Pericarditis, pleural effusion, and pneumonitis with transient mitochondrial antibodies.
(33/1198)
Four women with fever, arthromyalgias, pericarditis, pleural effusion, high erythrocyte sedimentation rates, and lymphopenia had mitochondrial antibodies in the serum in the absence of antinuclear antibody. Their illness lasted 5-12 weeks and the antibody test results became negative on remission. Absence of specific bacteriological findings, normal antistreptolysin O titres, resistance to antibiotics, and good response to steroids suggested that these cases represented a milder and less persistent form of the syndrome resembling systemic lupus erythematosus described by German authors. (+info)
Detection of Legionella species in respiratory specimens using PCR with sequencing confirmation.
(34/1198)
Legionella spp. are a common cause of community-acquired respiratory tract infections and an occasional cause of nosocomial pneumonia. A PCR method for the detection of legionellae in respiratory samples was evaluated and was compared to culture. The procedure can be performed in 6 to 8 h with a commercially available DNA extraction kit (Qiagen, Valencia, Calif.) and by PCR with gel detection. PCR is performed with primers previously determined to amplify a 386-bp product within the 16S rRNA gene of Legionella pneumophila. We can specifically detect the clinically significant Legionella species including L. pneumophila, L. micdadei, L. longbeachae, L. bozemanii, L. feeleii, and L. dumoffii. The assay detects 10 fg (approximately two organisms) of legionella DNA in each PCR. Of 212 clinical specimens examined by culture, 100% of the culture-positive samples (31 of 31) were positive by this assay. By gel detection of amplification products, 12 of 181 culture-negative samples were positive for Legionella species by PCR, resulting in 93% specificity. Four of the 12 samples with discrepant results (culture negative, PCR positive) were confirmed to be positive for Legionella species by sequencing of the amplicons. The legionella-specific PCR assay that is described demonstrates high sensitivity and high specificity for routine detection of legionellae in respiratory samples. (+info)
Monoclonality or oligoclonality of human herpesvirus 8 terminal repeat sequences in Kaposi's sarcoma and other diseases.
(35/1198)
BACKGROUND: Infection with human herpesvirus 8 (HHV8), also termed Kaposi's sarcoma (KS)-associated herpesvirus, is associated with all forms of KS, with primary effusion lymphoma (PEL), and with some forms of multicentric Castleman's disease (MCD), but the pathogenic role of HHV8 in these tumors and the clonal nature of KS are still unclear. The purpose of this study was to examine whether the number of terminal repeats (TRs) contained in the fused TR region of HHV8 could be used as a marker of clonality in HHV8-associated tumors. METHODS: Pulsed-field gel electrophoresis (PFGE) and multiple-probe Southern blot analysis of the HHV8 TR region were performed on high-molecular-weight DNA obtained from tumoral KS, PEL, and MCD lesions. RESULTS: These analysis showed that the fused TR region contains a large but variable number of TR units (ranging from 16 to 75) and that the viral genome is present as extrachromosomal circular DNA in these tumors in vivo, with occasional ladders of heterogeneous linear termini reflecting lytic replication. All PEL tumors and PEL-derived cell lines as well as some KS tumors contained monoclonal or oligoclonal fused TR fragments; however, the TR region appeared polyclonal in MCD tumors and in a few KS lesions. CONCLUSION: Several KS and PEL lesions are monoclonal expansions of a single infected cell, suggesting that HHV8 infection precedes tumor growth and thus supporting an etiologic role of latent HHV8 in these proliferations. Our finding that nodular KS lesions display all possible patterns of clonality supports the model according to which KS begins as a polyclonal disease with subsequent evolution to a monoclonal process. (+info)
Unilateral pleural effusion complicating central venous catheterisation.
(36/1198)
Acute respiratory distress developed in two preterm babies because of unilateral hydrothorax secondary to the migration of a central venous catheter into the pulmonary vasculature. Prompt recognition of the problem and rapid treatment are essential and life saving. This complication of intravenous alimentation catheters has not been previously reported in the neonatal age group. (+info)
Myelomatous effusion with poor response to chemotherapy.
