摘要目的:探讨2型糖尿病(T2DM)合并周围神经病变(DPN)患者血清补体因子B(CFB)、补体因子D(CFD)的水平及意义。方法:选取2019年10月至2020年10月于济宁医学院附属医院内分泌科住院的T2DM患者110例，根据是否合并DPN分为糖尿病周围神经病变组( n＝60)和单纯T2DM组( n＝50)；另选取同期于体检中心的体检人群52例为正常对照组( n＝52)。ELISA法测定各组血清CFB、CFD、TNF-α的水平，分析CFB、CFD与各临床指标的相关性，采用logistic回归分析DPN的影响因素。 结果:糖尿病周围神经病变组CFB、CFD水平高于T2DM组和正常对照组[CFB：(845.43±101.10)μg/ml vs (792.19±116.59)μg/ml、(739.20±123.43)μg/ml， P<0.05]、[CFD：(491.71±41.03)mg/L vs (467.58±45.16)mg/L、(445.16±50.47)mg/L， P<0.05]。Pearson相关分析显示，血清CFB的水平与糖化血红蛋白(HbA 1c)、空腹血糖(FPG)、肿瘤坏死因子-α(TNF-α)呈正相关(均 P<0.05)，与游离三碘甲状腺原氨(FT3)、总胆红素(TBIL)呈负相关(均 P<0.05)。血清CFD的水平与收缩压、HbA 1c、FPG、TNF-α呈正相关(均 P<0.05)，与FT3、TBIL呈负相关(均 P<0.05)。Logistic回归分析显示，排除收缩压、HbA 1c、FPG、FT3、DBIL、TBIL、TNF-α等混杂因素后，CFB和CFD仍是DPN发生和发展的影响因素。 结论:(1)DPN患者血清CFB、CFD水平显著升高，提示CFB、CFD可能参与了DPN的发生和发展。(2)DPN患者血清TNF-α水平显著升高，验证了TNF-α在DPN发病过程中的作用。

abstractsObjective:To investigate the serum level and significance of complement factor B (CFB) and complement factor D (CFD) in patients with type 2 diabetes mellitus (T2DM) and diabetic peripheral neuropathy (DPN).Methods:From October 2019 to October 2020, 110 patients with T2DM in the endocrinology department of Affiliated Hospital of Jining Medical College were divided into DPN group ( n=60) and simple T2DM group ( n=50) according to whether or not DPN was combined. In addition, 52 cases of physical examination population in the physical examination center in the same period were selected as the normal control group ( n=52). The serum levels of CFB, CFD and tumor necrosis factor-α (TNF-α) were measured by enzyme linked immunosorbent assay (ELISA). The correlation between CFB, CFD and clinical indexes was analyzed, and the influencing factors of DPN were analyzed by logistic regression. Results:The serum levels of CFB and CFD in DPN group were higher than those in T2DM group and normal control group [CFB: (845.43±101.10)μg/ml vs (792.19±116.59)μg/ml, (739.20±123.43)μg/ml, P<0.05], [CFD: (491.71±41.03)mg/L vs (467.58±45.16)mg/L, (445.16±50.47)mg/L, P<0. 05]. Pearson correlation analysis showed that the serum level of CFB was positively correlated with glycosylated hemoglobin (HbA 1c), fasting plasma glucose (FPG) and TNF-α (all P<0.05) and negatively correlated with triiodothyronine (FT3) and total bilirubin (TBIL) (all P<0.05). Serum CFD level was positively correlated with systolic blood pressure, HbA 1c, FPG and TNF-α (all P<0.05), but negatively correlated with FT3 and TBIL (all P<0.05). Logistic regression analysis showed that CFB and CFD were still influential factors for the occurrence and development of DPN after excluding confounding factors such as systolic blood pressure, HbA 1c, FPG, FT3, DBIL, TBIL and TNF-α. Conclusions:(1) Serum CFB and CFD levels were significantly increased in DPN patients, suggesting that CFB and CFD may be involved in the occurrence and development of DPN. (2) Serum TNF-α level was significantly increased in DPN patients, confirming the role of TNF-α in the pathogenesis of DPN.