Tumour necrosis factor alpha in the diagnostic assessment of pleural effusion.
(65/1198)
We investigated the role of tumour necrosis factor-alpha (TNF) in the evaluation of pleural effusion aetiology. Using a commercially-available ELISA kit, concentrations of TNF were measured in the serum and pleural fluid of patients with malignant effusions (n=19), uncomplicated parapneumonic effusions (n=13), and exudative (n=13) and transudative (n=13) effusions due to congestive heart failure (CHFex and CHFtr, respectively). Serum TNF did not differ significantly between the four groups (p>0.05). In the group with malignancy, pleural fluid TNF was significantly higher than in the other groups (p<0.001), which were not significant different from each other (p>0.05). However, a considerable overlap between all four groups was found. Pleural fluid TNF was significantly higher than serum TNF in the malignant and the uncomplicated parapneumonic groups (p<0.001), and there was a significant positive correlation between serum TNF and pleural fluid TNF in the group with uncomplicated parapneumonic effusion (r=0.7, p<0.005), in the group with CHFex (r=0.54, p<0.01), and in the group with CHFtr (r=0. 8, p<0.005), but not in the group with malignancy. Pleural fluid TNF:serum TNF (TNF ratio) was significantly higher in the malignancy group than in the other groups (p<0.001); no significant difference was found between the other three groups (p>0.05). At an optimal cut-off point of 2.0 for TNF ratio, determined by ROC analysis for discrimination between malignant and non-malignant groups, sensitivity was 84%, specificity 90%, and total accuracy 88% (p<0. 0001). TNF ratio might be helpful in the diagnostic assessment of exudative pleural effusion. (+info)
Pulmonary endothelinergic system in experimental congestive heart failure.
(66/1198)
OBJECTIVES: Endothelin-1 (ET-1), plays an important role in the pathophysiology of CHF and the pulmonary endothelium is an early hemodynamic target in diastolic left ventricular dysfunction. Therefore we hypothesized that the lung is a main source of humoral endothelin in CHF and that its secretion is proportional to the degree of heart failure. METHODS AND RESULTS: We used rats with coronary artery ligation as an experimental model of either compensated or decompensated heart failure, depending on infarct size. Reverse transcriptase polymerase chain reaction (RT-PCR) revealed that in the lung, the expression of preproET-1 mRNA was higher in decompensated HF than in control and compensated HF rats (P<0.001). Run-on assay demonstrated that ET-1 overexpression is regulated at a transcriptional level (P<0.01). In contrast, there was no change in ET-1 mRNA expression in aortae, left ventricular myocardium and skeletal muscle. The expression of endothelin-converting enzyme (ECE)-1 mRNA was not modified and the expression of ET(B) receptor mRNA in the congestive lung was significantly lower than in control and compensated HF rats (P<0.0001), while the expression of ET(A) receptor mRNA did not differ between groups. The lung and plasma ET-1 peptide levels were respectively 4.2 and 9 fold higher in the rats with decompensated HF than in control rats (P<0.05; P<0.0001). Organoculture experiments showed that the lung ET-1 peptide secretion level in rats with decompensated HF was higher than that in control rats (P<0.01). In contrast, there was no change in ET-1 peptide secretion by the left ventricular myocardium and skeletal muscle. In plasma of rats with decompensated HF, the rate of bigET-1 conversion to ET-1 was 22%. ET-1 peptide was also present in the pleural effusion of decompensated heart failure. Plasma ET-1 concentration was significantly correlated with upstream markers of left ventricular diastolic dysfunction, with the expression of preproET-1 mRNA in the lung, with lung and pleural ET-1 concentration and with the expression ratio of ET-1/ET(B) receptor mRNA. CONCLUSION: Taken together, these data suggest that overexpression of ET-1 and down-regulation of ET(B) receptors in the lung are determinants of circulating endothelin in CHF. As a corollary, increased plasma endothelin may provide evidence of pulmonary endothelial dysfunction in CHF. (+info)
Elevated IL-5 levels in pleural fluid of patients with paragonimiasis westermani.
(67/1198)
To investigate the pathogenic mechanisms of eosinophilic pleural effusion in patients with paragonimiasis, we measured the levels of IL-5, granulocyte-macrophage colony-stimulating factor (GM-CSF) and interferon-gamma (IFN-gamma) in pleural effusions. Samples were obtained from 11 patients with Paragonimus westermani infection. In addition, samples from 12 patients with pleural transudates, 16 with tuberculous pleurisy, seven with empyema and 20 with lung cancer were also examined. Eosinophilia was remarkable in peripheral blood (range 4-34%, median 23.4%) and pleural fluid (range 0-95%, median 71%) of paragonimiasis patients. IL-5 concentrations in pleural effusions of paragonimiasis were markedly higher than those in other groups. Although marked elevation of GM-CSF and IFN-gamma levels was observed in pleural effusion of empyema and tuberculosis patients, it was marginal in the pleural effusion of paragonimiasis patients. In paragonimiasis patients, IL-5 levels in the pleural effusion correlated well with the percentage of eosinophils in peripheral blood and pleural fluid. Such a correlation was not observed between GM-CSF levels in pleural effusion and percentages of eosinophils in pleural fluid or peripheral blood. Our findings suggest that in paragonimiasis IL-5 in the local inflammatory site is particularly important in mediating eosinophilia in peripheral blood and pleural effusion. (+info)
Contralateral pleural effusion during chemotherapy for tuberculous pleural effusion.
