Biomarker Levels During Indwelling Pleural cAtheter Sample Testing (BLAST)
Some patients that have a tunneled pleural catheter will not have the pleural fluid (water around the lung) return after some time (pleurodesis). The purpose of this study is to understand how the investigators can predict who will achieve pleurodesis and how this occurs by studying the pleural effusion.
Malignant Pleural Effusions
|Study Design:||Observational Model: Cohort
Time Perspective: Prospective
|Official Title:||TGF-B as a Marker of Pleurodesis in Patients With Tunneled Pleural Catheters|
- To determine the median time to pleurodesis [ Time Frame: 12 week follow up ] [ Designated as safety issue: No ]Duration of follow-up will be 12 weeks. After 12 weeks, all patients who do not achieve spontaneous pleurodesis will adhere to the standard drainage protocol.
- TGF-B levels over time [ Time Frame: 12 weeks ] [ Designated as safety issue: No ]To determine the threshold TGF-B level to determine accuracy of predicting auto-pleurodesis
Biospecimen Retention: Samples Without DNA
Pleural fluid attained during drainage of indwelling pleural catheter
|Study Start Date:||January 2014|
|Estimated Study Completion Date:||January 2016|
|Estimated Primary Completion Date:||January 2016 (Final data collection date for primary outcome measure)|
|Indwelling tunneled pleural catheter|
An alternative and emerging treatment for malignant pleural effusions is the placement of a chronic indwelling pleural catheter.
Tunneled pleural catheters (TPC) are ideal for treatment of MPE associated with a trapped or non-expandable lung which will not have sufficient visceral and parietal pleura apposition for chemical pleurodesis. Transforming growth factor-Beta 1 (TGF-β) is a profibrotic cytokine, and a potent inducer of Plasminogen activator inhibitor-1 (PAI-1) in human pleural mesothelial cells. PAI-1 inhibits protease-dependent fibrinolytic activity and along with TGF-β, its concentration is increased in exudative and tuberculous pleural effusion. TGF-β levels in pleural fluid have been shown to correlate with pleural thickness in tuberculosis pleurisy and empyema in rabbits.
TGF-β is a multifunctional cytokine primarily produced by mesothelial cells in the pleural space, but can also originate from lung parenchymal macrophages that migrate to the pleural space. In humans, TGF-β consists of three isoforms (TGF-β1, TGF-β2, and TGF-β3). They share many biological activities and their actions on cells are qualitatively similar in most cases. TGF-β stimulates the extracellular matrix production and studies support that TGF-β over-production is a key regulator in pleural fibrosis and chemical pleurodesis. Moreover, TGF-β signaling for the production of PAI-1 is clearly noted in human mesothelial cells of different origins. Different inflammatory stimuli in the pleural space including malignancy and infection may activate TGF-β up-regulation and enhanced production which in turns results in PAI-1 expression.
Please refer to this study by its ClinicalTrials.gov identifier: NCT02092155
|Contact: Karen Oakjones-Burgessemail@example.com|
|Contact: Ricardo Ortizfirstname.lastname@example.org|
|United States, Maryland|
|Johns Hopkins University||Recruiting|
|Baltimore, Maryland, United States, 21287|
|Contact: Karen Oakjones-Burgess 410-955-5288|
|Principal Investigator:||Lonny Yarmus, DO||Johns Hopkins University|