Tissue Inhibitor of Metalloproteinase-1 Is Responsible for Residual Pleural Thickening in Pleural Tuberculosis

• DOI: 10.1620/tjem.235.327
• Publication Date: 2015-04-08T01:42:34Z
• Authors: Ki-Eun Hwang; Young-Jun Shon; Byong-Ki Cha; Mi-Jeong Park; Min-Su Chu; Young-Jun Kim; Eun-Taik Jeong; Hak-Ryul Kim
• Keywords: Pleural thickening; Pathogenesis

Residual pleural thickening (RPT) is the most frequent complication associated with tuberculosis, and may occur even after successful anti-tuberculosis medications. Matrix metalloproteinases (MMPs) are zinc-dependent proteinases capable of degrading all components extracellular matrix. The proteolytic action MMPs be involved in pathogenesis tuberculosis. MMP-9, secreted by monocytes lymphocyte, lead to long-term fibrosis. aim present study was determine whether MMP-2 and/or MMP-9 their specific inhibitors, tissue inhibitors metalloproteinase 1 (TIMP-1) TIMP-2, could used predict RPT. This retrospective enrolled 52 patients diagnosed Levels MMP-2, TIMP-1, TIM-2 were determined fluid ELISA. RPT measured on chest X-ray at completion treatment final follow-up. average periods medication follow-up 6.7 7.6 months, respectively. or levels had no significant correlation > 2 mm higher TIMP-1 (p = 0.00 p 0.001, respectively). However, lower TIMP-2 0.005). In a logistic regression model, elevated medications conclusion, responsible for development helpful predicting