Pancreaticopleural fistula (PPF) is a rare complication of chronic pancreatitis described more commonly in adults with alcoholic and necrotizing pancreatitis. We report a rare case of ruptured mediastinal pseudocyst with the formation of PPF in a 15-year-old boy who presented with progressive dyspnea and large left-sided pleural effusion that recurred despite repeated drainage. On the basis of imaging findings and pleural fluid analysis, the diagnosis of PPF with ruptured mediastinal pseudocyst was made. The diagnosis of PPF should be considered in patients with non-resolving large left-sided pleural effusions. The diagnosis can be confirmed either by significantly raised amylase levels in pleural fluid or direct visualization of the fistula on Computed tomography/magnetic resonance cholangiopancreatography.
ObjectivePre-treatment biomarkers to estimate overall survival (OS) for malignant pleural effusion (MPE) are unidentified, especially those in pleural fluid. We evaluated the relationship between OS and total protein–chloride ratio in malignant pleural effusion (PE TPClR).Materials and MethodsA retrospective study was undertaken to identify patients from 2006 to 2018 who had pathologically or cytologically confirmed MPE and received no tumor-targeted therapy. We recorded the pre-treatment clinicopathologic characteristics and follow-up status. OS was estimated by the Kaplan–Meier method, and the association between variables and OS was evaluated by Cox proportional hazards models.ResultsWe screened 214 patients who met the eligibility criteria. The optimal cutoff value for the PE TPClR was set at 0.53. The univariate analysis showed that there was a significant correlation between PE TPClR and OS (P < 0.001). The multivariate analysis between OS and the variables selected from the univariate analysis showed that the levels of neutrophil, alkaline phosphatase, neuron-specific enolase, platelets, albumin in peripheral blood, and white blood cells in pleural effusion were also independent predictors of OS.ConclusionIn patients with MPE, pre-treatment PE TPClR independently predicts OS. Although further research is necessary to generalize our results, this information will help clinicians and patients to determine the most appropriate treatment for MPE patients.
Exposure to silica nanoparticles has been associated with pleural effusions (PEs) in animal models and case series. We hypothesized that some PEs labelled as “idiopathic” could, in fact, be secondary to inhalation of silica.
A retrospective case control study was designed utilizing a prospectively maintained pleural database. Cases, represented by idiopathic PEs, were matched by age and gender to control patients who had been diagnosed with malignant, cardiac, or infectious PEs. A survey consisting of questions about occupational life and possibility of silica inhalation was conducted. In a subgroup of patients, pleural fluid concentrations of silica were quantified by plasma atomic emission spectrometry analysis. Also, the pleural biopsy of a silica-exposed case was subjected to an energy dispersive X-ray spectroscopy (EDX) to identify the mineral, the size of which was determined by electron microscopy.
A total of 118 patients (59 cases and 59 controls) completed the survey. There were 25 (42%, 95% CI 31–55%) and 13 (22%, 95% CI 13–34%) silica-exposed workers in case and control groups, respectively. The exposure attributable fraction was 0.62 (95% CI 0.14–0.83). Four of eight exposed cases showed detectable levels of silica in the pleural fluid (mean 2.37 mg/L), as compared to none of 16 tested controls. Silica nanoparticles of 6–7 nm were identified in the pleural biopsy of an exposed case patient.
It is plausible that some idiopathic PEs could actually be caused by occupational silica inhalation.
Đặt vấn đề: Dựa vào tính chất các mẫu dịch khoang cơ thể có hiện diện các mảnh DNA lơ lửng giúp thực hiện chẩn đoán đột biến EGFR. Từ nguyên lý này, chúng tôi thực hiện nghiên cứu với các mục tiêu sau: Khảo sát tỉ lệ dương tính đột biến EGFR trong các mẫu dịch khoang cơ thể; và hảo sát tỉ lệ chẩn đoán đột biến gen EGFR trong mẫu bệnh phẩm mô học đúc khối parafin với mẫu dịch khoang cơ thể trên cùng một bệnh nhân.
Phương pháp nghiên cứu: Hồi cứu, thống kê mô tả cắt ngang. Các trường hợp ung thư phổi không tế bào nhỏ được chẩn đoán đột biến EGFR bằng mẫu bệnh phẩm đúc khối paraffine với Test EGFR Version 1 và mẫu bệnh phẩm dịch các khoang cơ thể (Dịch màng phổi, dịch màng tim, dịch màng bụng, dịch não tủy) với Test EGFR Version 2.
Kết quả: Có 117 ca bệnh trong nghiên cứu: Kết quả chẩn đoán đột biến gen EGFR trên mẫu mô học đúc khối paraffine: (+) 49 ca # 41,88%, tương đương với các thống kê ở trong nước và thế giới (Châu Á). Đa số vẫn là hai loại đột biến nhạy thuốc TKIs Exon 19 Deletion và Exon 21 L858R (53% và 23%). Kết quả chẩn đoán đột biến EGFR trên các mẫu dịch khoang cơ thể: Đa số mẫu dịch khoang cơ thể thực hiện chẩn đoán đột biến EGFR là dịch màng phổi (91 ca # 77,77%). Tỉ lệ phát hiện đột biến trong mẫu dịch màng phổi và dịch não tủy cao nhất (29,67% & 83,33%). So sánh tỉ lệ phát hiện đột biến EGFR trên mẫu dịch khoang cơ thể (35 /117 ca # 29,91%) với tỉ lệ phát hiện trên mẫu mô học thấp hơn có ý nghĩa thống kê (29,91% ↔ 41,88% với P = 0,0125). So sánh với các nghiên cứu khác trên thế giới cho thấy đa số các nghiên cứu cho kết quả cao hơn so với nghiên cứu tại bệnh viện Phạm Ngọc Thạch.
