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目的 观察氦氖激光并紫外线照射充氧自血回输 (L -UBIO)治疗慢性肝炎的治疗效果及其对内源性一氧化氮 (NO)水平、自然杀伤细胞 (NK细胞 )活性和血液粘度的影响。方法 将70例慢性肝炎随机分成联合治疗组 (L -UBIO组 )和保肝药物治疗组 (对照组 ) ,每组 35例。L -U BIO组采自体血 2 0 0ml经激光并紫外线照射充氧 15min回输 ,每周 3次 ,10次为 1疗程。观察治疗前后ALT、TBIL、NO、NK细胞及血液粘度的变化。结果 治疗结束时L -UBIO组显效 2 1例 ,有效10例 ,总有效率为 88%。对照组显效 12例 ,有效 8例 ,总有效率为 5 7%。L -UBIO组显著高于对照组 (χ2 =8.74,P <0 .0 1) ;ALT和TBIL降低幅度L -UBIO组显著高于对照组 (t =2 .0 0 4,2 .0 12 ,P <0 .0 5 ) ;L -UBIO组治疗前NO为 (46 .5± 10 .5 ) μmol/L ,治疗后升至 (6 1.5± 10 .9) μmpl/L (t =2 .16 4,P <0 .0 5 ) ;L -UBIO组治疗前后NK细胞活性和血液粘度指标均无明显变化。结论 激光并紫外线照射充氧自血回输治疗慢性肝炎 ,具有促进肝功能恢复和改善临床症状的作用。其作用机制可能与NO水平升高有关。
Objective To observe the therapeutic effect of He-Ne laser and UV-B irradiation on chronic hepatitis and its effects on the levels of endogenous nitric oxide (NO), natural killer (NK) cells and blood viscosity Impact. Methods Seventy patients with chronic hepatitis were randomly divided into combined treatment group (L -UBIO group) and hepatoprotective therapy group (control group), 35 cases in each group. L-U BIO group collected autologous blood 200ml by laser and ultraviolet radiation oxygenation 15min back, 3 times a week, 10 times for a course of treatment. The changes of ALT, TBIL, NO, NK cells and blood viscosity before and after treatment were observed. Results At the end of treatment, 21 cases were markedly effective in L-UBIO group, 10 cases were effective and the total effective rate was 88%. The control group markedly effective in 12 cases, effective in 8 cases, the total effective rate was 57%. L-UBIO group was significantly higher than the control group (χ2 = 8.74, P <0.01); ALT and TBIL decreased significantly in the L-UBIO group than in the control group (t = 2.040,2.012, P <0.05). The NO level in L-UBIO group was (46.5 ± 10.5) μmol / L before treatment and reached (6 1.5 ± 10.9) μmpl / L after t 4, P <0.05). There was no significant change in NK cell activity and blood viscosity before and after L-UBIO treatment. Conclusion Laser and ultraviolet irradiation oxygenation and autotransfusion in the treatment of chronic hepatitis can promote the recovery of liver function and improve the clinical symptoms. Its mechanism may be related to the increase of NO level.