Biomarker Levels During Indwelling Pleural cAtheter Sample Testing

• Conditions: Malignant Pleural Effusions

• Registration Number: NCT02092155
• Lead Sponsor: Johns Hopkins University

Brief Summary

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.

Detailed Description

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 malignant pleural effusion (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.

Study Timeline

• Study Start: 2014-01
• Study First Submitted: 2014-03-17
• Study First Submitted QC: 2014-03-19
• Study First Posted: 2014-03-20
• Status Verified: 2024-12
• Last Update Submitted: 2024-12-05
• Last Update Posted: 2024-12-09
• Primary Completion: 2025-12
• Study Completion: 2025-12

Recruitment & Eligibility

• Status: ENROLLING_BY_INVITATION
• Sex: All
• Target Recruitment: 95

Inclusion Criteria

Not provided

Exclusion Criteria

Not provided

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
To determine the median time to pleurodesis	12 week follow up	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.

Secondary Outcome Measures

Name	Time	Method
TGF-B levels over time	12 weeks	To determine the threshold TGF-B level to determine accuracy of predicting auto-pleurodesis

Trial Locations

Locations (1)

Johns Hopkins University; 🇺🇸 Baltimore, Maryland, United States