T Helper Cell Subsets in the Pleural Fluid of Tuberculous Patients Differentiate Patients With Non-Tuberculous Pleural Effusions.

Background: Tuberculous pleural effusion (TPE) is one of the most common forms of extrapulmonary tuberculosis (Tb). Patients with TPE or malignant pleural effusions (MPE) frequently have a similar lymphocytic pleural fluid profile. Since the etiology of PE in various diseases is different, identifying the cellular components may provide diagnostic clues for understanding the pathogenesis. Objective: We determined the frequency of T helper (Th) subtypes in the PEs for differentiation of Tb and non-Tb patients. Methods: Thirty patients with TPE, 30 patients with MPE, 14 patients with empyema (EMP), and 14 patients with parapneumonic effusion (PPE) were enrolled between December 2018 and December 2019. Five-milliliter fresh PE in tubes containing heparin as an anticoagulant was obtained from patients. The frequencies of CD4+IL-9+, CD4+IL-22+, CD+IL-17+, and regulatory T-cells CD4+CD25+ FOXP3+ (Treg) were determined by flow cytometry. Results: Treg cells have a lower frequency in TPE patients [4.2 (0.362-17.24)] compared with non-TPE patients [26.3 (3.349-76.93, p < 0.0001)]. The frequency of CD4+IL-9+ cells was significantly lower in TPE patients [3.67 (0.87-47.83)] compared with non-TPE groups [13.05 (1.67-61.45), p < 0.0001]. On the contrary, there was no significant difference in the frequency of CD4+IL-17+ and CD4+IL-22+ cells between TPE and non-TPE patients (p = 0.906 and p = 0.2188). Receiver-operator curve (ROC) analysis demonstrated that CD4+CD25+FOXP3+ T cells [optimal cutoff value = 13.6 (%), sensitivity 90%, specificity 75.86%] could be considered as predictor for TPE. However, adenosine deaminase [cutoff value 27.5 (IU/l), sensitivity 90%, specificity 96.5%] levels had an even greater predictive capacity. Conclusion: ADA, Treg cells, and CD4+IL-9+ cells may differentiate TPE from non-TPE patients. However, these results need validation in an independent large cohort.

Cytomorphology, Immunophenotype, and cytogenetic profile of leukemic serous effusions.

BACKGROUND: Serous effusions (SE) in leukemic patients can be due to infections, therapy, volume overload, lymphatic obstruction or malignancy having implications on treatment and mortality. The objective of the present study is to highlight the spectrum of cytomorphology, immunophenotype, and cytogenetics in leukemic serous effusions (LSE). MATERIALS: Present study is retrospective and descriptive. We reviewed all the SE, which were reported as suspicious or positive of leukemic infiltration from 2016 to 2019 for cytomorphological features. CSF and effusions involved by lymphomas were excluded. Cyto-diagnosis was compared with primary proven diagnosis (by ancillary techniques) and disconcordant cases were analyzed. RESULTS: Out of total 9723 effusions, only 0.4% (n = 40) showed leukemic involvement and included nine cases of AML, three of B-ALL, 13 T-ALL, 2 MPAL, 6 CML, 5CLL, one each of chronic myelomonocytic leukemia and AML with myelodysplasia. The most common site of involvement was the pleural cavity (n = 30), followed by the peritoneal cavity (n = 7) and the pericardial cavity (n = 3). T -ALL (41.9%) was the most common leukemia involving pleural fluid followed by AML (23.3%). CML (42.8%) was the most common leukemia involving the ascitic fluid followed by B-ALL (28.6%). Accurate diagnosis was given on cytomorphology in 72.5% (29/40) cases and 15.0% (6/40) were reported as non-Hodgkin lymphoma. CONCLUSION: Cytology is an effective tool available to make a diagnosis of LSE. Nuclear indentations in large atypical cells and cells with eosinophilic granular cytoplasm with sparse or abundant eosinophils in the background are an important clue in favor of leukemia over lymphoma.

Rapidly recurring massive pleural effusion as the initial presentation of sarcoidosis: A case report.

