The Effects of Urokinase Instillation Therapy via Percutaneous Transthoracic Catheter Drainage in Loculated Tuberculous Pleural Effusion: A randomized prospective study / 결핵

BACKGROUND: Tuberculous pleural effusion responds well to the anti-tuberculosis agents in general, so no further aggressive therapeutic managements to drain the tuberculous effusion is necessary except in case of diagnostic thoracentesis. But in clinical practice, we often see some patients who later decortication need due to dyspnea caused by pleural thickening despite the completion of anti-tuberculosis therapy in the patients with tuberculous effusion. Especially, the patients with loculated tuberculous effusion might have increased chance of pleural thickening after treatment. The purpose of this study was that intrapleural urokinase instillation could reduce the pleural thickining in the treatment of loculated tuberculous pleural effusion. METHODS: Thirty-seven patients initially diagnosed as having loculated tuberculous pleural effusion were randomly assigned to receive either the combined treatment of urokinase instillation and anti-tuberculosis agents(UK group) and anti-tuberculosis agents(Non-UK group) alone. The 16 patients in UK group received a single radiographically guided pig-tail catheter ranging in size from 10 to 12 French. 100,000 units of urokinase was dissolved in 150 ml of normal saline and instilled into the pleural cavity via pig-tail catheter every day, also this group was treated with anti-tuberculosis agents. While the 21 patients in Non-UK group were teated with anti-tuberculosis agents only except diagnostic thoracentesis. Then we evaluated the residual pleural thickening after treatment for their loculated tuberculous pleural effusion between the two groups. Also the duration of symptoms and the pleural fluid biochemistry like WBC counts, pH, lactic dehydrogenase (LDH), glucose, proteins, and adenosine deaminase (ADA) were compared. RESULTS: 1) The residual pleural thickening (RPT) (5.08 +/- 6.77 mm) of UK group was significantly lower than that (20.32 +/- 26.37 mm) of Non-UK group (Por=10 mm(5.23 +/- 3.89 wks) was significantly longer than the patients with RPT or=10 mm and the patients with RPT <10 mm. CONCLUSION: The treatment of loculated tuberculous pleural effusion with the urokinase instillation via percutaneous transthoraic catheter was effective to reduce the pleural thickening.

The effect of Insulin like growth factor-I (IGF-I) and IGF binding protein-3 (IGFBP-3) on cellular proliferation in mouse 3T3 fibroblast cells / 결핵

BACKGROUND: Cell growth is a balance between cell proliferation and cell death. Insulin-like growth factor-I(IGF-I), which binds IGF-I receptor (IGF-IR), mediates cellular proliferation as a potent mitogen. IGF binding protein-3 (IGFBP-3) as a circulating major IGFBP can inhibit or enhance the effects of IGF-I on cellular growth by binding IGFs. METHODS: We investigated the expressions of mRNA of IGF-I and IGF-IR by northern blot and phosphorylation of IGF-IR with the treatment of IGF-I by western blot in 3T3 fibroblast cells. The cellular proliferations of 3T3 cells with the treatments of IGF-I were evaluated using 3H-thymidine incorporation and MTT assay. Also to observe the effect of IGFBP-3 on cellular proliferation, 3T3 cells were treated with anti-IGFBP-3 and alpha IR3(monoclonal antibody to IGF-IR) alone or in combination. RESULTS: Our results demonstrated that 3T3 cells showed mRNA expressions of IGF-I and IGF-IR and the IGF-I increased phosphorylation of IGF-IR. The treatments of 3T3 cells with IGF-I increased cellular proliferation in 5% and 1% seruma-containing media, not in serum-free media. The addition of anti-IGFBP-3 to neutralize IGFBP-3 showed 2-fold increase of cellular proliferation, and also co-incubation of anti-IGFBP-3 and alpha IR3 together showed similar increase of cellular proliferation in 3T3 cells. Interestingly, when the cells were prethreated with alpha IR3 for 4 hr, prior to the simultaneous addition of alpha IR3 and anti-IGFBP-3, anti-IGFBP-3-mediated cellular proliferation was decreased to control level. All of these results suggest that free IGF-I released from IGF-I/IGFBP-3 complex would be involved in the cellular proliferation. CONCLUSION: IGF-I action by binding IGF-I.