Radial Probe Ultrasound-Guided Cryobiopsy.

Fluoroscopy-guided transbronchial forceps biopsy has a low diagnostic yield in patients with radiographic suspicion of interstitial lung disease. Cryobiopsy has a higher diagnostic yield likely due to preserved lung architecture and larger biopsies; however, there is an increased risk of major airway bleeding and pneumothorax. Simultaneous use of endobronchial balloon blocker allows for containment of bleeding after cryobiopsy to the affected lobe. In the current article we describe use of radial ultrasound in identification of a target lung parenchyma without a major blood vessel adjacent to distal bronchi. After fluoroscopic marking of the selected airway a 3 second cryobiopsy was performed after localization of cryoprobe. Simultaneous use of radial ultrasound and fluoroscopy can possibly decrease bleeding complication associated with cryobiopsy in patients with suspected interstitial lung disease.

Transbronchial Saline Injection to Allow Visualization and Biopsy of Peripheral Lung Nodule on Linear Endobronchial Ultrasound.

Two peripheral lung nodules suspicious for lung cancer were noted in a patient. Surgical and CT-guided transthoracic needle biopsies were deemed to be high risk given advanced emphysema. The patient received nondiagnostic electromagnetic navigation bronchoscopy and endobronchial ultrasound (EBUS)-guided mediastinal needle biopsies. Repeat bronchoscopy was then performed. The lung nodules were difficult to visualize with both convex probe EBUS and electromagnetic navigation bronchoscopy guidance. Normal saline injection into vicinity of the peripheral lung nodule was then used in hopes of filling airspace with fluid and improving visualization of the lung nodule. After saline injection the nodule was visualized on convex probe EBUS, allowing for diagnostic needle aspirations.

Boerhaave Syndrome Presenting as Tension Pneumothorax: First Reported North American Case.

Tension pneumothorax is a rare and potentially life-threatening clinical complication. A 43-year-old Caucasian woman with type 1 diabetes mellitus presented with nausea and retching and examination revealed dehydration. Laboratory parameters were consistent with a diagnosis of diabetic ketoacidosis, which responded to therapy. Suddenly, 30 hours later, she developed cardiorespiratory compromise due to a tension pneumothorax. After emergent decompression and catheter placement, computerized tomographic scan of the chest demonstrated esophageal-pleural fistula confirming Boerhaave syndrome as the etiology for the pneumothorax. The patient underwent emergent esophagectomy with pleural washout with a subsequent gastric pull-up surgery. Boerhaave syndrome frequently presents atypically with chest pain, dyspnea, and nausea. It communicates with the left pleural space in 80% to 90% of cases, but <5% of cases involve the right pleural cavity. Unexplained and rapidly progressive pleural effusions have been associated with this entity. Only 4 cases of Boerhaave syndrome causing tension pneumothorax have been reported in the literature so far.

Chronic inflammation and cancer: emerging roles of triggering receptors expressed on myeloid cells.

Inflammation is tightly regulated by a vast system that is intricately interconnected with innate immunity. Aberrations in expression or signaling, such as in innate immune receptors, can create excessive inflammation and, when chronic, often promote oncogenesis. The triggering receptor expressed on myeloid cells receptor family has been characterized as a major player in the amplification and signaling of the inflammatory response. In a number of chronic inflammatory conditions and malignancies, the triggering receptor expressed on myeloid cells has been implicated in disease severity and progression. In this article, the current understanding of triggering receptor expressed on myeloid cells function in pre-malignant, malignant and chronic inflammatory conditions is critically reviewed. The potential for therapeutic application is also discussed.

Diagnostic value of tumor antigens in malignant pleural effusion: a meta-analysis.

The diagnostic value of tumor markers, carcinoembryonic antigen (CEA), cancer antigen (CA) 15-3, CA 19-9, CA 125, cytokeratin fragment (CYFRA), and neuron-specific enolase (NSE) in pleural fluid to differentiate between benign and malignant pleural effusion (MPE) has not yet been clearly established. A review of English language studies using human subjects was performed. Sensitivity and specificity values of the chosen tumor markers were pooled using a random effects model to generate hierarchical summary receiver operator curves to determine the diagnostic performance of each tumor marker. A total of 49 studies were included in the final analysis. Pooled sensitivity and specificity values for chosen tumor markers for diagnosing MPE are as follows: CEA, 0.549 and 0.962; CA 15-3, 0.507 and 0.983; CA 19-9, 0.376 and 0.980; CA 125, 0.575 and 0.928; CYFRA, 0.625 and 0.932; NSE, 0.613 and 0.884. The use of individual tumor markers in diagnosing MPE has many benefits (cost, invasiveness, and so forth). Although these tumor markers exhibit high specificity, the low sensitivity of each marker limits the diagnostic value. We conclude that tumor markers used individually are of insufficient diagnostic accuracy for clinical use. Tumor markers used in various combinations or from serum may have some potential worth further investigation.

