Serum neurotrophin profiles in dermatomyositis complicated with interstitial lung damage / 中华风湿病学杂志

ABSTRACT

Objective To investigate the profiles of serum nerve grow factor profile (NGF),neurotrophin (NT)-3,as well as brain-derived neurotrophic factor (BDNF) in patients with dermatomyositis (DM) complicated with interstitial lung damage (ILD).Methods Forty-seven patients were divided into 2 groups:ILD group (30 patients) and non-ILD group (17 patients).Twenty healthy blood donors were used as controls.Serum levels of NGF,NT-3,as well as BDNF were measured serum by enzyme-linked immunosorbent assay (ELISA).ANOVA was used to compare serum level of NTs.When a significant difference was found,the exact P-values were calculated using the student's t-test or t-test followed by Bonferroni's correction.Pearson test was used for correlation analysis.Results The serum NGF levels in healthy control group,the non-ILD group and the ILD group were (182±43),(308±72),(480±96) pg/ml respectively.There was statistically significant difference between the three groups (F=90.3,P＜0.01),and the serum NGF levels were elevated significantly in ILD and non-ILD patient groups as compared with healthy controls (t=12.9 and t=6.5 respectively,both P＜0.01).The serum level of NGF was significantly higher in ILD group than that in the non-ILD group (t=6.4,P＜0.01).There was no significant difference in the serum levels of NT-3 among the two patient groups and healthy controls.On the contrary,BDNF levels were significantly decreased in both ILD [(792± 106) pg/ml] and non-ILD patients groups [(963±93) pg/ml] when compared with healthy controls [(1 281±107) pg/ml] (t=15.9 and t=9.6 respectively,both P＜0.01).The decrease was also significant in ILD group when compared with non-ILD group (t=5.6,P＜0.01).Moreover,NGF and BDNF both showed significant correlation with serum C-reactive protein (CRP) level in ILD group by applying Pearson correlation analysis (r=0.56,P＜0.01; r=-0.48,P＜0.05 respectively).Conclusion Neurotrophins may play an import role in the pathogenesis of DM.