Ueno Yasuaki, Nakamura Masanao, Watanabe Osamu, Yamamura Takeshi, Funasaka Kohei, Ohno Eizaburo, Miyahara Ryoji, Kawashima Hiroki, Goto Hidemi, Hirooka Yoshiki
Department of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Department of Endoscopy, Nagoya University Hospital, Nagoya, Japan.
Nagoya J Med Sci. 2016 Aug;78(3):323-8.
The patient was a 72 year old man who had been given non-steroidal anti-inflammatory drug (NSAID) for two years. He repeatedly developed small intestinal ileus; therefore, he underwent several imaging examinations, but the cause was not identified. He subsequently underwent a double-balloon endoscopy (DBE). The membranous stenoses were detected in the jejunum, and the biopsy specimens were taken during the DBE. The membranous stenoses in the gastrointestinal tract were characteristic of NSAID-induced enteropathy, and he was endoscopically and histopathologically diagnosed with NSAID-induced small intestinal disorder. NSAID administration was withdrawn, and the balloon dilation was conducted for small intestinal stenosis. After that, no small intestinal ileus developed again. Some studies were conducted on the mechanism of NSAID-induced small intestinal dysfunction, but the drug that was administered to the patient was a highly selective NSAID for cyclooxygenase (COX)-2, and there are few studies that reported a dysfunctional mechanism induced by this drug. In the tissue sampled by DBE, apoptotic bodies were found; therefore, it was suggested that the stenoses in this case were caused by the COX-2 inhibitor from the relationship between COX-2 inhibition and apoptosis. Further studies are necessary to investigate the mechanism of NSAID enteropathy.
该患者为一名72岁男性,已服用非甾体抗炎药(NSAID)两年。他反复出现小肠梗阻;因此,他接受了多项影像学检查,但病因未明确。随后他接受了双气囊小肠镜检查(DBE)。在空肠发现了膜性狭窄,并在DBE期间采集了活检标本。胃肠道的膜性狭窄是NSAID诱导的肠病的特征,他在内镜和组织病理学上被诊断为NSAID诱导的小肠疾病。停用了NSAID,并对小肠狭窄进行了球囊扩张。此后,未再次出现小肠梗阻。对NSAID诱导的小肠功能障碍的机制进行了一些研究,但给予该患者的药物是一种对环氧化酶(COX)-2具有高度选择性的NSAID,很少有研究报道这种药物诱导的功能障碍机制。在DBE采集的组织中发现了凋亡小体;因此,从COX-2抑制与凋亡的关系来看,提示该病例中的狭窄是由COX-2抑制剂引起的。有必要进一步研究NSAID肠病的机制。