痛风汤剂益肾养肝合剂治疗痛风性肾病33例临床观察

目的: 探讨痛风汤剂与益肾养肝合剂同用治疗痛风性肾病的临床疗效.方法: 将痛风性肾病患者58例分为两组,治疗组33例予痛风汤剂加益肾养肝合剂治疗,对照组25例只予痛风汤剂治疗.观察两组治疗前后血尿酸,肾功能,血、尿β2-微球蛋白指标的变化.结果: 治疗组在改善临床症状、肾功能,降低血尿酸、尿β2-微球蛋白(β2-MG)方面均优于对照组.结论: 对痛风性肾病患者的治疗,痛风汤剂与益肾养肝合剂同用扶正祛邪的治疗方法较好,能够改善肾小管功能.     

痛风丸治疗痛风的实验研究

目的：观察痛风丸对痛风性关节炎、高尿酸血症的影响及镇痛作用。方法：用尿酸钠致大鼠踝关节肿胀、酵母膏致小鼠高尿酸血症及小鼠冰醋酸所致的扭体反应，观察其抗痛风的作用。结果：痛风丸可明显减轻痛风模型大鼠的关节肿胀程度、降低高尿酸血症模型小鼠的血尿酸、减少扭体次数。结论：痛风丸对痛风的急性发作有一定的治疗作用。     

MRI对痛风性膝关节炎诊断的准确性研究

目的探讨MRI对痛风性膝关节炎诊断的准确性。方法回顾性分析张家港澳洋医院2015年7月至2019年2月收治的31例慢性痛风患者膝关节双能量CT和MRI检查图像,以双能量CT为金标准,检验MRI对痛风石检出的敏感性、特异性、阳性预测值、阴性预测值和准确性。结果 4例患者行双侧膝关节双能量CT和MRI检查,共35个膝关节纳入研究。MRI对痛风石检出的特异性为0. 977(95%CI:0. 930～0. 994),敏感性为0. 648(95%CI:0. 551～0. 735),阳性预测值为96. 0%,阴性预测值为77. 0%,准确性为82. 8%。结论与双能量CT相比,MRI具有较高的特异性和准确性,对痛风性关节炎的诊断潜力较大。     

陈以平治疗痛风性肾病的经验

介绍陈以平教授治疗痛风性肾病的经验。陈师认为,该病的病因病机,在于肾虚脾弱,湿浊瘀阻;辨证施治,注重培补脾肾,活血化瘀;遣方用药,经方为主,参以中和尿酸之品。并附验案2则。     

自拟清热利湿解毒方联合中药外敷治疗急性痛风性关节炎64例临床观察

Objective To study the effect of treating gouty arthritis with Chinese herbal medicines. Methods 64 patients were randomly recruited into a control group and a treatment group, with 32 cases in each group. The treatment group was treated with taking self-made Qingrelishijiedu formula orally and applying Sanhuang powder externally, while the control group was treated with Xinhuang tablets. Results The cure rate of the healing group was 95.45% in comparison with 86.06%in the control group, showing obvious difference (t=3.25, P＜0.05). The level of blood uric acid of both group reduced after the treatment. The level of blood uric acid of the treatment group was (498.2±79.1) μmol/L before the treatment and (338.6±39.9 ) μmol/L after the treatment, contrasting to (492.3 ± 87.5 ) μ mol/L and ( 396.2 ± 67.3 ) μmol/L in the control group. The difference was also statistically obvious (t=3.09, P＜0.05). Conclusion The effect of treating gouty arthritis by Chinese herbal medicine both orally taken and externally applied was better than western medicine exclusively.     

痛风病的国内外认识及治疗进展与思考

痛风病是指与高尿酸血症、尿酸盐沉积密切相关的进展性代谢疾病,已成为我国第二大类代谢疾病。通过梳理和总结国内外痛风相关疾病的指南和专家共识以及中医对痛风病的认识,对痛风病的中西医认识进展进行综述。以及基于对痛风病的认识,总结中西医治疗痛风病的研究进展,以期为痛风病的诊疗及研究提供参考。     

急性痛风性关节炎的中西医结合治疗及护理

目的探讨急性痛风性关节炎中西医结合治疗及护理方法。方法临床观察62例患者,随机分成治疗组31例,对照组31例,详细总结了急性痛风性关节炎急性期中西医结合治疗疗效及护理方法和缓解期健康教育及出院指导。结果治疗组在关节疼痛缓解时间,关节疼痛消失时间,治疗总有效率方面均优于对照组,均显示有明显统计学差异(P<0.05)。     