(68/1198)
A 25 year old woman developed a right pleural effusion 6 weeks after commencement of short course chemotherapy for left sided tuberculous pleural effusion. Since the patient improved following continuation of the same treatment, it is presumed to be a case of paradoxical response to anti-tuberculosis treatment. (+info)
Pleural effusion in sarcoidosis: a report of six cases.
(69/1198)
Six (4 percent) of 150 patients with sarcoidosis had a pleural effusion. A review of the literature revealed seven more patients with pleural sarcoidosis. Analysis of the 13 patients reported so far did not reveal any clinical, radiological, or laboratory feature which may be of diagnostic significance. The diagnosis of pleural sarcoidosis was based on clinical or radiographic grounds and histological evidence of noncaseating granulomata. In three of the patients pleural fluid resolved spontaneously; the other three were treated with corticosteroids. It is suggested that pleural involvement in sarcoidosis, especially in Negroes, may be more frequent than is generally realized and the effusion may occur either at the time of initial presentation or later in the course of the disease. (+info)
Yellow nail syndrome: does protein leakage play a role?
(70/1198)
Yellow nail syndrome is characterized by primary lymphoedema, recurrent pleural effusion and yellow discoloration of the nails. Although mechanical lymphatic obstruction is assumed to be the underlying pathology, it cannot explain the common finding of high albumin concentration in the pleural space. This paper describes a case of yellow nail syndrome presenting with the classical triad of lymphoedema, recurrent pleural effusion and yellow discoloration of the nails, associated with persistent hypoalbuminaemia and increased enteric loss of albumin. Based on the findings in this case and those in the literature, it is speculated that increased microvascular permeability may contribute to the pathogenesis of this syndrome. (+info)
Boerhaave syndrome: report of a case treated non-operatively.
(71/1198)
An unique case of Boerhaave's Syndrome is presented in which the patient survived without any surgical treatment. We believe that this was due to non-contamination of the mediastinal and pleural cavities as shown by serial contrast roentgenograms of the esophagus. (+info)
Expression profile of human herpesvirus 8 (HHV-8) in pyothorax associated lymphoma and in effusion lymphoma.
(72/1198)
AIMS: Pyothorax associated lymphoma (PAL) occurs in a clinical setting of longstanding pyothorax or chronic inflammation of the pleura. Like primary effusion lymphoma, it has an association with Epstein-Barr virus (EBV), and is confined to the pleural cavity, but has differing morphological and phenotypic features. Human herpesvirus 8 (HHV-8) has been consistently reported in primary effusion lymphoma. This study examines the immunophenotype of two European cases of PAL, investigates the presence of HHV-8 and its expression profile, and assesses whether PAL is similar to other effusion lymphomas. METHODS: Material was obtained from two European cases of PAL. Immunocytochemical analysis was performed using antibodies against CD45, CD20, CD79a, CD45RAA, CD3, CD43, CD45RO (UCHL1), CD30, BCL-2, CD68, epithelial membrane antigen (EMA), BCL-6, p53, Ki-67, kappa light chain, lambda light chain, and the EBV antigens latent membrane protein 1 (LMP-1) and EBV encoded nuclear antigen 2 (EBNA-2). The cases were examined for HHV-8 by means of polymerase chain reaction in situ hybridisation (PCR-ISH), solution phase PCR, in situ hybridisation (ISH), and real time quantitative TaqMan PCR to HHV-8 open reading frame 26 (ORF-26) and viral (v) cyclin encoding regions. The expression profile of HHV-8 in PAL and in BC-1 and BC-3 cells was assessed by RNA TaqMan PCR to the HHV-8 genes encoding v-cyclin, v-IL-6, and G protein coupled receptor (GPCR). RESULTS: Both cases expressed CD24, CD20, CD79a, BCL-2, light chain restriction, and high Ki-67 staining. EBV was identified by EBER-ISH in one case. HHV-8 was not identified by solution phase PCR, but was detected by PCR-ISH (sensitivity of 1 viral genome copy/cell) in 35% of the cells and by TaqMan PCR, which showed 50-100 HHV-8 copies/2,000 cell genome equivalents (sensitivity of 1 viral genome in 10(6) contaminating sequences). HHV-8 v-IL-6, v-cyclin, and GPCR encoded transcripts were identified using RNA TaqMan PCR. v-IL-6 was high in PAL and in BC-1 and BC-3 cells. CONCLUSION: The presence of HHV-8 in one of two patients with PAL raises interesting questions in relation to the pathobiology of the condition. Clearly, the results indicate that HHV-8 is not an obligate pathogen, necessary for the effusion phenotype, but might contribute to it by its secretion of specific cytokines. (+info)