机构地区:[1]天津市第五中心医院内分泌科,天津市300450 [2]天津市第五中心医院消化科,天津市300450 [3]天津市第五中心医院普外科,天津市300450 [4]天津市第五中心医院中心实验室,天津市早产儿器官发育表观遗传重点实验室,天津市300450
出 处:《世界华人消化杂志》2022年第19期845-849,共5页World Chinese Journal of Digestology
基 金:天津市自然科学基金资助项目,No.19JCZDJC35200;国家自然科学基金资助项目,No.81471175.
摘 要:背景质子泵抑制剂通过阻碍胃壁细胞H+-K+-ATP酶发挥抑制胃酸分泌的作用.除常见的药物过敏等不良反应外,质子泵抑制剂还可能导致痛风患者出现急性痛风发作,但临床医师对质子泵抑制剂可能引起痛风性关节炎急性发作的认识不足,其发病机制尚不明确.目的分析奥美拉唑及其S异构体(艾斯奥美拉唑)诱发痛风性关节炎急性发作的临床特点.方法选择2020-11/2021-05在天津市第五中心医院住院治疗,应用奥美拉唑及其S异构体后出现痛风性关节炎急性发作的11例患者的病例资料进行分析.结果患者男性9例(81.8%),女性2例(18.2%);平均年龄(56.73±15.40)岁.临床诊断为慢性胃炎6例(54.5%)、急性上消化道出血2例(18.2%)、十二指肠球部溃疡1例(9.1%)、肠炎1例(9.1%)、空肠间质瘤伴出血1例(9.1%).应用奥美拉唑6例(54.5%)、艾斯奥美拉唑5例(45.5%),均为静脉给药.应用奥美拉唑及其S异构体至痛风性关节炎急性发作时间为(4.73±4.10)d.临床表现为单关节或者多个关节红肿疼痛.11例患者尿酸水平均高于正常,且应用奥美拉唑及其S异构体后尿酸水平较应用前显著升高(t=-0.81,P=0.00).贫血患者与无贫血患者相比,出现痛风性关节炎急性发作的时间无显著差异(t=-0.37,P=0.72);肌酐升高患者与肌酐正常者相比,出现痛风性关节炎急性发作的时间无明显差异(t=0.48,P=0.65);静脉应用奥美拉唑与艾斯奥美拉唑相比,出现痛风性关节炎急性发作的时间无明显差别(t=0.78,P=0.46).结论奥美拉唑及其S异构体诱发痛风性关节炎急性发作,可能与其抑制肾脏H+-K+-ATP酶,使尿酸排泄减少有关.BACKGROUND Proton pump inhibitors inhibit gastric acid secretion by blocking H+-K+-ATPase in gastric parietal cells.In addition to common adverse reactions such as drug allergies,proton pump inhibitors may also cause acute gout attacks in patients with gout,but clinicians do not know enough that proton pump inhibitors may cause the acute attack of gouty arthritis,whose pathogenesis is still unclear.AIM To analyze the clinical characteristics of acute gout arthritis induced by omeprazole and its S-isomer(esomeprazole).METHODS The clinical data of 11 patients who were hospitalized at Tianjin Fifth Central Hospital from November 2020 to May 2021 and developed an acute attack of gout arthritis after using omeprazole and its S-isomer were analyzed.RESULTS There were nine(81.8%)males and two(18.2%)females.The mean age was 56.73±15.4 years.The clinical diagnoses were chronic gastritis in six(54.5%)cases,acute upper gastrointestinal bleeding in two(18.2%),duodenal bulb ulcer in one(9.1%),enteritis in one(9.1%),and jejunal stromal tumor with bleeding in one(9.1%).Five(45.5%)cases used esomeprazole,and six used omeprazole;both were intravenously administered.Clinical manifestations were redness,swelling,and pain of single or multiple joints.The uric acid levels of the 11 patients were all higher than normal,and the uric acid level after using omeprazole and its S-isomer was significantly higher than before(t=-0.81,P=0.00).The time between using omeprazole and its S-isomer to onset of acute gout arthritis was 4.73±4.10 d;there was no significant difference in the time between patients with and without anemia(t=-0.37,P=0.72),between patients with elevated creatinine levels and those with normal creatinine levels(t=0.48,P=0.65),and between patients who received esomeprazole compared with those who received omeprazole(t=0.78,P=0.46).CONCLUSION Omeprazole and its S-isomer induce the acute attack of gout arthritis,which may be related to the inhibition of renal H+-K+-ATPase and the reduction of uric acid excretion.
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