原发性病理性十二指肠胃反流患者的胃电活动和胃排空研究

The study on gastric electrical activity and gastric emptying in patients with primary pathological duodenogastric reflux

目的通过分析原发性病理性十二指肠胃反流（DGR）患者胆汁反流程度与体表胃电节律变化以及胃排空运动之间的关系，探讨原发性病理性DGR致病因素。方法收集2007年1月至2008年4月青岛市立医院门诊诊断为原发性病理性DGR患者58例（DGR组）和健康者21例（对照组）进行24h胃内胆红素监测、胃镜、胃电图和胃排空检测，分析胃电参数及其与胃排空、胆汁反流和Hp之间的关系。结果①原发性病理性DGR患者的餐前及餐后胃电慢波主频率[（1．94±0．04）cpm比（2．93±0．07）cpm；（2．12±0．03）cpm比（3．35±0．05）cpm]、餐前及餐后正常胃电慢波百分比（74．46%±0．56％比85．55％±1．06％；63．97％±0．64％比86．13％±1．49％）、餐前／餐后功率比（PR）（1．68±0．02比2．75±0．09）均低于对照组（P〈0．05）。原发性病理性DGR患者的餐前及餐后胃动过缓百分比（18．04％±0．36％比7．76％±0．78％；23．73％±0．91％比8．47％±0．55％）、餐前及餐后胃动过速百分比（8．93％±0．26oA比5．75％±0．66％；13．02％±0．40％比7．66％±0．27%）均高于对照组（P〈0．05）。②高反流组患者的餐前及餐后胃电慢波主频率[（1．68±0．07）cpm比（2．13±0．07）cpm；（2．18±0．09）cpm比（2．76±0．06）]、餐前及餐后正常胃电慢波百分比（69．71％±0．43％比80．35％±0．68％；56．36％±0．85％比72．34％±0．80％）、餐前／餐后功率比（PR）（1．47±0．04比2．02±0．04）均低于低反流组（P〈0．05）。高反流组患者的餐前及餐后胃动过缓百分比（22．94％±0．68％比13．47％±0．61％；29．61oA±1．14%比17．55％±0．51％）、餐前及餐后胃动过速百分比（9．94％±0．54％比7．02％±0．42％；17．04％±0．70％比10．71％±0．20％）均高于低反流组（P〈0．05）；③Hp阳性组和Hp阴性组餐前、餐后各胃电参数差异均无统计学意义（P〉0．05）；④DGR患者胃钡条排空者明显低于对照组（37．9％比90．5％，P〈0．05）。DGR组胃排空延迟较对照组明显增多，两者比较差异，（60．3％比9．5％，P〈0．05）。高反流组与低反流组比较胃排空延迟率差异无统计学意义（69．0％比51．7％，P〉0．05）。结论原发性病理性DGR患者存在胃电节律紊乱和胃运动功能障碍，这可能是病理性DGR的一个重要原因。

Objective To explore the etiological factors of primary pathological duodenogastric reflux （DGR） through investigating the relationship between severity of bile refulx, the changes of surface gastric electric rhythm and gastric emptying movement in primary pathological DGR patients. Methods From January 2007 to April 2008 in Qingdao Municipal Hospital, 58 cases of outpatients diagnosed as primary pathological DGR and 21 healthy individuals （control group） were collected and underwent 24-hour gastric bilirubin monitoring, gastric endoscopy, gastric electric rhythm, and gastric emptying test. The relationship between gastric electric parameters and gastric emptying, bilirubin reflux, Hp infection was analyzed. Results 1. The main frequency in fasting and postprandial of primary pathological DGR Patients [（1. 94±0.04） cpm vs （2. 93±0.07） cpm; （2. 12±0.03） cpm vs （3.35±0.05） cpm], the percentage of normal gastric slow wave in fasting and postprandial （74.46± 0.56 vs 85.55 ± 1.06 ; 63.97 ± 0.64 vs 86.13 ± 1.49 ）, and fasting/postprandial power ratio （PR） （1. 68±0.02 vs 2.75±0.09） were all lower than those of control group （P〈0.05）. The percentage of bradygastria in fasting and postprandial of DGR patients （18.04± 0.36 vs 7. 76 ±0. 78; 23. 73± 0.91 vs 8. 47±0.55）, the percentage of taehygastria in fasting and postprandial （8. 93±0.26 vs 5.75 ±0.66;13.02±0.40 vs 7.66±0.27） were higher than that of control group （P〈0.05）. 2. The main frequency of severe reflux patients in fasting and postprandial [（1. 68±0.07） cpm vs （2. 13±0.07） cpm; （2.18±0.09） cpm vs （2. 76±0.06） cpm], the percentage of normal gastric slow wave in fasting and postprandial （69. 71±0. 43 vs 80. 35±0. 68; 56. 36±0. 85 vs 72. 34±0. 80）, fasting / postprandial PR （1. 47±0.04 vs 2. 02±0.04） were lower than those of mild-reflux group （P〈0.05）. The percentage of bradygastria in fasting and postprandial of severe reflux patients （22.94 ± 0.68 vs 13.47±0. 61;29. 61 ± 1. 14 vs 17.55 ±0. 51） and the percentage of tachygastria in fasting and postprandial （9.94±0.54 vs 7. 02±0.42; 17. 04±0. 70 vs 10.71 ±0.20） were higher than that of mild-reflux group （P〈0.05）. 3. There was no significant difference of gastric electrical parameters in fasting and postprandial between Hp-positive and Hp-negative groups （P〉 0.05）. 4. The ratio of gastric emptying in DGR group was significantly lower than that of control group （37.9 % vs 90.5 %, P〈0.05）. The gastric emptying delay in DGR group significantly increased compared with control group （60. 3% vs 9. 5%, P〈0.05）. There was no significant difference in gastric emptying delay between severe-reflux group and light-reflux group （69.0% vs 51. 7%, P〉0. 05）. Conclusions There is dysfuntion of gastric myoelectrical activity and gastric motility in primary pathological DGR patients, which may be an important mechanism in pathological DGR.