(37/1198)
While pleural effusion in multiple myeloma is relatively infrequent, myelomatous pleural effusion is extremely rare. We experienced a 61-year-old woman with IgD-lambda multiple myeloma and pleural effusion. The diagnosis was made originally by pleural biopsy, pleural fluid cytology and immunoelectropheresis of pleural fluid. Transient improvement of the pleural effusion was observed after administration of combination chemotherapy of vincristine, melphalan, cyclophosphamide, prednisone (VMCP)/vincristine, cyclophosphamide, adriamycin, prednisone (VCAP). Two months later, myelomatous pleural effusion recurred and no response to salvage therapy was observed. We reviewed the clinical feature of this case and literature concerning myelomatous pleural effusion. (+info)
PRIMARY PURPOSE: Formation of ascites and pleural effusion (PE) is a common problem for patients with advanced-stage cancer. These fluid accumulations cause severe symptoms such as abdominal distention, shortness of breath, cachexia, anorexia, and fatigue. Preclinical models have demonstrated that vascular endothelial growth factor (VEGF) plays a pivotal role in the accumulation of malignant PE or ascites. This study investigated whether blockade of VEGF activity would reduce biological activity of PE and ascites on endothelial cells of cancer patients. PATIENTS AND METHODS: The activity of VEGF in PE and ascites of 58 patients (39 with PE and 19 with ascites) was measured. An endothelial cell proliferation assay with human umbilical vein endothelial cells was used to determine the biological activity of ascites and PE. RESULTS: VEGF concentrations ranged from 67-6,245 pg/ml. A significantly higher concentration of VEGF was detected in the ascites and PE of patients with cancer (median, 1,290 pg/ml) than in patients with nonmalignant disease (median, 250 pg/ml; p = 0.02). Of the 58 PE and ascites samples, 41 were biologically active, based on a two- to fourfold stimulation of endothelial cell proliferation in 72 hours. VEGF concentrations were significantly higher in the biologically active samples compared with the 17 nonactive samples (2,056 pg/ml versus 771 pg/ml; p = 0.02). Coincubation of the samples with either a neutralizing polyclonal antibody against VEGF or SU5416, a small molecule inhibitor of the VEGF receptor Flk-1/KDR, inhibited endothelial cell proliferation by 66% and 100%, respectively. The inhibition caused by the antibody and that caused by SU5416 correlated significantly (r = 0.8, p<0.001). CONCLUSION: We conclude that malignant ascites and PE contain high levels of biologically active VEGF. This study strongly supports the hypothesis that blockade of VEGF, such as that afforded by SU5416, may benefit cancer patients with recurrent ascites or PE formation. (+info)
The role of thoracic ultrasonography for evaluation of patients with decompensated chronic heart failure.
(39/1198)
OBJECTIVES: This study examined the usefulness of thoracic ultrasonography for evaluation of fluid accumulation in patients with decompensated chronic heart failure (CHF) in comparison with physical signs, upright posteroanterior chest X-ray and echocardiography. BACKGROUND: Decompensated CHF is frequently accompanied by pleural effusion, suggesting that pleural effusion is a useful marker for confirming the diagnosis of the uncontrolled stage of CHF. Thoracic ultrasonography seems to be adequate for this purpose. METHODS: Patients with uncontrolled CHF and an interpretable physical examination, chest X-ray, ultrasonogram for the heart and thorax and thoracic X-ray computed tomographic (CT) scan were enrolled in the study (n = 60). Patients free from thoracic and cardiovascular diseases served as a control (n = 22). Thoracic CT scan was used as the gold standard for the presence or absence of pleural effusion. Variables used to predict body fluid accumulation included the following: pulmonary rales, jugular venous distension or peripheral edema, roentgenographic evidence of pulmonary edema or pleural fluid, pericardial or pleural effusion on ultrasonographic study. RESULTS: The reported incidence of pleural effusion detected by thoracic ultrasonography was high (91%). The incidence of physical signs and roentgenographic signs of body fluid accumulation, however, was modest (56%) to low (33%). The best clinical variable for identifying patients with decompensated CHF was the detection of pleural fluid by thoracic ultrasonography (91% predictive accuracy). This variable also had high interobserver agreement (95% overall agreement, kappa = 0.70). There was only 41% to 65% predictive accuracy of other clinical variables, with 72% to 95% agreement (kappa = 0.400-0.848). CONCLUSIONS: Thoracic ultrasonography is a simple, sensitive and accurate method for the evaluation of body fluid accumulation in patients with decompensated CHF. This technique can be used to assist in making the diagnosis of decompensated CHF if other causes of pleural effusion have been clinically ruled out. (+info)
Paragonimiasis westermani with multifocal lesions in lungs and skin.
(40/1198)
We report a case of Paragonimus westermani infection with a reticulonodular lesion in the right lung, left pleural effusion, and a mobile subcutaneous mass. Analyses of pleural effusion and bronchoalveolar lavage fluid (BALF) showed marked eosinophilia and high levels of eosinophil cationic protein and interleukin (IL)-5. Transbronchial lung biopsy revealed the presence of pneumonia with mild eosinophilic infiltration but remarkable lymphocytic infiltration. In this patient, high IL-5 levels in both BALF and pleural effusion could explain the remarkable eosinophilia. (+info)