山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2009年
25期
7-10
,共4页
姜东春%韩俊岭%李莉%韩莹
薑東春%韓俊嶺%李莉%韓瑩
강동춘%한준령%리리%한형
十二指肠胃反流,病理性,原发性%胆汁监测%致病因素
十二指腸胃反流,病理性,原髮性%膽汁鑑測%緻病因素
십이지장위반류,병이성,원발성%담즙감측%치병인소
duodenogastric reflux,pathological,primary%bile monitoring%pathogenic factors
目的 探讨原发性病理性十二指肠胃反流(DGR)胃黏膜病变、幽门螺杆菌(Hp)感染、胆汁反流之间的关系.方法 应用便携式胆汁监测仪监测86例原发性病理性DGR患者胃内24 h胆汁反流情况;另取胃黏膜组织活检,分别行快速尿素酶试验、改良Giemsa染色和HE染色,判断有无Hp感染,并观察胃黏膜慢性炎症、活动性、萎缩、肠化等组织学特征.结果 ①将患者根据有无Hp感染分为Hp阳性组和Hp阴性组,Hp阳性组胃窦部黏膜病理积分、胆红素吸收值≥0.25的时间百分比均显著低于Hp阴性组(P均＜0.05);两组胆红素吸收值≥0.25的时间百分比和胃窦、胃角部黏膜病理积分均呈显著正相关(P均＜0.05).②将患者根据胆汁反流程度分为高反流组和低反流组,高反流组Hp阳性率显著低于低反流组(P＜0.05),胃窦和胃角部黏膜肠上皮化生的检出率、胃窦部黏膜病理积分均显著高于低反流组(P均＜0.05).结论 原发性病理性DGR导致胃窦黏膜损伤的主要因素可能为胆汁反流,随胆汁反流程度加重,胃窦黏膜损伤程度加重;胆汁反流可能抑制Hp在胃窦部定植,Hp感染可能与胆汁反流协同作用导致胃体部黏膜损伤.
目的 探討原髮性病理性十二指腸胃反流(DGR)胃黏膜病變、幽門螺桿菌(Hp)感染、膽汁反流之間的關繫.方法 應用便攜式膽汁鑑測儀鑑測86例原髮性病理性DGR患者胃內24 h膽汁反流情況;另取胃黏膜組織活檢,分彆行快速尿素酶試驗、改良Giemsa染色和HE染色,判斷有無Hp感染,併觀察胃黏膜慢性炎癥、活動性、萎縮、腸化等組織學特徵.結果 ①將患者根據有無Hp感染分為Hp暘性組和Hp陰性組,Hp暘性組胃竇部黏膜病理積分、膽紅素吸收值≥0.25的時間百分比均顯著低于Hp陰性組(P均＜0.05);兩組膽紅素吸收值≥0.25的時間百分比和胃竇、胃角部黏膜病理積分均呈顯著正相關(P均＜0.05).②將患者根據膽汁反流程度分為高反流組和低反流組,高反流組Hp暘性率顯著低于低反流組(P＜0.05),胃竇和胃角部黏膜腸上皮化生的檢齣率、胃竇部黏膜病理積分均顯著高于低反流組(P均＜0.05).結論 原髮性病理性DGR導緻胃竇黏膜損傷的主要因素可能為膽汁反流,隨膽汁反流程度加重,胃竇黏膜損傷程度加重;膽汁反流可能抑製Hp在胃竇部定植,Hp感染可能與膽汁反流協同作用導緻胃體部黏膜損傷.
목적 탐토원발성병이성십이지장위반류(DGR)위점막병변、유문라간균(Hp)감염、담즙반류지간적관계.방법 응용편휴식담즙감측의감측86례원발성병이성DGR환자위내24 h담즙반류정황;령취위점막조직활검,분별행쾌속뇨소매시험、개량Giemsa염색화HE염색,판단유무Hp감염,병관찰위점막만성염증、활동성、위축、장화등조직학특정.결과 ①장환자근거유무Hp감염분위Hp양성조화Hp음성조,Hp양성조위두부점막병리적분、담홍소흡수치≥0.25적시간백분비균현저저우Hp음성조(P균＜0.05);량조담홍소흡수치≥0.25적시간백분비화위두、위각부점막병리적분균정현저정상관(P균＜0.05).②장환자근거담즙반류정도분위고반류조화저반류조,고반류조Hp양성솔현저저우저반류조(P＜0.05),위두화위각부점막장상피화생적검출솔、위두부점막병리적분균현저고우저반류조(P균＜0.05).결론 원발성병이성DGR도치위두점막손상적주요인소가능위담즙반류,수담즙반류정도가중,위두점막손상정도가중;담즙반류가능억제Hp재위두부정식,Hp감염가능여담즙반류협동작용도치위체부점막손상.
Objective To study the relationship among the gastric mucosal lesions caused by primary pathological duodenogastric reflux , the Hp infection, the bile reflux assessed with bilirubin absorbance. Methods 24 hours intragastric bile reflux of 86 cases in primary pathological duodenogastric reflux were measured using Bilitec 2000. Endoscopy and gastric mucosa biopsies were performed in all cases for examination with rapid urease test, improved Giemsa staining and HE staining in order to diagnose Hp infection and define the lesions of gastric mucosa. The degree of chronic inflammation, activity, atrophy, intestinal metaplasia of gastric mucosa were observed. Results ① All cases were divided into two groups, Hp positive group and Hp negative group, based on the diagnosis of Hp infection. The time percentage of bilirubin absorbance≥0.25 in Hp positive group was significantly lower than that in Hp negative group(P＜0.05). The time percentage of bilirubin absorbance≥0.25 was positively correlated with New Sydney system pathological scores of gastric antrum and gastric anguli in two groups. ②Based on the severity of bile reflux, all cases were divided into two groups, high reflux group and low reflux group. Hp infection rate in high reflux group was significantly lower than that in low reflux group(P＜0.05). The frequency of intestinal metaplasia of gastric antrum and anguli, the New Sydney system pathological scores of gastric antrum in high reflux group were significantly higher than that in low reflux group(P＜0.05). Conclusions Bile reflux is possibly the main cause to mucosal lesions of gastric antrum in primary pathological duodenogastric reflux. Bile reflux may inhibit Hp to locate in gastric antrum. Hp infection and bile reflux can contribute to mucosal lesions of gastric body cooperatively.
