis, helping identify the driver oncogenes and resistance-leading mutations for targeted therapies.

Background Incidence of childhood complicated community acquired pneumonia (cCAP) is increasing worldwide. Necrotising pneumonia (NP), empyema and complicated parapneumonic effusion (CPPE) are the most common local complications. Methods This retrospective observational study describes clinical characteristics, aetiology and management of children hospitalized with cCAP in one of the largest tertiary centers in Egypt, over 5 years (December 2017 till September 2022). Results A total of 158 cases were identified. Seasonal variation was observed, as more cases were hospitalized during Winter and Spring. NP, empyema and CPPE, were diagnosed in 85 (54%), 52 (33%) and 21 (13%) children, respectively. 54 (64%) of children presented with NP had associated empyema or CPPE. The yield of pleural fluid, sputum and blood cultures were 23%, 18% and 17%, respectively. Community acquired MRSA was the predominant causative organism, followed by S pneumoniae . 87% of the patients had pleural interventions. 29 (18%) children received fibrinolytics. Three children presented with CAP and highly septated effusion, developed NP and persistent air leaks following fibrinolytic administration. Patients had prolonged hospitalization (median 17 days). 15 (10%) children had surgery. Children presented with NP had more morbidities and longer length of hospital stay, compared to children presented with CPPE and empyema. ICU admission, mechanical ventilation, severe anemia requiring blood transfusion, broncho-pleural fistula and surgical interventions were significantly higher in NP cohort. We report 5 mortalities, 4 of them below 1 year of age. Conclusions This study describes the largest cohort of children hospitalized with cCAP from Egypt till this date. Management of cCAP remains challenging worldwide and the current guidelines requires updating. Improvement of microbial detection and reporting is needed to promote antimicrobial stewardship.