Mulholland G, Ardill J E, Fillmore D, Chittajallu R S, Fullarton G M, McColl K E
University Department of Medicine and Therapeutics, Western Infirmary, Glasgow.
Gut. 1993 Jun;34(6):757-61. doi: 10.1136/gut.34.6.757.
Helicobacter pylori infection increases the serum concentration of gastrin, and this may be one of the mechanisms by which it predisposes to duodenal ulceration. Different forms of circulating gastrin were studied both basally and postprandially in 13 duodenal ulcer patients before and one month after eradication of H pylori. Three antisera that are specific for particular regions of the gastrin molecules were used. Gel chromatography indicated that > 90% of the circulating gastrin consisted of gastrin (G) 17 and G34 both before and after eradicating the infection. The basal median total immunoreactive gastrin concentration fell from 26 pmol/l (range 11-43) to 19 pmol/l (8-39) (p < 0.05), entirely because of a fall in G17 from 6 pmol/l (< 2.4-25) to < 2.4 pmol/l (< 2.4-23) (p < 0.001). The median (range) basal G34 values were similar before (15 pmol (2-36)) and after (10 pmol (2-30)) eradication. The median total immunoreactive gastrin concentration determined 20 minutes postprandially fell from 59 pmol/l (38-114) to 33 pmol/l (19-88) (p < 0.005), and again this was entirely the result of a fall in G17 from 43 pmol/l (9-95) to 17 pmol/l (< 2.4-52) (p < 0.001). The median postprandial G34 values were similar before (13 pmol/l, range 6-42) and after (15 pmol/l, range 6-30) eradication. Eating stimulated a noticeable rise in G17 but little change in G34, both in the presence and absence of H pylori. The finding that H pylori infection selectively increases G17 explains why the infection causes mainly postprandial hypergastrinaemia. G17 is increased selectively because H pylori predominantly affects the antral mucosa which is the main source of G17 whereas G34 is mainly duodenal in origin. This study also indicates that the increased concentration of gastrin in H pylori infection is the result of an increase in one of the main biologically active forms of the hormone.
幽门螺杆菌感染会增加胃泌素的血清浓度，这可能是其易引发十二指肠溃疡的机制之一。对13例十二指肠溃疡患者在根除幽门螺杆菌之前及之后1个月，分别在基础状态和餐后研究了不同形式的循环胃泌素。使用了三种对胃泌素分子特定区域具有特异性的抗血清。凝胶色谱法表明，在根除感染前后，循环胃泌素中>90%由胃泌素（G）17和G34组成。基础状态下总的免疫反应性胃泌素浓度中位数从26 pmol/l（范围11 - 43）降至19 pmol/l（8 - 39）（p < 0.05），完全是因为G17从6 pmol/l（<2.4 - 25）降至<2.4 pmol/l（<2.4 - 23）（p < 0.001）。根除前后基础状态下G34值的中位数（范围）相似，根除前为15 pmol（2 - 36），根除后为10 pmol（2 - 30）。餐后20分钟测定的总的免疫反应性胃泌素浓度中位数从59 pmol/l（38 - 114）降至33 pmol/l（19 - 88）（p < 0.005），同样这完全是G17从43 pmol/l（9 - 95）降至17 pmol/l（<2.4 - 52）（p < 0.001）的结果。根除前后餐后G34值的中位数相似，根除前为13 pmol/l（范围6 - 42），根除后为15 pmol/l（范围6 - 30）。无论有无幽门螺杆菌感染，进食均会刺激G17显著升高，但G34变化不大。幽门螺杆菌感染选择性增加G17这一发现解释了为何该感染主要导致餐后高胃泌素血症。G17被选择性增加是因为幽门螺杆菌主要影响胃窦黏膜，而胃窦黏膜是G17的主要来源，而G34主要起源于十二指肠。本研究还表明，幽门螺杆菌感染时胃泌素浓度升高是该激素主要生物活性形式之一增加的结果。
