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小肠细菌过度生长和胃食管反流病(5)
丁文京
3、肠道气体影响食管下括约肌
碳水化合物发酵对健康人的胃和食管运动有影响。Piche等人研究口服低聚果糖(fructooligosaccharides, FOS)对胃食管反流病患者结肠发酵的影响。他们采用交叉设计,对9例有症状的胃食管反流病患者进行2天和7天的10g纤维/天饮食,每天3次,饭后服用6.6g 低聚果糖或安慰剂。每一个周期都被至少3周的清洗所分隔。在第7天,在禁食条件下和含有6.6g 低聚果糖或安慰剂的试验餐后记录食道运动和pH值。监测呼出气中氢浓度用以反映结肠发酵和血浆胰高血糖素样肽1(GLP-1)、肽YY和胆囊收缩素浓度。结果显示,与安慰剂相比,低聚果糖导致短暂性食管下括约肌松弛和反流发作、食管酸暴露和胃食管反流病症状评分显著增加。服用低聚果糖后GLP-1的血浆综合反应显著高于安慰剂。该研究表明不可消化碳水化合物的结肠发酵增加了胃食管反流的发生率,增加了胃食管反流的次数,以及增加了胃食管反流的症状。尽管可能涉及不同的机制,但GLP-1的过量释放可能至少部分解释了这些效应(Piche, et al., 2003.)。
4、小肠细菌过度生长导致胃食管反流病的潜在机制
不同角度的研究揭示胃食管反流病和小肠细菌过度生长可能存在高度的相关性,小肠细菌过度生长可能是导致胃食管反流病的一个重要因素。小肠产气时,由于细菌酵解食物导致产气增加,气体可以向各个方向扩散,部分气体上升经过胃和食管外溢,带动胃内容物进入食管,甚至进入咽喉和呼气器官,导致胃食管反流病和食管外疾病。小肠气体增加造成腹内压增加,压迫胃,导致胃内容物向食管挤压,也可以导致导致胃食管反流病和食管外疾病。在临床实践中发现胃食管反流病的病人经常伴有腹胀、腹痛、嗳气、打嗝、多屁等症状,与小肠细菌过度生长的症状高度一致。用食管多通道阻抗-pH检测技术也看到气体反流和气体与液体并存的混合反流。临床症状和检查结果都揭示小肠细菌过度生长可能是导致胃食管反流病的一个重要因素。
Dodds等人评估了10例反流性食管炎患者胃食管反流的机制,并将结果与10例对照组进行了比较。患者有更多的反流发作(12小时内35±15次,对照组为9±8次),食管下括约肌压力较低(13±8毫米汞柱,对照组为29±9次)(P<0.001)。他们提出胃食管反流病的发生有三种不同的机制:(1)食管下括约肌暂时完全松弛,(2)腹腔内压暂时升高,(3)或与食管下括约肌静息压低相关的自发性自由反流。对照组94%的反流是由短暂的括约肌松弛引起的。在这些病人中,65%的反流伴随着短暂的括约肌松弛,17%伴随着腹腔内压力的短暂增加,18%是自发的自由反流。个别患者的主要反流机制各不相同:一些患者的静息括约肌压力和反流主要发生在短暂括约肌松弛期间,而其他静息括约肌压力较低的患者的自发自由反流或反流则发生在腹内压力增加期间(Dodds, et al., 1982.)。
小结:小肠细菌过多生长引起胃食管反流的途径
1、小肠内细菌产生的气体会导致小肠扩张。这种膨胀向上推压胃。对胃的额外压力会导致胃内容物推压食管下括约肌(LES)并通过回流进入食管。
2、细菌产生的气体可以向上排出。这种气体通过在阀门上产生压力来减弱食管下括约肌。在打嗝过程中,气体通过食管下括约肌反流入食管。
3、细菌过度生长导致无法合成某些消化酶,降低小肠将蛋白质分解为氨基酸的能力,并阻止营养物质的吸收,导致消化过程减慢。消化过程的减慢导致小肠内食物的增加。体积的增加会对胃和左心室造成压力,从而导致胃酸反流、烧心和胃食管反流。
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