BACKGROUND: Transforming growth factor-β1 (TGF-β1) plays a major role in pleural fibrosis and chemical pleurodesis. Approximately 50% of patients with tunneled pleural catheters (TPCs) for malignant pleural effusions (MPEs) will have autopleurodesis. Pleural TGF-β1 levels have never been measured in the setting of TPC drainage and may predict autopleurodesis. METHODS: Pleural fluid was collected prospectively in subjects with MPE and planned TPC insertion. Pleural fluid was collected at time 0 (T0, thoracentecis before TPC placement), time 1 (T1, TPC insertion), and time 2 (T2, 2 wk after TPC insertion). The MPE levels of TGF-β1, vascular endothelial growth factor, and plasminogen activator inhibitor-1 were measured using ELISA. Lactate dehydrogenase levels were also measured at T0. Patients were followed up for autopleurodesis and TPC removal. RESULTS: Nineteen samples were collected from 9 patients with MPE who underwent TPC placement. Three patients died before the study completion. The median level of TGF-β1 of 1243 pg/mL (range, 620 to 4547 pg/mL) at T1 in 6 patients showed a statistically significant rise to 2857 pg/mL (range, 2120 to 7160 pg/mL) after TPC placement (P=0.004, R=0.898). There was no statistically significant increase in TGF-β1 levels from T0 to T1. There was a linear relationship between TGF-β1 and lactate dehydrogenase at T0 (R=0.635). Plasminogen activator inhibitor-1 levels increased from T1 to T2, but was not statistically significant. There was no significant rise in vascular endothelial growth factor from T1 to T2. CONCLUSIONS: TPC insertion results in an independent increase in TGF-β1 levels in MPE.
BACKGROUND: Transforming growth factor-β1 (TGF-β1) plays a major role in pleural fibrosis and chemical pleurodesis. Approximately 50% of patients with tunneled pleural catheters (TPCs) for malignant pleural effusions (MPEs) will have autopleurodesis. Pleural TGF-β1 levels have never been measured in the setting of TPC drainage and may predict autopleurodesis. METHODS:Pleural fluid was collected prospectively in subjects with MPE and planned TPC insertion. Pleural fluid was collected at time 0 (T0, thoracentecis before TPC placement), time 1 (T1, TPC insertion), and time 2 (T2, 2 wk after TPC insertion). The MPE levels of TGF-β1, vascular endothelial growth factor, and plasminogen activator inhibitor-1 were measured using ELISA. Lactate dehydrogenase levels were also measured at T0. Patients were followed up for autopleurodesis and TPC removal. RESULTS: Nineteen samples were collected from 9 patients with MPE who underwent TPC placement. Three patients died before the study completion. The median level of TGF-β1 of 1243 pg/mL (range, 620 to 4547 pg/mL) at T1 in 6 patients showed a statistically significant rise to 2857 pg/mL (range, 2120 to 7160 pg/mL) after TPC placement (P=0.004, R=0.898). There was no statistically significant increase in TGF-β1 levels from T0 to T1. There was a linear relationship between TGF-β1 and lactate dehydrogenase at T0 (R=0.635). Plasminogen activator inhibitor-1 levels increased from T1 to T2, but was not statistically significant. There was no significant rise in vascular endothelial growth factor from T1 to T2. CONCLUSIONS:TPC insertion results in an independent increase in TGF-β1 levels in MPE.
Authors: Samira Shojaee; S Shojaee; Janet Dawson; J Dawson; Ray W Shepherd; R W Shepherd; Hans J Lee; H J Lee Journal: Lung Date: 2014-12 Impact factor: 2.584