中华儿科杂志
中華兒科雜誌
중화인과잡지
Chinese Journal of Pediatrics
2008年
4期
257-262
,共6页
马鸣%陈洁%张雁翼%李中跃%江米足%余金丹
馬鳴%陳潔%張雁翼%李中躍%江米足%餘金丹
마명%진길%장안익%리중약%강미족%여금단
十二指肠胃反流%胆汁反流%胃黏膜%螺杆菌,幽门%儿童
十二指腸胃反流%膽汁反流%胃黏膜%螺桿菌,幽門%兒童
십이지장위반류%담즙반류%위점막%라간균,유문%인동
Duodenogastric reflux%Bile reflux%Gastric mucosa%Helicobacter pvlori%Child
目的 观察儿童原发性十二指肠胃反流(DGR)对胃黏膜的损伤作用,并初步探讨DGR与临床症状、幽门螺杆菌感染和胃内酸度的关系.方法 对81例因腹痛、饱胀、恶心、呕吐等上消化道症状就诊的患儿,进行临床症状评分、胃镜检查、胃窦黏膜组织病理学检查和24 h胃内胆红素监测,其中51例同步行24 h胃内pH监测.以胆汁反流总时间百分比作为胆汁反流程度的指标.根据胃窦黏膜的胃镜下改变以及组织病理学特征变化有无进行分组,分别比较2组的胆汁反流程度.并对胃内胆汁反流与临床症状评分、胃内酸度以及Hp感染等进行相关性分析.结果 胃窦黏膜有充血者[17.1%(0.5%～53.2%)]较无充血者[6.5%(0～58.6%)](Z=-1.980),有黄染者[19.8%(0.5%～58.6%)]较无黄染者[8.8%(0-38.0%)](Z=-2.956),胆汁反流总时间百分比高,差异均有统计学意义(P＜0.05或0.01);胃窦黏膜组织病理学检查,有肠化组胆汁反流总时间百分比[29.0%(1.9%～58.6%)]较无肠化组[14.3%(0～53.7%)]长,差异有统计学意义(Z=-2.026,P＜0.05).有慢性炎症组与无慢性炎症组、有活动性组与无活动性组相比,胆汁反流程度差异无统计学意义(P＞0.05).胆汁反流严重度与饱胀症状正相关(r=0.258,P＜0.05),与Hp感染(r=0.016)和胃内酸度(r=0.124)元明显相关性(P均＞0.05).结论 原发性DGR可致儿童胃窦黏膜损伤,胃镜下主要表现为胃窦黏膜充血和黄染,病理组织学变化上与肠上皮化生有关,与炎症细胞浸润无关.DGR与Hp感染和胃内酸度均无关,DGR可能是一个独立的致病因素,与Hp感染和胃酸一起共同对胃黏膜造成损伤.
目的 觀察兒童原髮性十二指腸胃反流(DGR)對胃黏膜的損傷作用,併初步探討DGR與臨床癥狀、幽門螺桿菌感染和胃內痠度的關繫.方法 對81例因腹痛、飽脹、噁心、嘔吐等上消化道癥狀就診的患兒,進行臨床癥狀評分、胃鏡檢查、胃竇黏膜組織病理學檢查和24 h胃內膽紅素鑑測,其中51例同步行24 h胃內pH鑑測.以膽汁反流總時間百分比作為膽汁反流程度的指標.根據胃竇黏膜的胃鏡下改變以及組織病理學特徵變化有無進行分組,分彆比較2組的膽汁反流程度.併對胃內膽汁反流與臨床癥狀評分、胃內痠度以及Hp感染等進行相關性分析.結果 胃竇黏膜有充血者[17.1%(0.5%～53.2%)]較無充血者[6.5%(0～58.6%)](Z=-1.980),有黃染者[19.8%(0.5%～58.6%)]較無黃染者[8.8%(0-38.0%)](Z=-2.956),膽汁反流總時間百分比高,差異均有統計學意義(P＜0.05或0.01);胃竇黏膜組織病理學檢查,有腸化組膽汁反流總時間百分比[29.0%(1.9%～58.6%)]較無腸化組[14.3%(0～53.7%)]長,差異有統計學意義(Z=-2.026,P＜0.05).有慢性炎癥組與無慢性炎癥組、有活動性組與無活動性組相比,膽汁反流程度差異無統計學意義(P＞0.05).膽汁反流嚴重度與飽脹癥狀正相關(r=0.258,P＜0.05),與Hp感染(r=0.016)和胃內痠度(r=0.124)元明顯相關性(P均＞0.05).結論 原髮性DGR可緻兒童胃竇黏膜損傷,胃鏡下主要錶現為胃竇黏膜充血和黃染,病理組織學變化上與腸上皮化生有關,與炎癥細胞浸潤無關.DGR與Hp感染和胃內痠度均無關,DGR可能是一箇獨立的緻病因素,與Hp感染和胃痠一起共同對胃黏膜造成損傷.