Kết luận: Khảo sát chẩn đoán đột biến EGFR trong dịch các khoang cơ thể, đặc biệt trong các mẫu dịch có quá ít tế bào ác tính, kết quả dương tính 29,91%. Tỉ lệ cao nhất trong dịch màng phổi và dịch não tủy. Tuy nhiên, khả năng phát hiện đột biến EGFR trong các dịch khoang cơ thể thấp hơn so với trên các bệnh phẩm mô học (29.91% < 41,88%). Và đô tương đồng giữa hai loại bệnh phẩm này là 71,42%. Cần nâng cao kỹ thuật thực hiện chẩn đoán đột biến EGFR trong mẫu dịch khoang cơ thể với các phương pháp có độ nhạy cao hơn: ddPCR, NGS…
DIAGNOSTIC EGFR GENE MUTATIONS IN NON SMALL CELL LUNG CANCER WITH SPECIMENS OF BODY CAVITY FLUIDS
Introduction: Based on the nature of the body cavity fluid samples, there is the presence of suspended DNA fragments that help to make an EGFR mutation diagnosis. From this principle, we have conducted this research with the following objectives: Investigate the positive rate of EGFR mutations in body cavity fluid samples, and explore the diagnosis rate of EGFR gene mutations in paraffin block histology samples with body cavity fluid samples in the same patients.
Methods: In a retrospective study, cases of NSCLC were diagnosed with EGFR mutations by paraffin block histological specimens with Test EGFR Version 1 and body cavity fluid samples (pleural fluid, pericardial fluid, peritoneal fluid, cerebrospinal fluid) with Test EGFR Version 2.
Results: There are 117 cases in the research: Results of EGFR mutation diagnosis on paraffin block histology: (+) 49 cases # 41.88%, equivalent to statistics in Vietnam and the World (Asia). The majority are still two types of drug - sensitive mutants TKIs: Exon 19 Deletion and Exon 21 L858R (53% and 23%). Results of diagnosis of EGFR mutation in samples of body cavity fluids: Most samples of body cavity performing diagnosis of EGFR mutation were pleural fluid (91 cases # 77.77%). The highest rate of detection of mutations in pleural and cerebrospinal fluid samples (29.67% & 83.33%). Comparing the rate of detection of EGFR mutation in body fluid samples (35/117 cases # 29.91%) with the statistically lower rate of detection in histological samples (29.91%-41, 88% with P = 0.0125). Compared with other studies in the world, most studies have higher results than those at Pham Ngoc Thach Hospital.
Conclusion: Survey on the diagnosis of EGFR mutations in body cavity fluid samples, especially in fluid samples with too few malignant cells, showed positive results of 29.91%. The highest percentage is in pleural fluid and cerebrospinal fluid. However, the ability to detect EGFR mutations in body cavity fluid samples was lower than in histological specimens (29.91% < 41.88%). And the similarity between these two samples is 71.42%. Therefore, it is necessary to improve the technique of performing EGFR mutation diagnosis in body cavity fluid samples with more sensitive methods: ddPCR, NGS...
Keywords: Non small cell lung cancer (NSCLC), Formalin - Fixed Paraffin - Embedded Tissue (FFPET), Body cavity fluids, Cell Free DNA, Cellular DNA.
Pleural effusions appearing within the first 30 postoperative days following coronary artery bypass grafting (CABG) are classified as early and believed to be directly related to the surgery. The characteristics of such effusions are well-described. Orthotopic heart transplantation is also known to be complicated by pleural effusions; however, their characteristics have not been systematically reported. We assessed the features of early postoperative pleural effusions after heart transplantation and compared them to those of early effusions following CABG.
We retrospectively collected demographic, clinical, and laboratory data for patients who underwent either orthotopic heart transplantation (study group) or CABG (comparison group) at our institution and whose postoperative course within 30 days was complicated by new or worsening pleural effusion that prompted drainage. Patients subjected to analysis consisted only of those with sufficiently complete laboratory profiles to permit adequate characterization of the nature of their pleural fluid.
Out of 251 orthotopic heart transplant recipients, seven (2.8%) were found to have sufficiently complete pleural fluid results to be included in the study group. Out of 1,506 patients who underwent CABG, 32 (2.1%) had sufficiently complete pleural fluid results and formed the comparison group. The radiological appearance of pleural effusions in both groups was similar: bilateral in at least half and exclusively moderate to large. Effusions complicating both surgeries were exudative in close to 90% of cases. For those with available leukocyte differential counts, the pleural fluid of the post-orthotopic heart transplantation group was more often neutrophilic (3/5, 60%), whereas the fluid of the post-coronary artery bypass grafting group was more often lymphocytic (22/32, 69%) and tended to be hemorrhagic (median RBC count 33,000 cells/µL vs. 10,000 cells/µL). None of the comparisons of pleural fluid characteristics between the two groups reached statistical significance.
This small, descriptive study is the first to systematically report the fluid characteristics of pleural effusions complicating orthotopic heart transplantation within the first 30 postoperative days and to compare this group to those who developed effusions after CABG. Our findings revealed both similarities and differences in the pleural fluid characteristics between these two types of patients.
BackgroundTuberculous 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.ObjectiveWe determined the frequency of T helper (Th) subtypes in the PEs for differentiation of Tb and non-Tb patients.MethodsThirty 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.ResultsTreg 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.ConclusionADA, Treg cells, and CD4+IL-9+ cells may differentiate TPE from non-TPE patients. However, these results need validation in an independent large cohort.