Objective: To investigate the association of the serum levels of high mobility group protein B1 (HMGB1) and advanced glycosylation end-product receptor (RAGE) in patients with acute lung injury secondary to acute aortic dissection (AAD).
Methods: From March 2016 to May 2018, 56 consecutive patients with AAD who were diagnosed by CTA of the whole aorta and echocardiography were enrolled. According to the values of oxygenation index (PaO2/FiO2) during oxygen inhalation in a resting state, the patients were divided into lung injury group (21 cases) and non-lung injury group (35 cases), and 30 individuals undergoing health maintenance examination were randomly selected as control group. Blood samples were drawn once per 4 h in the AAD patients after admission, and in the control group, fasting blood samples were taken only once from the elbow vein in the morning. The serum levels of HMGB1 and RAGE were measured by ELISA and PaO2 values were detected for calculating PaO2/FiO2.
Results: In both groups of AAD patients, the serum levels of HMGB1 and RAGE at 24 h after admission were significantly higher than those in the healthy control group, and which were also significantly higher in lung injury group than those in non-lung injury group (all P<0.05). In both groups of AAD patients, the serum levels of HMGB1 and RAGE were continuously increased, while the PaO2/FiO2 values were gradually decreased, and all reached a peak value within 48-60 h after admission. The changing amplitudes of the 3 variables were all significantly greater in lung injury group than those in non-lung injury group (all P<0.05). After they reached the peak values, the HMGB1 and RAGE levels gradually decreased, while the PaO2/FiO2 values correspondingly increased as time elapsed. In AAD patients, both HMGB1 and RAGE levels presented a significantly negative correlation with PaO2/FiO2 value (r=–0.940, –0.794).
Conclusion: The HMGB1/RAGE signaling pathway may play an important role in the occurrence of lung injury in AAD, and lung injury may be worsened with the increase of HMGB1 and RAGE levels. Monitoring of the HMGB1 and RAGE levels can help to evaluate the risk of lung injury after AAD. Further investigations of the HMGB1/RAGE signaling pathway may provide interventional targets for lung injury after AAD.