RATIONALE: Sarcoidosis is a multisystem granulomatous disease with unknown etiology. It affects mainly the lungs, but it can affect almost any other organ. Nevertheless, pleural involvement with the development of pleural effusion is relatively rare. It is usually mild and responsive to treatment with systemic steroids. Here we present a case of rapidly recurring massive unilateral pleural effusion caused by sarcoidosis that was resistant to systemic steroids. PATIENT CONCERNS: A 55-year-old lady presented with shortness of breath of 2-months duration. No other respiratory symptoms were reported. On physical examination, there were signs of left-sided pleural effusion, splenomegaly, and inguinal lymph nodes. These findings were confirmed by chest x-ray showing massive pleural effusion. Work up of the effusion revealed an exudative effusion with lymphocyte predominance. Pan-computed tomography scan revealed multiple thoracic, abdominal and inguinal lymphadenopathy; additionally, a left-sided pleural effusion and an enlarged spleen; that contained variable hypodense nodular lesions. Positron emission tomography-computed tomography showed intense uptake in the spleen and the lymph nodes. Inguinal lymph node biopsy showed non-necrotizing granulomatous inflammation. Due to suspicion of malignancy, left medical thoracoscopy was done, and biopsy of the parietal pleura showed nonspecific inflammation without evidence of malignancy or tuberculosis. DIAGNOSIS: Sarcoidosis was diagnosed based on the finding of the non-necrotizing granulomatous inflammation with no evidence of malignancy or infection on several microbiological and pathological samples. INTERVENTIONS: The patient was treated with repeated pleural fluid drainage. Steroids failed to prevent pleural effusion recurrence. Surgical left side pleurodesis was eventually performed. OUTCOMES: At more than 1 year follow up, the patient showed no recurrence of pleural effusion or development of any other symptoms. LESSONS: Sarcoidosis may rarely present with massive pleural effusion, as this presentation is rare; it is imperative to rule out other causes of massive pleural effusion. Massive pleural effusion in sarcoidosis may be steroid-resistant. Pleurodesis may have a role in such a scenario.

Molecular testing on serous effusions.

Serous effusions constitute a significant part of the material processed and diagnosed by cytopathology laboratories. Effusions may occur in a variety of clinical settings and the differential diagnosis between these conditions often requires ancillary tests. Immunohistochemistry is still the most frequently used method in this context. However, a wide array of other methods measuring the expression of DNA, mRNA, noncoding RNA, proteins, and other compounds may be applied to the diagnosis of serous effusions, particularly in the setting of cancer, as well as to studies focusing on tumor biology and understanding of tumor progression. In addition, as serous effusions provide ideal material for molecular testing, they have in recent years assumed central role as specimens informative of prediction in the context of targeted therapy, as well as prognostication. This review discusses recent studies in this field.

Root cause analysis of indeterminate diagnoses in serous fluids cytopathology.

INTRODUCTION: The International System for Reporting Serous Fluid Cytopathology proposed five diagnostic categories: Nondiagnostic (ND), Negative for Malignancy (NFM), Atypia of Undetermined Significance (AUS), Suspicious for Malignancy (SFM) and Malignant (MAL) (Primary or Metastatic). The indeterminate (AUS/SFM) categories are challenging for management. The goal of this study is to reveal the root causes contributing to indeterminate diagnoses (ID). MATERIALS AND METHODS: We searched our archives between 1 January 2017 and 30 June 2019, and performed a root cause analysis (RCA) using the "5 whys" method to determine the contributing factors of ID. RESULTS: Nine hundred eleven specimens were evaluated and diagnosed: ND (9, 1%), NFM (667, 73.2%), AUS (51, 5.6%), SFM (27, 3%) and MAL (157, 17.2%). More than one factor contributed to 38/78 ID. Low volume (<50 cc), and low cellularity were identified in 31 and 51 cases, respectively. Three cases were simply deferred to concurrent biopsy. Eleven cases were called atypical, favor reactive mesothelium despite confirmatory IHC. Atypical lymphoid population was reported in seven cases. Cellblocks (CB) were low in cellularity despite volume >1000 mL in 13 cases. Two mesotheliomas were underdiagnosed as suspicious. CONCLUSIONS: Low cellularity and low volume were the most common contributing factors, highlighting the importance of adequate sample collection. Adequate volume specimens with low cellularity may benefit from a close inspection and a second CB. Some IDs can be switched to NFM or MAL with careful consideration of clinical, radiologic findings and ancillary testing, and concurrent surgical pathology correlation when available.

