苯溴马隆对牙周炎并高尿酸血症患者炎性因子水平的影响

Influence of hyperuricemia on inflammatory factor in patients with periodontal disease and its therapy

目的探讨慢性牙周炎并高血尿酸血症(hyperuricemia,HUA)患者炎性因子水平变化及应用苯溴马隆治疗的效果。方法慢性牙周炎患者90例,血尿酸水平正常30例(血尿酸正常组),60例合并HUA者随机分为苯溴马隆治疗组和HUA组各30例,同期体检健康者30例为对照组,苯溴马隆治疗组给予苯溴马隆+碳酸氢钠片口服,HUA组仅口服碳酸氢钠片;比较各组以及苯溴马隆组和HUA组治疗前及治疗8周后炎性因子水平变化。结果 (1)苯溴马隆治疗组、HUA组治疗前血清高敏C反应蛋白(high sensitivity C-reactive protein,hs-CRP)[(3.51±0.90)、(3.42±0.84)mg/L]、白细胞介素-1β(interleukin-1β,IL-1β)[(4.81±0.53)、(4.79±0.58)ng/L]、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)[(49.15±8.59)、(48.24±8.96)μg/L]高于血尿酸正常组[hs-CRP(2.87±1.04)mg/L、IL-1β(3.04±0.52)ng/L、TNF-α(30.45±5.63)μg/L]及对照组[hs-CRP(0.89±0.31)mg/L、IL-1β(2.09±0.20)ng/L、TNF-α(18.07±3.92)μg/L],血尿酸正常组血清hs-CRP、IL-1β、TNF-α水平高于对照组(P<0.05),苯溴马隆组和HUA组以上指标比较差异无统计学意义(P>0.05);(2)治疗后苯溴马隆治疗组血尿酸[(282.19±43.91)μmol/L]、hs-CRP[(1.62±0.69)mg/L]、IL-1β[(2.97±0.44)ng/L]、TNF-α[(30.49±4.60)μg/L]较治疗前下降(P<0.05),与HUA组[血尿酸(429.21±50.20)μmol/L、hs-CRP(2.30±0.92)mg/L、IL-1β(4.31±0.39)ng/L、TNF-α(43.10±4.62)μg/L)比较差异有统计学意义(P<0.05);(3)牙周炎并HUA患者血尿酸水平与hs-CRP(r=0.83,P=0.000)、IL-1β(r=0.75,P=0.000)、TNF-α(r=0.80,P=0.000)呈正相关。结论 HUA可增加牙周炎患者炎症反应,苯溴马隆通过降低患者血尿酸水平来减轻炎症反应。

Objective To investigate the relationship of hyperuricemia with inflammatory factors in patients with chronic periodontal disease and the therapeutic effect of benzbromarone. Methods Ninety patients with chronic periodontitis were divided into normal uric acid group, benzbromarone group with hyperuricemia treated with oral administration of benzbromaron plus sodium bicarbonate, and hyperuricemia group treated with only oral administration of sodium bicarbonate, with 30 patients in each group. Another 30 healthy volunteers were as controls （control group）. The levels of inflammatory factors were compared among groups before and after 8-week treatment. Results Before treatment, the levels of high sensitivity C-reactive protein （hs-CRP）, interleukin 1β （IL-1β） and tumor necrosis factor-α （TNF-α） were significantly higher in benzbromarone group （（3.51 ±0. 90） mg/L, （4. 81 ± 0. 53） ng/L, （49. 15 ±8. 59） μg/L） and hyperuricemia group （（3.42±0.84） mg/L, （4.79±0.58） ng/L, （48.24±8.96）μg/L） than those in normal uric acid group （（2.87±1.04） mg/L, （3. 04±0. 52） ng/L, （30. 454-5. 63） μg/L） and control group （（0.89±0.31） mg/L, （2.09±0.20） ng/L, （18. 07±3.92） μg/L） （P〈0. 05）, and were higher in normal uric acid group than those in control group （P〈0.05）, and there were no significant differences between benzbromarone group and hyperuricemia group （P〉 0.05）. The levels of uric acid, hs-CRP, IL-1β and TNF-α were significantly lower after treatment （（282. 19±43. 91） μmol/L, （1.62±0.69） mg/L, （2.97±0.44） g/L, （30.49±4.60） μg/L） than those before treatment in benzbromarone group （P〈0.05）, showing significant differences in comparison with hyperuricemia group （（429.21±50.20） μmol/L, （2.30±0. 92） mg/L, （4. 31± 0. 39） ng/L, （43. 10±4. 62） μg/L） （P〈0.05）. The uric acid level in periodontitis patients complicated with hyperuricemia was positively correlated with hs-CRP （r= 0.83, P= 0. 000）, IL-1β （r= 0.75, P=0. 000） and TNF-α （r=0. 80, P=0. 000）. Conclusion Hyperuricemia could increase the levels of inflammatory factors, and benzbromarone could effectively alleviate the inflammatory ractions by decreasing the level of uric acid.