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根除幽门螺杆菌可降低长期使用奥美拉唑治疗期间的高胃泌素血症。

Eradicating Helicobacter pylori reduces hypergastrinaemia during long-term omeprazole treatment.

作者信息

el-Nujumi A, Williams C, Ardill J E, Oien K, McColl K E

机构信息

University Department of Medicine and Therapeutics, Western Infirmary, Glasgow, UK.

出版信息

Gut. 1998 Feb;42(2):159-65. doi: 10.1136/gut.42.2.159.

Abstract

BACKGROUND

Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.

AIMS

To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.

METHODS

Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.

RESULTS

In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylori eradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26-86) at initial presentation and increased to 64 ng/l (range 29-271) after seven months omeprazole, representing a median increase of 68% (p < 0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95).

CONCLUSION

Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long-term proton pump inhibitor treatment.

摘要

背景

质子泵抑制剂药物治疗和幽门螺杆菌感染均可导致人体高胃泌素血症。

目的

确定根除幽门螺杆菌是否是在后续质子泵抑制剂治疗期间降低高胃泌素血症的一种方法。

方法

幽门螺杆菌感染患者被随机分为抗幽门螺杆菌治疗组或对症治疗组。1个月后,所有患者均接受为期4周的奥美拉唑治疗,初始剂量为40mg/天,持续1个月,随后剂量为20mg/天,持续6个月。在每次治疗前后测量血清胃泌素浓度。

结果

在随机接受抗幽门螺杆菌治疗的患者中,感染根除使空腹胃泌素中位数降低了48%,进餐刺激后的胃泌素降低了46%。以抗幽门螺杆菌/对症治疗后1个月的胃泌素浓度作为基线,奥美拉唑治疗使幽门螺杆菌感染患者和幽门螺杆菌已根除患者的血清胃泌素增加了相似的百分比。因此,在未根除幽门螺杆菌的患者中,初次就诊时空腹胃泌素浓度中位数为38ng/l(范围26 - 86),奥美拉唑治疗7个月后升至64ng/l(范围29 - 271),中位数增加了68%(p < 0.005)。相比之下,在随机接受幽门螺杆菌根除治疗的患者中,初次就诊时空腹胃泌素中位数为54ng/l(范围17 - 226),奥美拉唑治疗7个月后为38ng/l(范围17 - 95),无变化。

结论

根除幽门螺杆菌是减少后续长期奥美拉唑治疗期间胃泌素升高的一种方法。鉴于高胃泌素血症的潜在有害影响,在开始长期质子泵抑制剂治疗前使患者幽门螺杆菌呈阴性可能是合适的。

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