Distinct compartmentalization of immune cells and mediators characterizes bullous pemphigoid disease.

Bullous pemphigoid (BP) is an autoimmune blistering disease characterized by recruitment of leucocytes into skin and release of damaging enzymes, resulting in epidermal detachment and blister formation. To better understand the role of leukotriene B4 (LTB4) and other inflammatory factors in BP pathophysiology, we conducted microscopic and immunohistochemical analyses of preserved skin biopsy sections and conducted flow cytometry and ELISA analyses of matched blood and blister fluid from BP patients. Neutrophils predominated in BP blister fluid, which also contained monocytes/macrophages and T cells, but few to no eosinophils and B cells. In contrast, BP skin histology showed a different pattern, with abundant neutrophils but eosinophils being the predominant immune cell type. LTB4 pathway and neutrophil activation markers were prevalent in BP skin lesions and strongly associated with perivascular neutrophils. Blister fluid neutrophils, monocytes/macrophages and eosinophils all exhibited increased surface expression of leukotriene A4 hydrolase and neutrophil elastase (P = .002 for both). Blister fluid was also enriched in interleukins (IL)-1α, IL-1ß, IL-8, IL-10, IL-18, monocyte colony-stimulating factor (M-CSF) and vascular endothelial growth factor (VEGF). Our findings suggest differential leucocyte recruitment from blood into dermis and from dermis into blister, which correlates with disease activity, and presents potential new treatment opportunities for BP.

The Use of a Novel Quantitative Marker of Echogenicity of Pleural Fluid in Parapneumonic Pleural Effusions.

Background: Thoracic ultrasound is an essential tool in the daily clinical care of pleural effusions and especially parapneumonic pleural effusions (PPEs), in terms of diagnosis, management, and follow-up. Hypoechogenicity index (HI) is a quantitative marker of pleural fluid echogenicity. We aimed to examine associations of HI with pleural inflammation in patients with PPE. Methods: All patients included underwent a thoracic ultrasound with HI determination at the first day of their admission for a PPE. Thoracentesis was performed in all patients. Demographics, laboratory measurements, and clinical data were collected prospectively and recorded in all subjects. Results: Twenty-four patients with PPE were included in the study. HI was statistically significantly correlated with intensity of inflammation as suggested by pleural fluid LDH (p < 0.001, r = -0.831), pleural fluid glucose (p=0.022, r = 0.474), and pleural fluid pH (p < 0.001, r = 0.811). HI was correlated with ADA levels (p=0.005, r = -0.552). We observed a statistically significant correlation of HI with pleural fluid total cell number (p < 0.001, r = -0.657) and polymorphonuclears percentage (p=0.02, r = -0.590), as well as days to afebrile (p=0.046, r = -0.411), duration of chest tube placement (p < 0.001, r = -0.806), and days of hospitalization (p=0.013, r = -0.501). Discussion. HI presents a fast, easily applicable, objective, and quantitative marker of pleural inflammation that reliably reflects the intensity of pleural inflammation and could potentially guide therapeutic management of PPE.

Idiopathic Pleural Effusions: Characteristics and Discrimination From Cytology-Negative Malignant Pleural Effusions.

