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目的研究地塞米松对一氧化碳中毒迟发性脑病(DEACMP)患者脑脊液中转化生长因子β1(TGF-β1)、结缔组织生长因子(CTGF)的干预及其意义。方法选取35例DEACMP患者为观察组,入院第1天、第29天留取脑脊液,并于第1天及之后隔日1次椎管注射地塞米松。同时选取35例同期入院的神经系统非脱髓鞘疾病患者为对照组,于入院第1天留取脑脊液。用酶联免疫吸附法测定脑脊液TGF-β1、CTGF水平;2组患者均于入院第1天行头颅CT。入院第29天判定疗效。结果观察组患者头颅CT均显示不同程度的脑室周围白质脱髓鞘改变;对照组患者头颅CT未见脑室周围白质脱髓鞘改变。与对照组入院第1天时比较,观察组入院第1天和第29天时脑脊液TGF-β1、CTGF水平均显著增高,差异均有统计学意义(P<0.05);观察组入院第29天时脑脊液TGF-β1、CTGF水平均显著低于入院第1天时,差异均有统计学意义(P<0.05)。结论 DEACMP患者发病机制可能与TGF-β1、CTGF过表达有关。地塞米松可能通过抑制TGF-β1、CTGF的过表达起到治疗DEACMP的作用。
Objective To investigate the interventional effect of dexamethasone on the expression of transforming growth factor β1 (TGF-β1) and connective tissue growth factor (CTGF) in cerebrospinal fluid of patients with delayed encephalopathy caused by carbon monoxide poisoning (DEACMP). Methods 35 patients with DEACMP were selected as observation group. Cerebrospinal fluid was collected on the first day and the 29th day after admission. Dexamethasone was injected into the vertebral canal on the first day and every other day. At the same time, 35 patients with neurological non-demyelinating disease admitted in the same period were selected as the control group, and cerebrospinal fluid was collected on the first day after admission. The levels of TGF-β1 and CTGF in cerebrospinal fluid were detected by enzyme-linked immunosorbent assay (ELISA). The skull CT was performed on the first day after admission in both groups. The first 29 days of admission to determine the efficacy. Results The head CT of the observation group showed varying degrees of periventricular white matter demyelination; in the control group, there was no change of periventricular white matter demyelination in the head CT. Compared with the control group on the first day after admission, the levels of TGF-β1 and CTGF in cerebrospinal fluid of the observation group were significantly increased on the first day and the 29th day of admission (P <0.05) β1, CTGF levels were significantly lower than the first day of admission, the differences were statistically significant (P <0.05). Conclusion The pathogenesis of DEACMP may be related to the overexpression of TGF-β1 and CTGF. Dexamethasone may play a role in the treatment of DEACMP by inhibiting the overexpression of TGF-β1 and CTGF.