Distinct profiles of gastritis in dyspepsia subgroups. Their different clinical responses to gastritis healing after Helicobacter pylori eradication.

Distinct profiles of gastritis in dyspepsia subgroups. Their different clinical responses to gastritis healing after Helicobacter pylori eradication.
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消化不良亚组中胃炎的不同特征。

DOI:
10.3109/00365529409094858
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发表时间:
1994
影响因子:
1.9
通讯作者:
Enrico Solcia
Enrico Solcia
中科院分区:
医学4区
文献类型:
--
作者:
E. Trespi;F. Broglia;Laura Villani;O. Luinetti;R. Fiocca;Enrico Solcia

文献摘要

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背景 幽门螺杆菌胃炎在非溃疡性消化不良(NUD)发病机制中的作用尚不清楚。 方法 通过适当的临床问卷调查和胃镜检查,我们从139例门诊消化不良患者中筛选出87例症状较重且具有群体特征的非溃疡性消化不良患者,其中35例为溃疡样(ULD)。38例为运动障碍样(DLD),14例为反流样消化不良(RLD)。根据悉尼系统对活检标本进行幽门螺杆菌胃炎评估。对70例幽门螺杆菌阳性患者给予奥美拉唑20 mg,每日2次,阿莫西林1g,每日3次,疗程2周。 结果 幽门螺杆菌在胃粘膜的定植率ULD(91%)和RLD(86%)高于DLD(68%)和无症状患者(42%)。与RLD患者相比,ULD患者的上颌窦活动度评分较高。根除幽门螺杆菌3个月和6个月后,ULD组(而不是DLD组)的排尿症状评分显著下降。 结论 幽门螺杆菌胃炎,尤其是活动性胃窦炎,似乎是ULD的致病因素之一。其在RLD和DLD发病机制中的作用有待进一步研究。
BACKGROUND A contribution of Helicobacter pylori gastritis to the pathogenesis of non-ulcer dyspepsia (NUD) remains uncertain. METHODS Administration of an appropriate clinical questionnaire followed by endoscopy allowed us to select, among 139 outpatients with dyspepsia, 87 non-ulcer dyspepsia patients with more severe and group-distinctive symptoms, 35 of whom were classified as having ulcer-like (ULD). 38 as dysmotility-like (DLD), and 14 as reflux-like dyspepsia (RLD). Biopsy specimens were evaluated for H. pylori gastritis in accordance with the Sydney system. The 70 H. pylori-positive cases were treated with omeprazole, 20 mg twice daily, and amoxycillin, 1 g three times daily for 2 weeks. RESULTS Higher rates of H. pylori colonization were found histologically in the gastric mucosa of ULD (91%) and RLD (86%) than in that of DLD (68%) or asymptomatic (42%) patients. ULD differed from RLD patients in their higher score of antritis activity. Three and 6 months after H. pylori eradication ULD (but not DLD) showed significant regression of dypspetic symptoms scores. CONCLUSIONS It seems likely that H. pylori gastritis, with special reference to active antritis, is among causative factors of ULD. Its role in the pathogenesis of RLD and DLD needs further investigation.