BACKGROUND: The etiology of pleural effusions often remained unknown notwithstanding surgical pleural biopsy and further clinical observation. A better understanding of clinical characteristics of patients with idiopathic pleural effusion (IPE) may improve the ability to differentiate between IPEs and cytology-negative malignant pleural effusions (MPEs) and facilitate the identification of patients requiring invasive investigation. However, little is known about the clinical factors that can help distinguish patients with IPE from those with cytology-negative MPE. MATERIALS AND METHODS: Patients who were diagnosed with IPE or cytology-negative MPE between 2010 and 2017 were enrolled in this retrospective study. Clinical, laboratory and radiologic characteristics were compared between patients with IPE and cytology-negative MPE. Diagnostic performances of predictors for IPE were assessed using receiver operating characteristic curves. RESULTS: Of 146 patients undergoing pleural biopsy owing to cytology-negative pleural effusion of uncertain cause, MPE was confirmed in 54 patients. IPE was ultimately diagnosed in 22 patients. Multivariate analysis demonstrated that a minimal amount of pleural effusion (odds ratio [OR] = 12.41, P = 0.039), presence of pleural nodularity (OR = 0.01, P < 0.001) and pleural fluid carcinoembryonic antigen levels less than 14 ng/mL (OR = 87.59, P = 0.002) were independent factors for distinguishing IPEs from cytology-negative MPEs. A combination of the absence of pleural nodularity with pleural fluid carcinoembryonic antigen levels less than 14 ng/mL yielded an area under the curve of 0.94 (sensitivity = 91% and specificity = 96%). CONCLUSIONS: Using these readily available parameters to identify IPE in patients with cytology-negative exudative effusion of unknown cause can help guide decision-making when choosing to perform an invasive pleural biopsy or to take a conservative approach.

Cytological and microbiological characteristics of middle ear effusions in brachycephalic dogs.

BACKGROUND: Middle ear effusion is common in brachycephalic dogs with similarities to otitis media with effusion in children. Association with the cranial and eustachian tube morphology and bacterial infection is suspected in both species. HYPOTHESIS/OBJECTIVES: To determine cytological and bacteriological features of middle ear effusions in dogs, provide information on histological features, and further assess the dog as a model of the human disease. ANIMALS: Sixteen live dogs, 3 postmortem cases of middle ear effusion, and 2 postmortem controls. METHODS: Prospective; clinical investigation using computed tomography, magnetic resonance imaging, video-otoscopy, myringotomy; cytological assessment of 30 and bacteriology of 28 effusions; histology and immunohistochemistry (CD3 for T-lymphocytes, Pax5 for B lymphocytes and MAC387 for macrophages) of 10 middle ear sections. RESULTS: Effusions were associated with neurological deficits in 6/16 (38%) and concurrent atopic dermatitis and otitis externa in 9/16 (56%) of live cases. Neutrophils and macrophages predominated on cytology (median 60 [range 2%-95.5%] and 27 [2%-96.5%]) whether culture of effusions was positive or not. In histology sections, the mucosa was thickened in affected dogs but submucosal gland dilatation occurred in affected and unaffected dogs. There was no bacterial growth from 22/28 (79%) of effusions. Bacteria isolated from the other 6 (21%) were predominantly Staphylococcus pseudintermedius (4/6, 67%). CONCLUSIONS AND CLINICAL IMPORTANCE: Clinical, morphological, and cytological findings in middle ear effusions of dogs and people suggest similar pathogeneses. Middle ear effusion of dogs could be a useful model of human otitis media with effusion. Such comparisons can improve understanding and management across species.

Bicavitary eosinophilic effusion in a dog with coccidioidomycosis.

This is a case of coccidioidomycosis in a dog, examined for vomiting and labored breathing. Physical examination and thoracic and abdominal imaging revealed pleural and peritoneal effusions, both of which exhibited neutrophilic inflammation with a substantial eosinophilic component. The dog had positive IgM and IgG coccidioidomycosis titers at initial evaluation. The eosinophilic component of the inflammation was attributed to coccidioidomycosis. The dog underwent approximately 6 months of fluconazole treatment, with both effusions and clinical signs improving after 6 weeks. Three months after cessation of antifungal treatment, the dog developed a mid-diaphyseal lytic and proliferative lesion in the left radius caused by Coccidioides spp. This case illustrates the importance of consideration of coccidioidomycosis when an eosinophilic cavitary effusion is present in dogs that live in or have traveled to endemic regions.

What's the Score? Do Pleural Effusion Clinical Scoring Systems Help in Management of Disease?