목적 관찰인동원발성십이지장위반류(DGR)대위점막적손상작용,병초보탐토DGR여림상증상、유문라간균감염화위내산도적관계.방법 대81례인복통、포창、악심、구토등상소화도증상취진적환인,진행림상증상평분、위경검사、위두점막조직병이학검사화24 h위내담홍소감측,기중51례동보행24 h위내pH감측.이담즙반류총시간백분비작위담즙반류정도적지표.근거위두점막적위경하개변이급조직병이학특정변화유무진행분조,분별비교2조적담즙반류정도.병대위내담즙반류여림상증상평분、위내산도이급Hp감염등진행상관성분석.결과 위두점막유충혈자[17.1%(0.5%～53.2%)]교무충혈자[6.5%(0～58.6%)](Z=-1.980),유황염자[19.8%(0.5%～58.6%)]교무황염자[8.8%(0-38.0%)](Z=-2.956),담즙반류총시간백분비고,차이균유통계학의의(P＜0.05혹0.01);위두점막조직병이학검사,유장화조담즙반류총시간백분비[29.0%(1.9%～58.6%)]교무장화조[14.3%(0～53.7%)]장,차이유통계학의의(Z=-2.026,P＜0.05).유만성염증조여무만성염증조、유활동성조여무활동성조상비,담즙반류정도차이무통계학의의(P＞0.05).담즙반류엄중도여포창증상정상관(r=0.258,P＜0.05),여Hp감염(r=0.016)화위내산도(r=0.124)원명현상관성(P균＞0.05).결론 원발성DGR가치인동위두점막손상,위경하주요표현위위두점막충혈화황염,병리조직학변화상여장상피화생유관,여염증세포침윤무관.DGR여Hp감염화위내산도균무관,DGR가능시일개독립적치병인소,여Hp감염화위산일기공동대위점막조성손상.
Objective Duodenogastric reflux (DGR) is a reverse flow of duodenal juice into stomach through pylorus composed of bile acid,pancreatic secretion,and intestinal secretion.The increased entero-gastric reflux results in mucosal injury that may relate not only to reflux gastritis but also esophagitis,gastric ulcers,carcinoma of stomach and esophagus.However,the exact mechanisms of gastric mucosal damage caused by DGR are still unknown.The objective of the present study is to investigate the pathogenic effect of primary DGR on gastric mucosa in children,and to explore the correlation of DGR with clinical symptoms,Hp infection and intragastric acidity.Method Totally 81 patients with upper gastrointestinal manifestations were enrolled and they were graded according to the symptom scores and underwent endoscopic,histological examinations and 24-hour intra-gastric bilirubin was monitored with Bilitec 2000.Of the 81 cases,51 underwent the 24-hour intra-gastric pH monitoring by ambulatory pH recorder simultaneously.The total fraction time of bile reflux was considered as a marker to evaluate the severity of DGR.The total fraction time of bile reflux was compared between the patients with positive and negative results under endoscopy and histologically.respectively.The correlations of the total fraction time of bile reflux with clinical symptom score,Hp infection,intragastric acidity were analyzed respectively.Result The total fraction time of bile reflux in the patients with hyperemia and yellow stain gastric antral mucosa under endoscopy was significantly higher than that without those changes[17.1%(0.5%～53.2%)vs.6.5%(0～58.6%),Z=-1.980,P<0.05;19.8%(0.5%～58.6%)vs.8.8%(0～38.0%),Z=-2.956,P<0.01 respectively].Histologically,the cases with intestinal metaplasia had significantly higher total fraction time of bile reflux than in the cases without intestinal metaplasia [29.0%(1.9%～58.6%)vs.14.3%(0～53.7%),Z=-2.026,P<0.05],but no significant difference was found either between the cases with and without chronic inflammation(P>0.05)or between the cases with and without active inflammation(P<0.05).The severity of bile reflux was positively correlated with the score of abdominal distention(r=0.258,P<0.05),but no correlation with either the severity of intragastric acid (r=-0.124,P>0.05),or Hp infection(r=0.016,P>0.05)was found.Conclusion Primary DGR could cause gastric mucosal lesions manifested mainly as hyperemia and bile-stained gastric antral mucosa under endoscopy and the gastric antral intestinal metaplasia histologically in children.There was no significant correlation between DGR and gastric mucosal inflammatory infihration.DGR had no relevance to Hp infection and intragastrie acidity.We conclude that DGR is probably an independent etiological factor and might play a synergistic role in the pathogenesis of gastric mucosal lesions along with gastric acid and Hp infection.
