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Title   ¾Ç¼º È丷À¯Ãâ¿¡¼­ ¼¶À¯¼Ò¿ëÇØ°è ¹°ÁúÀÇ º¯È­ ( Fibrinolytic Profiles in Malignant Pleural Effusion )
Publicationinfo   1996 Jan; 028(04): 705-710.
Key_word   Malignant pleural effusion, Plasminogen activators and Plasminogen activator inhibitor-1
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Abstract   Plasminogen activators(PAs) and their inhibitors, plasminogen activator inhibitor-l(PAI-l) are known to play an important role in tumor invasion and metastasis. The differentiation of malignant pleural effusion(PE) from non-malignant pleural effusion is important for the management of a patient. Since malignant PE is a form of metastasis, and malignant cells are considered to be able to produce PAs or PAI-1, it seems reasonable to assume that PAa and PAI-1 in PE will be in somewhat different from that in non-malignant PE. We examined urokinase- type plasminogeo activator(uPA) and uPA receptor(uPAR) and tissue-type plasminogen activator(tPA), PAI-1 antigen using ELISA method and conventional laboratory tests and adenosine deaminase(ADA) in PEs. Levels of uPA, uPAR, tPA and PAI-1 were significantly increased in malignant and tuberculous PE than transudates(p<0.05) but not statistically significant between malignant and tuberculous PE. ADA in PE showed significantly increased in tuberculous PE than malignant PE and transudate(p<0.05). These data suggests that measurement of uPA, uPAR, tPA, PAI-1 antigen in addition to ADA could be helpful to differentiate malignant PE from tuberculous PE and transudate.
Àú ÀÚ   ¹é½ÂÈ£(Seung Ho Baik),ÀüÁø¿ì(Jin Woo Jeon),¿øÁ¾È£(Jong Ho Won),È«´ë½Ä(Dae Sik Hong),¹ÚÈñ¼÷(Hee Sook Park)