Cellular and molecular immunology of lung cancer: therapeutic implications.

Although the incidence of lung cancer is declining, the prognosis remains poor. This is likely due to lack of early detection and only recent developments in selective cancer therapies. Key immune cells involved in the pathogenesis of lung cancer include CD4(+) T lymphocytes, macrophages, dendritic cells and NK cells. The growing understanding of these cells indicates a highly complex and intertwined network of their involvement in each stage of lung cancer. Immune cell types and numbers affect prognosis and could offer an opportunity for clinical therapeutic applications. However, an incomplete understanding of immune cell involvement and the underlying processes in lung cancer still remain. Deeper investigation focusing on the role of the immune cells will further the understanding of lung carcinogenesis and develop novel therapeutic approaches for the treatment and management of patients with more specialized and selective lung cancer.

Hemostatic implications of endothelial cell apoptosis in obstructive sleep apnea.

Patients with obstructive sleep apnea (OSA) are at increased risk of atherothrombosis independent of the Framingham risk factors. Studies on hemostasis factors in OSA are scarce and inconsistent. We sought to understand the variation in atherothrombotic propensity as a function of apoptotic circulating endothelial cells (CECs) in OSA by investigating the relationship between CEC apoptosis and plasma levels of hemostatic factors tissue factor (TF) and von Willebrand Factor (vWF) in apneic subjects. Apoptotic CECs were detected by flow cytometry in 35 male subjects free of cardiovascular diseases (AHI range 8-43) and 12 healthy male controls (AHI range 2-5) before and after 8 weeks of nasal continuous positive airway pressure (nCPAP). Quantitative determination of TF and vWF was performed using an enzyme-linked immunosorbent assay (ELISA) kit. The mean levels of TF (66.78 +/- 41.59 pg/ml) and vWF (189.70 +/- 69.24 IU/dl) were significantly higher in OSA patients compared with those in healthy subjects (42.83 +/- 14.18 pg/ml; and 124.48 +/- 31.43 IU/dl). Apoptotic CECs were elevated in patients with OSA and correlated strongly with TF and vWF levels (p = 0.02 and p < 0.001; respectively). There were no correlations between TF, vWF and apnea hypopnea index, or arousal index. Only the percentage of time spent <90% oxygen saturation was inversely associated with TF (r = 0.38; p = 0.02). Following nCPAP therapy, there was significant decrease in TF levels that correlated with decrease in apoptotic CECs. In patients with OSA, increased prothrombotic factors are strongly determined by apoptotic CECs. Treatment with nCPAP may alleviate the coagulation propensity.

Inhibition of delayed rectifier potassium channels and induction of arrhythmia: a novel effect of celecoxib and the mechanism underlying it.

Selective inhibitors of cyclooxygenase-2 (COX-2), such as rofecoxib (Vioxx), celecoxib (Celebrex), and valdecoxib (Bextra), have been developed for treating arthritis and other musculoskeletal complaints. Selective inhibition of COX-2 over COX-1 results in preferential decrease in prostacyclin production over thromboxane A2 production, thus leading to less gastric effects than those seen with nonselective COX inhibitors such as acetylsalicylic acid (aspirin). Here we show a novel effect of celecoxib via a mechanism that is independent of COX-2 inhibition. The drug inhibited the delayed rectifier (Kv2) potassium channels from Drosophila, rats, and humans and led to pronounced arrhythmia in Drosophila heart and arrhythmic beating of rat heart cells in culture. These effects occurred despite the genomic absence of cyclooxygenases in Drosophila and the failure of acetylsalicylic acid, a potent inhibitor of both COX-1 and COX-2, to inhibit rat Kv2.1 channels. A genetically null mutant of Drosophila Shab (Kv2) channels reproduced the cardiac effect of celecoxib, and the drug was unable to further enhance the effect of the mutation. These observations reveal an unanticipated effect of celecoxib on Drosophila hearts and on heart cells from rats, implicating the inhibition of Kv2 channels as the mechanism underlying this effect.