Pleural effusion is a common condition, affecting over 3,000 people per million population every year. More than 50 causes of pleural effusions are known, including pleural infection and malignant pleural disease. These conditions place a large burden on healthcare systems with one-fourth of patients with pleural infection having a length of hospital stay of more than 1 month. Malignant pleural effusion represents advanced malignant disease with a correspondingly high mortality. Prognostic models using clinical information in combination with blood or pleural fluid biomarkers predicting survival and other outcome measures are therefore a priority in improving clinical care, and potentially outcomes. Identifying patients with poor prognosis may help avoid discomfort and unnecessary interventions at the end of their lives, while, on the other hand, individuals with scores predicting a particularly good prognosis might be selected for more aggressive early treatment. Such scores must be based on data representing routine practice in a general hospital and variables chosen based on their clinical availability at clinical decision points (i.e., before treatment is instituted), making the findings widely applicable.

Clinical approach and review of causes of a chylothorax.

A chylothorax, also known as chylous pleural effusion, is an uncommon cause of pleural effusion with a wide differential diagnosis characterized by the accumulation of bacteriostatic chyle in the pleural space. The pleural fluid will have either or both triglycerides >110 mg/dL and the presence of chylomicrons. It may be encountered following a surgical intervention, usually in the chest, or underlying disease process. Management of a chylothorax requires a multidisciplinary approach employing medical therapy and possibly surgical intervention for post-operative patients and patients who have failed medical therapy. In this review, we aim to discuss the anatomy, fluid characteristics, etiology, and approach to the diagnosis of a chylothorax.

Muscle-strain injury exudate favors acute tissue healing and prolonged connective tissue formation in humans.

Traumatic strain injury in skeletal muscle is often associated with fluid accumulation at the site of rupture, but the role of this injury exudate (EX) in cellular responses and healing is unknown. We aimed to characterize the EX sampled from human hamstring or calf muscles following a strain injury (n = 12). The cytokine and growth-factor profile, gene expression, and transcriptome analysis of EX-derived cells were compared with blood taken simultaneously from the same individuals. Cellular responses to the EX were tested in 3-dimensional (3D) culture based on primary human fibroblasts and myoblasts isolated from hamstring muscles. The EX contained a highly proinflammatory profile with a substantial expression of angiogenic factors. The proinflammatory profile was present in samples taken early postinjury and in samples aspirated several weeks postinjury, suggesting persistent inflammation. Cells derived from the EX demonstrated an increased expression of fibrogenic, adipogenic, and angiogenesis-related genes in comparison with blood cells. The injury EX stimulated fibroblast proliferation 2-fold compared with plasma, whereas such an effect was not seen for myoblasts. Finally, in 3D cell culture, the EX induced an up-regulation of connective tissue-related genes. In summary, EX formation following a muscle-strain injury stimulates fibroblast proliferation and the synthesis of connective tissue in fibroblasts. This suggests that the EX promotes an acute tissue-healing response but potentially also contributes to the formation of fibrotic tissue in the later phases of tissue repair.-Bayer, M. L., Bang, L., Hoegberget-Kalisz, M., Svensson, R. B., Olesen, J. L., Karlsson, M. M., Schjerling, P., Hellsten, Y., Hoier, B., Magnusson, S. P., Kjaer, M. Muscle-strain injury exudate favors acute tissue healing and prolonged connective tissue formation in humans.

Cytological evaluation of pericardial fluids: A 5 years experience in tertiary care center.

BACKGROUND: Cytological examination of pericardial effusion fluids is important in diagnosing the etiology of underlying disease, staging, and prognosis of cancer. AIMS AND OBJECTIVES: (1) To study cytological evaluation of pericardial effusions in various pathological conditions in a tertiary care center. (2) To analyze their frequency and clincopathological correlation of the diagnosis. MATERIALS AND METHODS: Our study was a retrospective study performed in the Department of Pathology from 1st January 2012 to 31st December 2016. The study sample included all the pericardial effusions submitted in the pathology department for cytological evaluation. Clinical details and relevant parameters correlated with clinical findings. Each fluid underwent cytospin and cytocentrifuge along with preparation of conventional smears. RESULTS: Of 120 cases, 80% were of benign effusion and 20% were of malignant effusion. Male-to-female ratio was 1.44:1 with patient age ranging from 3 to 90 years. CONCLUSION: Benign effusions can been seen in younger age group and malignant ones in the older age group. The preliminary pericardial fluid analysis in resource-limited settings is the most convenient and cost-effective method for accurate diagnosis. It reduces the demand of invasive investigations and its complications. At times, it is the first test to point toward underlying malignant process thereby affecting the prognosis, survival, and treatment outcome of the patient.

