Umegaki Eiji, Kuramoto Takanori, Kojima Yuichi, Nouda Sadaharu, Ishida Kumi, Takeuchi Toshihisa, Inoue Takuya, Tokioka Satoshi, Higuchi Kazuhide
The Second Department of Internal Medicine, Osaka Medical College, Japan.
Intern Med. 2014;53(4):283-90. doi: 10.2169/internalmedicine.53.1572.
A treatment strategy to inhibit nonsteroidal anti-inflammatory drug (NSAID)-induced small intestinal lesions has not yet been established. To clarify whether monotherapy with a gastromucoprotective drug, geranylgeranylacetone (GGA), inhibits NSAID-induced acute mucosal injury of the upper digestive tract and small intestine.
A prospective, randomized, comparative study. All procedures were performed at Osaka Medical College. The subjects, thirty healthy adult volunteers, were randomly divided into two groups. In the NSAID-GGA group, 75 mg/day of diclofenac sodium and 150 mg/day of GGA were orally administered for two weeks. In the NSAID-FAM group, 75 mg/day of diclofenac sodium and 20 mg/day of famotidine (FAM) were orally administered for two weeks. esophagogastroduodenoscopy (EGD) and video capsule endoscopy (VCE) were performed before and two weeks after drug administration. In addition, we measured fecal occult blood reactions and the fecal calprotectin levels.
No significant differences were observed between the groups in the mean increase in esophageal/gastroduodenal lesions. The mean increases in the scores in the NSAID-FAM group (NSAID-GGA group) of small bowel lesions were as follows: erythema: 1.93 ± 0.67 (0.30 ± 0.60), erosions: 1.13 ± 0.54 (0.38 ± 0.35), ulcers: 0.73 ± 0.33 (0.07 ± 0.07) and edema: 0.53 ± 0.44 (0.07 ± 0.07). The scores for erythema and ulcers were significantly lower in the NSAID-GGA group than in the NSAID-FAM group (p=0.032 and 0.0165, respectively).
We compared the prophylactic effects of a mucoprotective drug, GGA, and an H2RA, famotidine, on mucosal injury involving the esophagus to the small intestine related to the two-week oral administration of diclofenac sodium in healthy volunteers. In the upper digestive tract, the prophylactic effects were similar between the two drugs. However, in the small intestine, GGA more markedly inhibited the development of lesions compared to famotidine.
尚未确立抑制非甾体抗炎药（NSAID）引起的小肠病变的治疗策略。为阐明胃黏膜保护药物香叶基香叶基丙酮（GGA）单药治疗是否能抑制NSAID引起的上消化道和小肠急性黏膜损伤。
一项前瞻性、随机、对照研究。所有操作均在大阪医科大学进行。30名健康成年志愿者被随机分为两组。在NSAID-GGA组，口服双氯芬酸钠75mg/天和GGA 150mg/天，持续两周。在NSAID-FAM组，口服双氯芬酸钠75mg/天和法莫替丁（FAM）20mg/天，持续两周。在给药前及给药两周后进行食管胃十二指肠镜检查（EGD）和视频胶囊内镜检查（VCE）。此外，我们还检测了粪便潜血反应和粪便钙卫蛋白水平。
两组食管/胃十二指肠病变的平均增加量无显著差异。NSAID-FAM组（NSAID-GGA组）小肠病变评分的平均增加情况如下：红斑：1.93±0.67（0.30±0.60），糜烂：1.13±0.54（0.38±0.35），溃疡：0.73±0.33（0.07±0.07），水肿：0.53±0.44（0.07±0.07）。NSAID-GGA组的红斑和溃疡评分显著低于NSAID-FAM组（分别为p=0.032和0.0165）。
我们比较了黏膜保护药物GGA和H2受体拮抗剂法莫替丁对健康志愿者口服双氯芬酸钠两周相关的食管至小肠黏膜损伤的预防作用。在上消化道，两种药物的预防效果相似。然而，在小肠中，与法莫替丁相比，GGA更显著地抑制了病变的发展。
