动态监测胃食管反流患者食管24hpH值及压力

Study of 24 h esophageal pH monitoring and manometryin gastroesophageal reflux patients

目的：探讨胃食管反流（ＧＥＲ）的食管酸暴露与动力学改变特征。方法：采用２４ｈ食管ｐＨ值及压力联合动态监测，研究２７例ＧＥＲ患者（按食管炎０级、Ⅰ～Ⅱ级、Ⅲ～Ⅳ级分为３组）和１３例对照组患者的食管酸反流特征，及反流发生时食管体部动力改变，并以静态食管测压观察下食管括约肌（ＬＥＳ）静息压变化。结果：３个反流组总的、卧位和立位反流时间百分比均显著低于对照组（Ｐ＜０．０１）。Ⅲ～Ⅳ级食管炎组ＬＥＳ静息压显著低于其他各组（Ｐ＜０．０５），ＬＥＳ长度各组间无明显差异。３个反流组反流期食管蠕动频率均显著低于对照组（Ｐ＜０．０１）；伴食管炎的两组顺行性蠕动百分比较对照组明显降低（Ｐ＜０．０５），其他食管运动（同步、孤立、逆行）各组间无显著差异。Ⅲ～Ⅳ级食管炎组反流期食管蠕动波幅显著低于对照组，蠕动波间期各组间无显著差异。结论：ＧＥＲ患者的酸暴露程度与食管炎程度无显著的对应关系。ＬＥＳ静息压降低和反流发生后食管蠕动减少、频率减慢、幅度降低。

Objective: To investigate the characteristic changes of esophageal acid exposure time and esophageal motility in patients with gastroesophageal reflux (GER). Methods: Ambulatory 24 h esophageal pH monitoring and manometry were carried out in 27 patients with GER. Among these patients, there were 7 cases without esophagitis, 9 with grade Ⅰor Ⅱesophagitis and 11 with grade Ⅲ or Ⅳ esophagitis confirmed by endoscopy. Resting pressure of lower esophageal sphincter (LES) was also studied by means of stationary esophageal manometry. The results were compared with those of 13 controls. Results: The percentages of total, supine and upright acid exposure time were greater in patients with GER than those in controls (P<0.01), while there were no differences among the three groups. LES resting pressure was lower in patients with severe esophagitis than those in controls (P<0.05), however, there were no differences of length of LES among all groups. During the attack of acid reflux, the frequency of esophageal peristalses was lower in patients with GER (P<0.01). The percentage of esophageal peristalses was lower in patients with esophagitis (P<0.05), and the amplitude of esophageal peristalses was decreased in patients with grade Ⅲ～Ⅳesophagitis (P<0.05). Conclusion: Esophageal acid exposure time is not correlated with the severity of esophagitis. Lowed LES resting pressure, and decreased frequency and amplitude of esophageal peristalses during the attack of reflux may play important roles in the pathogenesis of reflux esophagitis.