Cognate Interaction With CD4+ T Cells Instructs Tumor-Associated Macrophages to Acquire M1-Like Phenotype.

The immunosuppressive tumor microenvironment (TME) established by tumor cells, stromal cells and inhibitory immune cells counteracts the function of tumor reactive T cells. Tumor associated macrophages (TAMs) showing functional plasticity contribute to this process as so called M2-like macrophages can suppress the function of effector T cells and promote their differentiation into regulatory T cells (Tregs). Furthermore, tumor antigen specific CD4+ T effector cells can essentially sustain anti-tumoral immune responses as shown for various tumor entities, thus suggesting that cognate interaction between tumor antigen-specific CD4+ Th1 cells and TAMs might shift the intra-tumoral M1/M2 ratio toward M1. This study demonstrates repolarization of M2-like PECs upon MHC II-restricted interaction with tumor specific CD4+ Th1 cells in vitro as shown by extensive gene and protein expression analyses. Moreover, adoptive transfer of OVA-specific OT-II cells into C57BL/6 mice bearing OVA expressing IAb-/- tumors resulted in increased accumulation of M1-like TAMs with enhanced M1 associated gene and protein expression profiles. Thus, this paper highlights a so far underestimated function of the CD4+ Th1/TAM axis in re-conditioning the immunosuppressive tumor microenvironment.

Bacteriology and cytology of otic exudates in 41 cavalier King Charles spaniels with primary secretory otitis media.

BACKGROUND: Primary secretory otitis media (PSOM) in the cavalier King Charles spaniel (CKCS) is similar to otitis media with effusion (OME) in humans. A proposed aetiology of OME is inflammation of the middle ear mucosa, usually due to bacterial infection, leading to auditory tube dysfunction. HYPOTHESIS/OBJECTIVES: Our objective was to characterize the microbiological and cytological findings of otic exudates from the external ear canal (EEC) (n = 68) and middle ear (ME) (n = 69) from 41 CKCSs with PSOM. METHODS AND MATERIALS: Swab samples from the EEC and mucus aspirated from the ME after performing a myringotomy were obtained for bacterial culture and cytological analysis. RESULTS: Fifty-five of 68 (81%) EEC and 46 of 69 (67%) ME yielded no bacterial growth. Thirty-eight of the 68 (56%) ears had no microbial growth from neither the EEC nor ME; seven (10%) had bacteria isolated from the EEC only; 17 (25%) had bacteria isolated from the ME only, and six (8%) had bacteria isolated from both EEC and ME. Thirty-four total bacterial isolates were cultured from ME. The most common bacterial species isolated were coagulase-negative staphylococci, followed by Staphylococcus pseudintermedius. Otic cytology identified coccoid organisms in only three of 68 EEC and four of 69 ME. CONCLUSIONS: The role of bacteria in the pathogenesis of PSOM in CKCS is unclear. The majority of the EEC and ME of the CKCS with PSOM were negative by conventional bacterial culture and the cytological presence of bacteria was not correlated with culture positives. The potential role of noncultivable microbiota in PSOM requires exploration using molecular methods.

Cellular content plays a crucial role in Non-typeable Haemophilus influenzae infection of preinflamed Junbo mouse middle ear.

Non-typeable Haemophilus influenzae (NTHi) is a major pathogen causing acute otitis media (AOM). The relationship between the cellular content of the middle ear fluid (MEF) during AOM and infection of NTHi is poorly understood. Using the Junbo mouse, a characterised NTHi infection model, we analysed the cellular content of MEF and correlated the data with NTHi titres. The MEF of the Junbo mouse was heterogeneous between ears and was graded from 1 to 5; 1 being highly serous/clear and 5 being heavily viscous/opaque. At seven-day post-intranasal inoculation, NTHi was not found in grade-1 or 2 fluids, and the proportion of MEF that supported NTHi increased with the grade. Analyses by flow cytometry indicated that the cellular content was highest in grade-4 and 5 fluids, with a greater proportion of necrotic cells and a low-live cell count. NTHi infection of the middle ear increased the cell count and led to infiltration of immune cells and changes in the cytokine and chemokine levels. Following NTHi inoculation, high-grade infected MEFs had greater neutrophil infiltration whereas monocyte infiltration was significantly higher in serous noninfected low-grade fluids. These data underline a role for immune cells, specifically monocytes and neutrophils, and cell necrosis in NTHi infection of the Junbo mouse middle ear.

