Lipscomb G R, Painter J, Riley S, Gillott T, Rees W
Dept. of Medicine, North Manchester General Hospital, UK.
Scand J Gastroenterol. 1998 Aug;33(8):790-4. doi: 10.1080/00365529850171413.
Non-steroidal anti-inflammatory drugs (NSAIDs) frequently damage the gastrointestinal tract, but with continued administration this usually resolves by a process of adaptation. There is evidence that the acute injury can be reduced by acid suppression, and animal models have shown that salivary epidermal growth factor (EGF) is an important factor in gastric mucosal adaptation. We therefore wanted to assess the effect of acid suppression and salivary EGF output during naproxen-induced acute gastric injury and subsequent adaptation.
Healthy subjects were given a 14-day course of naproxen with different regimens of ranitidine and placebo. Before and on three occasions during treatment subjects provided a salivary sample for EGF and underwent gastroscopy to assess gastric damage.
Similar gastric damage occurred after 24 h in all groups and resolved in most subjects. Base-line salivary EGF output was similar in all groups but increased in the placebo/ranitidine group on day 3 and in the ranitidine group on day 9.
Acid suppression with ranitidine did not prevent acute gastric injury. Adaptation may be associated with an increase in salivary EGF output.
非甾体抗炎药（NSAIDs）常对胃肠道造成损害，但持续用药后这种损害通常会通过适应性过程而缓解。有证据表明，抑制胃酸可减轻急性损伤，动物模型显示唾液表皮生长因子（EGF）是胃黏膜适应性的一个重要因素。因此，我们想评估在萘普生诱导的急性胃损伤及随后的适应性过程中抑制胃酸和唾液EGF分泌量的影响。
健康受试者接受为期14天的萘普生治疗，并搭配不同方案的雷尼替丁和安慰剂。治疗前及治疗期间的三个时间点，受试者提供唾液样本用于检测EGF，并接受胃镜检查以评估胃损伤情况。
所有组在24小时后均出现相似的胃损伤，且大多数受试者的损伤得到缓解。所有组的唾液EGF基础分泌量相似，但安慰剂/雷尼替丁组在第3天、雷尼替丁组在第9天唾液EGF分泌量增加。
雷尼替丁抑制胃酸并不能预防急性胃损伤。适应性可能与唾液EGF分泌量增加有关。