四妙汤加味配合中药外敷治疗痛风性关节炎的临床研究

目的：探讨四妙汤加减配合中药外敷治疗痛风性关节炎的临床疗效。方法收集2010年1月至2013年8月本院就诊痛风性关节炎患者76例,按病例尾号随机分为两组各38例,两组患者治疗期间均进食低热量饮食,并加大日饮水量（＞2000 ml）,戒烟酒,禁食高嘌呤食物。对照组急性期口服秋水仙碱片、吲哚美辛肠溶片,缓解期口服双氯芬酸钠缓释片。治疗组在对照组治疗基础上加用四妙汤加味并配合外敷自拟消肿止痛散治疗。治疗7d后观察并记录患者治疗前后的中医症状积分、关节炎症状积分、症状缓解时间,红细胞沉降率（ESR）、C反应蛋白（CRP）、血尿酸（UA）、白细胞介素-1β（IL-1β）、白细胞介素-18（IL-18）。结果两组治疗后CRP、ESR[治疗组分别为（22.06±10.31）mg/L、（25.18±17.80）mm/h,对照组分别为（14.11±7.32） mg/L、（24.16±22.09） mm/h]均较同组治疗前降低[治疗组分别为（82.16±21.37）mg/L、（72.13±32.36）mm/h,对照组分别为（52.46±22.26）mg/L、（62.72±33.31）mm/h, P＜0.01],治疗组ESR低于对照组（P＜0.05）。两组治疗后IL-1？、IL-18[治疗组为（55.26±16.31）pg/ml、（187.32±50.38）pg/ml,对照组为（57.25±18.21）pg/ml、（178.49±52.60）pg/ml]均较同组治疗前[治疗组分别为（106.11±41.02）pg/ml、（398.15±132.52）pg/ml,对照组分别为（109.23±40.12）pg/ml、（397.16±141.21）pg/ml]明显降低（P＜0.01）。治疗后治疗组完全缓解时间为（4.02±2.08）d,对照组为（4.95±2.68）d,两组完全缓解时间比较,差异有统计学意义（P＜0.05）。结论四妙汤加减配合中药外敷可减少中医症状积分、关节炎症状积分,缩短症状缓解时间;降低ESR、CRP、UA水平,增强机体免疫力。     

赵纪生教授论治痛风性肾病

赵纪生教授认为痛风性肾病中医多为先天不足,后天失养所致,病机多属本虚标实,虚实夹杂。本虚为脾肾气虚,气阴两虚,标实为痰瘀湿浊互结,中医治疗注重辨证施治,标本兼顾,以健脾益肾,清利湿浊;益气养阴,清化痰湿;滋补肝肾,活血化瘀为主,强调内外结合,注重调护,把理气活血化瘀法贯穿于始终。     

The inhibitor effect of RKIP on inflammasome activation and inflammasome-dependent diseases

Aberrant inflammasome activation contributes to the pathogenesis of various human diseases, including atherosclerosis, gout, and metabolic disorders. Elucidation of the underlying mechanism involved in the negative regulation of the inflammasome is important for developing new therapeutic targets for these diseases. Here, we showed that Raf kinase inhibitor protein (RKIP) negatively regulates the activation of the NLRP1, NLRP3, and NLRC4 inflammasomes. RKIP deficiency enhanced caspase-1 activation and IL-1β secretion via NLRP1, NLRP3, and NLRC4 inflammasome activation in primary macrophages. The overexpression of RKIP in THP-1 cells inhibited NLRP1, NLRP3, and NLRC4 inflammasome activation. RKIP-deficient mice showed increased sensitivity to Alum-induced peritonitis and Salmonella typhimurium-induced inflammation, indicating that RKIP inhibits NLRP3 and NLRC4 inflammasome activation in vivo. Mechanistically, RKIP directly binds to apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) and competes with NLRP1, NLRP3, or NLRC4 to interact with ASC, thus interrupting inflammasome assembly and activation. The depletion of RKIP aggravated inflammasome-related diseases such as monosodium urate (MSU)-induced gouty arthritis and high-fat diet (HFD)-induced metabolic disorders. Furthermore, the expression of RKIP was substantially downregulated in patients with gouty arthritis or type 2 diabetes (T2D) compared to healthy controls. Collectively, our findings suggest that RKIP negatively regulates NLRP1, NLRP3, and NLRC4 inflammasome activation and is a potential therapeutic target for the treatment of inflammasome-related diseases.