The value of exfoliative cell cytology in the diagnosis of exudative pleural effusions.

The sensitivity and specificity of exfoliative cell cytology for the diagnosis of exudative pleural effusions varies widely according to the etiologic causes. The aim of this study is to assess the diagnostic value of exfoliative cell cytology for the identification of exudative pleural effusions. This is a retrospective study of the patients with an exudative pleural effusion admitted at our clinic in the last twenty years. We have conducted the clinical, the cytological findings, and the diagnostic results of six hundred patients from hospital records.  Male to female ratio was 2.2:1 with a mean age of 42.8 years (range 18-78 years) among the patients. Samples were processed and evaluated according to the standard methods. Cytology results were reviewed and the patients were stratified according to the final diagnosis of their disease. Of the six hundred exudative effusions, 240 were malignant on exfoliative cytology pleural fluid alone. Adenocarcinoma was the most common type of malignancy. Tuberculosis was the second most frequent etiology for the exudative effusions followed by infection and collagen vascular diseases. Diagnostic accuracy of cytology showed a good correlation with the final diagnosis with an overall 70.1% sensitivity, 62.5% specificity, and a 95.9% positive predictive value for all exudative pleural effusions. Cytologic examination of the pleural fluid is a simple non-invasive procedure as the initial step for the diagnostic work up of patients with a pleural effusion.  Exfoliative cytology provides high a final diagnostic yield for the identification of an exudative pleural effusion etiology. Furthermore, cytologic analysis leads the clinician into the correct diagnostic pathway as the most informative laboratory tool even when it was not diagnostic by itself for equivocal cases.

Pediatric pleural tuberculosis.

Background: Pleural tuberculosis (TB) diagnosis is sometimes controversial because the microbiologic confirmation ratio is very low in pleural fluid. There are few pediatric pleural TB case series in the literature. Methods: We retrospectively evaluated our TB cases below 18 years of age and extracted pleural TB cases. Results: Seven cases with pleural TB were identified. About 42.9% of the patients had isolated pleural TB whereas 57.1% of the patients had accompanying pulmonary TB. Lymphocytic pleural effusion and increased adenosine deaminase (ADA) (>40 U/L) level are found in 85.7% of the patients. Six patients had uncomplicated effusion (transudate) according to Light's criteria and one had complicated effusion (exudate). Lung decortication was needed in three patients. All patients were given 6 months anti-TB medication and recovered completely. Conclusion: In the lymphocyte-predominant pleural effusion, an increased ADA level highly supported TB disease. The complicated effusion (exudate) in pleural TB is not rule; uncomplicated effusion (transudate) could be seen.

Carbimazole-induced eosinophilic pleural effusion.

We report the case of a 41-year-old woman who presented with a unilateral exudative effusion with prominent eosinophils on pleural cytology. Carbimazole had been started 4 weeks prior to presentation. No immediate cause was identified on imaging or laboratory testing. The effusion persisted at 2-month follow-up. Further investigation at this time, including autoimmune serology was negative. At 2-month follow-up, the effusion was loculated on ultrasound imaging and had a low fluid pH on diagnostic aspiration, in keeping with an empyema. The patient received treatment for pleural empyema, including antibiotics, intercostal drain insertion and video-assisted thoracoscopic pleural biopsy. Carbimazole was stopped, and following treatment for the empyema, the effusion did not reaccumulate.This case illustrates the diagnostic difficulties that pleural effusions may present. It demonstrates that drug reactions should be considered in the differential diagnosis following thorough investigation for other potential causes and also describes the complications that may occur.