慢性萎缩性胃炎胃泌素、生长抑素、表皮生长因子、血管活性肠肽的测定及临床意义

Changes of gastrointestinal hormones in chronic atrophic gastritis and their clinical significance

目的:通过对照慢性萎缩性胃炎(CAG)及胃癌患者胃泌素、生长抑素(SS)、表皮生长因子(EGF)和血管活性肠肽(VIP)水平,探讨上述胃肠激素在CAG的临床意义,为CAG的内分泌治疗提供理论与实验依据.方法:应用放免法检测经胃镜及病理证实的67例CAG患者,18例胃癌患者,15例正常人血中胃泌素、EGF、VIP和SS水平.结果:与正常人血清胃泌素、EGF含量[(64.19±35.34)×10-3ng/ml,(1.76±0.35)ng/ml]相比,CAG患者血清内这两种物质含量均明显升高[(115.23±60.62)×10-3ng/ml,(152.60±82.93)ng/ml],P<0.01,且随萎缩病变加重呈上升趋势,伴肠化生者[(137.20±60.23)×10-3ng/ml,(2.71±1.02)ng/ml]升高最为显著,接近胃癌水平[(152.60±72.93)×10-3ng/ml,(2.86±1.23)ng/ml],P>0.05.CAG患者VIP含量(9.42±2.34)×10-3ng/ml显著低于正常水平(16.34±8.18)×10-3ng/ml,P<0.01,但较胃癌患者(6.98±2.13)×10-3ng/ml显著增高,P<0.01.且随萎缩病变加重呈下降趋势,伴肠化生时(7.68±2.96)×10-3ng/ml仅略高于胃癌.血浆SS含量以CAG患者为最低(61.90±28.36)×10-3ng/ml显著低于正常人(96.28±35.18)×10-3ng/ml,P<0.01及胃癌患者(114.96±47.12)×10-3ng/ml且随萎缩病变加重呈下降趋势,伴肠化生时最低(40.17±20.34)×10-3ng/ml.结论:CAG存在胃泌素,EGF水平的增高及SS、VIP水平的减低,使胃黏膜的生理功能、生物学行为发生改变,致CAG沿着肠化生-不典型增生癌变发展,适当应用上述胃肠激素或其拮抗剂可能阻止CAG的发展,并使之逆转.

AIM:To investigate the changes of gastrin, epidermal growth factor (EGF), vasoactive intestinal polypeptide (VIP), somatostatin (SS) and their clinical significance in chronic atrophic gastritis (CAG), and meanwhile to supply theoretical and experimental basis for the endocrinal therapy of CAG. METHODS:The serum levels of gastrin, EGF, VIP and SS were measured in 67 cases of CAG patients, 18 gastric cancers and 15 normal controls by radioimmunoassay. RESULTS:The serum levels gastrin and EGF were obviously higher in CAG patients (115.23± 60.23 )× 10-3 ng/ml, (152.60 ± 82.93) ng/ml than those in normal persons (64.19± 35.34)× 10-3 ng/ml,(1.76± 0.35)ng/ml (P <0.01), but significantly lower than those in gastric cancer (152.60± 72.93)×10-3 ng/ml,(2.86±1.23) ng/ml (P <0.01). There was an increasing tendency in the content of gastrin and EGF with the development of atrophy, which was close to the level of gastric cancer in CAG patients accompanied by intestinal metaplasia (137.20 ± 60.23)× 10-3 ng/ml, (2.71 ± 1.02) ng/ml (P <0.05). The serum levels of SS and VIP were obviously lower in CAG (61.90 ± 28.36) × 10-3 ng/ml,(9.42 ± 2.34)× 10-3 ng/ml than those in normal persons (96.28 ± 35.18) × 10-3 ng/ml,(16.34 ± 8.18)× 10-3 ng/ml. The more serious atrophy was accpmpaind with lower level of SS and VIP. Furthermore, the serum level of SS was lower in CAG than those in gastric cancer (114.96± 47.12) ×10-3 ng/ml, but the serum level of VIP was higher than the latter (6.98±2.13) ×10-3 ng/ml.CONCLUSION:CAG is accompanied with the increasing of gastrin, EGF and the decreasing of SS and VIP, which may change the physiological functions and biological behaviors of the gastric mucosa and lead CAG to gastric cancer. If properly using these gastrointestinal hormones or their blocker, it may block the development of CAG.