BackgroundReexpansion pulmonary edema (REPE) is known as a rare and fatal complication after tube thoracostomy.ObjectivesWe investigated the risk factors for the development of REPE in patients with spontaneous pneumothorax.MethodsWe selected patients who were diagnosed with spontaneous pneumothorax and were initially treated with tube thoracostomy between August 1, 2003 and December 31, 2011. The patients’ electronic medical records, including operative notes and chest x-ray and computed tomography scans, were reviewed.ResultsREPE developed in 49 of the 306 patients (16.0%). REPE was more common in patients with diabetes (14.3% vs 3.9%, P = 0.004) or tension pneumothorax (46.8% vs 16.2%, P = 0.000). The pneumothorax was larger in patients with REPE than without REPE (57.0 ± 16.0% vs 34.2 ± 17.6%, P = 0.000), and the incidence of REPE increased with the size of pneumothorax. On multivariate analysis, diabetes mellitus [(odds ratio (OR) = 9.93, P = 0.003), and the size of pneumothorax (OR = 1.07, P = 0.000) were independent risk factors of REPE.ConclusionsThe presence of diabetes increases the risk of REPE development in patients with spontaneous pneumothorax. The risk of REPE also increases significantly with the size of pneumothorax.
PurposeThis study was designed to investigate the change of peroxisome proliferator-activated receptor gamma (PPARγ) after the infection of the human coronary artery smooth muscle cells (HCSMCs) with Chlamydia pneumoniae (C. pneumoniae) and the effect of PPARγ agonist on the expression of PPARγ of C. pneumoniae-infected HCSMCs.Materials and MethodsTo determine the effect of PPARγ agonist on the proliferation of C. pneumoniae-infected HCSMCs, rosiglitazone at various concentrations was applied 1 hour before inoculation of HCSMCs.ResultsThe expression of PPARγ mRNA in HCSMCs increased from 3 hours after C. pneumoniae infection and reached that of noninfected HCSMCs at 24 hours (p < 0.05). The expression of PPARγ protein in HCSMCs also increased from 3 hours after C. pneumoniae and persisted until 24 hours as compared with that of noninfected HCSMCs (p < 0.05). The pretreatment of HCSMCs with rosiglitazone followed by the infection with C. pneumoniae augmented the expression of PPARγ mRNA and protein (p < 0.05) and decreased cell proliferation.ConclusionOur results showed that the expression of PPARγ increases in response to C. pneumoniae infection and rosiglitazone further augmented the expression of PPARγ. It is suggested that rosiglitazone could ameliorate the chronic inflammation in the vessel wall induced by C. pneumoniae by augmenting PPARγ expression.
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