Rademaker J W, Hunt R H
Division of Gastroenterology, McMaster University Medical Centre, Hamilton, Ontario, Canada.
Scand J Gastroenterol Suppl. 1990;175:19-26. doi: 10.3109/00365529009093123.
Medical therapy for peptic ulcer disease has been targeted at inhibiting acid secretion based on the belief that ulcers occur due to an imbalance between aggressive and protective factors. New antisecretory agents are unlikely to show any dramatic improvement over the success and safety of histamine H2 receptor antagonists or the recently introduced H+K+ATPase proton pump antagonist omeprazole. The development of specific muscarinic M3 and gastrin receptor antagonists will provide useful agents to suppress acid and pepsinogen secretion by alternative means and may prevent the associated hypergastrinaemia seen with anti-secretory therapy. Enhancement of mucosal defence by site protective agents will be based on a better understanding of the vascular and immune factors involved in maintaining mucosal integrity and the growth factors that regulate wound healing. Molecular techniques are likely to produce the 'model anti-ulcer' agent which will effectively inhibit acid secretion and also enhance wound healing thus providing a cure for this chronic disease.
消化性溃疡疾病的药物治疗一直以抑制胃酸分泌为目标，这是基于一种观点，即溃疡的发生是由于攻击因素和保护因素之间的失衡。新的抗分泌药物在成功率和安全性方面不太可能比组胺H2受体拮抗剂或最近推出的H⁺K⁺ATP酶质子泵拮抗剂奥美拉唑有任何显著改善。特异性毒蕈碱M3和胃泌素受体拮抗剂的开发将提供有用的药物，通过其他方式抑制胃酸和胃蛋白酶原分泌，并可能预防抗分泌治疗中出现的相关高胃泌素血症。通过局部保护剂增强黏膜防御将基于对维持黏膜完整性所涉及的血管和免疫因素以及调节伤口愈合的生长因子的更好理解。分子技术可能会产生“理想的抗溃疡”药物，它将有效抑制胃酸分泌并促进伤口愈合，从而治愈这种慢性疾病。
