Omeprazole does not reduce gastroesophageal reflux: New insights using multichannel intraluminal impedance technology

Omeprazole does not reduce gastroesophageal reflux: New insights using multichannel intraluminal impedance technology
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DOI:
10.1016/j.gassur.2004.08.001
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发表时间:
2004-11-01
影响因子:
3.2
通讯作者:
DeMeester, TR
DeMeester, TR
中科院分区:
医学3区
文献类型:
--
作者:
Tamhankar, AP;Peters, JH;DeMeester, TR

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质子泵抑制剂是胃食管反流病医疗管理的支柱。虽然它们可以缓解大多数症状,但反流可能会持续存在。我们假设奥美拉唑不能减少胃食管反流的总量,而只是改变其pH值特征。6名无症状志愿者在服用奥美拉唑(BID 20 mg) 7天前后进行24小时阻抗pH监测。通过食管下括约肌(LES)上方5 cm处的pH测量,将反流事件分为酸性(pH < 4)、弱酸(pH bbbb4但降低> 1个pH单位)和非酸性(pH bbbb4但降低< 1个pH单位)。胃pH传感器位于LES下方10 cm处,用于验证奥美拉唑的作用。阻抗检测到奥美拉唑治疗前共116次反流发作,治疗后96次。每位受试者反流发作的中位数(18次对16次,P = 0.4)、反流发作的中位数持续时间(4.7分钟对3.6分钟,P = 0.5)和反流发作的总持续时间(27.2分钟对42.4分钟,P = 0.5)在奥美拉唑前后相似。服用奥美拉唑后,胃酸反流发生率从服用前的63%降至2.1% (P < 0.0001),而非胃酸反流发生率增加(15%至76%,P < 0.0001)。弱酸反流发作无变化(22.4% ~ 21.8%,P = 1.0)。pH值大于4的反流发生率从37%上升到98% (P < 0.0001)。在正常受试者中,奥美拉唑治疗不影响反流发作次数或持续时间;相反,它将胃酸反流转化为较少的胃酸反流,从而使食道暴露于改变的胃液中。这些观察结果可以解释质子泵抑制剂治疗后症状的持续和粘膜损伤的出现。(C) 2004消化道外科学会。
Proton pump inhibitors are the mainstay of medical management in gastroesophageal reflux disease. Although they provide relief from most symptoms, reflux may persist. We hypothesize that omeprazole does not reduce the total amount of gastroesophageal reflux but simply alters its pH characteristics. Six asymptomatic volunteers had combined 24-hour impedance pH monitoring before and after 7 days of omeprazole (20 mg BID). Multichannel intraluminal impedance was used to identify reflux episodes, which were classified as acid (pH < 4), weak acid (pH > 4 but decrease > 1 pH unit) and nonacid (pH > 4 and decrease < 1 pH unit) by pH measurements 5 cm above the lower esophageal sphincter (LES). A gastric pH sensor located 10 cm below the LES was used to verify the action of omeprazole. Impedance detected a total of 116 reflux episodes before and 96 episodes after omeprazole treatment. The median number of reflux episodes (18 versus 16, P = 0.4), median duration of reflux episodes (4.7 versus 3.6 minutes, P = 0.5), and total duration of reflux episodes (27.2 versus 42.4 minutes, P = 0.5) per subject were similar before and after omeprazole. Acid reflux episodes were reduced from 63% before to 2.1% after omeprazole (P < 0.0001), whereas nonacid reflux episodes increased (15% to 76%, P < 0.0001). Weak acid reflux episodes did not change (22.4% to 21.8%, P = 1.0). The proportion of reflux episodes greater than pH 4 increased from 37% to 98% (P < 0.0001). In normal subjects, omeprazole treatment does not affect the number of reflux episodes or their duration; rather it converts acid reflux to less acid reflux, thus exposing esophagus to altered gastric juice. These observations may explain the persistence of symptoms and emergence of mucosal injury white on proton pump inhibitor therapy. (C) 2004 The Society for surgery of the Alimentary Tract.