Diffuse Lung Disease: Diffuse Lung Disease: Connective Tissue Disease |

Increased Expression of Urotensin II and Its Clinical Significance in Patients With Pulmonary Fibrosis FREE TO VIEW

Yan Ding, MD; Fan Lin; Ya Chen; Wei Yan; Juan Wang; Ming Chen; Yi Liu; Wan Yao
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Peking University Third Hospital, Beijing, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A209. doi:10.1016/j.chest.2016.02.216
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SESSION TITLE: Diffuse Lung Disease: Connective Tissue Disease

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: As a new peptide with angiogenic and pro-fibrogenic features, Urotensin II might play a role in pulmonary fibrosis. We aim to evaluate Urotensin II levels in patients with different extent of pulmonary fibrosis, their associations with fibrosis and other clinical indexes, and predictive value in fibrosis progression.

METHODS: Seventy-eight consecutive patients with pulmonary fibrosis were included, and divided into four groups according to extent of fibrosis of the total lung: non-fibrosis (0%), mild fibrosis (1-25%), moderate fibrosis (26-50%) and severe fibrosis (51-100%). All the patients underwent bronchoalveolar lavage, and were evaluated for HRCT scores, pulmonary function test, cytological analysis of bronchoalveolar lavage fluid, Urotensin II and endothelin-1 levels of both plasma and bronchoalveolar lavage fluid, and the follow-up pulmonary fibrosis progression in HRCT.

RESULTS: Urotensin II levels (pg/ml) of bronchoalveolar lavage fluid and plasma were significantly higher in patients with moderate (15.00-4.96 and 15.52-4.29) or severe fibrosis (19.26-5.06 and 15.59-4.55) than in non-fibrosis (11.57-3.53 and 12.80-3.24) (P< 0.05), and were positively correlated with reticulation score, honeycombing score, global disease severity score, the percentage of CD8+T-cells of bronchoalveolar lavage fluid and endothelin-1 levels, while negatively with total lung capacity %, diffusion capacity for carbon monoxide %, percentage of CD4+ T-cells (P< 0.05). Baseline Urotensin II levels in bronchoalveolar lavage fluid predicted subsequent pulmonary fibrosis progression independently.

CONCLUSIONS: Urotensin II might be an important mediator in pulmonary fibrosis. However further studies should be conducted to verify the findings of the current study.

CLINICAL IMPLICATIONS: Our findings suggest UII might be an important mediator in fibrosis pathogenesis, which might have some instructional therapy significance.

DISCLOSURE: The following authors have nothing to disclose: Yan Ding, Fan Lin, Ya Chen, Wei Yan, Juan Wang, Ming Chen, Yi Liu, Wan Yao

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