Future treatment of peptic ulcers.
Drugs which abolish acid secretion and promise improved ulcer healing rates have produced dysplasia and tumours in experimental animals given large doses for long periods. Solutions to this problem will be based on better understanding of the mechanisms involved. Healing rates might be improved by combining inhibitors of acid secretion with ulcer protectors which, unlike currently available agents, are designed to work well in the presence of diminished acid secretion. Drugs which increase mucosal defence might best be used to prevent ulceration, so the need is to develop agents which are safe for long term use.
Calam
J
J
D000818:Animals; D000897:Anti-Ulcer Agents / Q000627:therapeutic use*; D004815:Epidermal Growth Factor / Q000627:therapeutic use; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D010434:Pepsin A / Q000037:antagonists & inhibitors; D010437:Peptic Ulcer / Q000188:drug therapy* / Q000382:microbiology; D011377:Proglumide / Q000627:therapeutic use; D011459:Prostaglandins E, Synthetic / Q000627:therapeutic use; D013004:Somatostatin / Q000627:therapeutic use; D013270:Stomach / Q000382:microbiology; D014945:Wound Healing / Q000187:drug effects
D000897:Anti-Ulcer Agents; D011459:Prostaglandins E, Synthetic; D013004:Somatostatin; D004815:Epidermal Growth Factor; D010434:Pepsin A; D011377:Proglumide