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[ColonTODAY 045 - Aspirin/NSAID-associated enteropathy]

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[2016-6-24. ¾Öµ¶ÀÚ ÆíÁö]

50¼¼ ³²ÀÚ·Î 7³âÀü ±Þ¼º½É±Ù°æ»öÁõÀ¸·Î °ü»óµ¿¸Æ ½ºÅÙÆ® ÈÄ ¾Æ½ºÇǸ°, ÇÁ¸®±×·¼(clopidogrel resinate)À» µå½Ã°í °è½Ê´Ï´Ù. ½ÅÀåÀÌ½Ä ÈÄ ¼Ò·Ðµµ 2.5mg/day¿Í ¾Æµå¹Ù±×¶øÀ̶ó´Â ¸é¿ª¾ïÁ¦Á¦¸¦ µå½Ã°í °è½Ê´Ï´Ù.

ÃÖ±Ù ¼³»ç¿Í Ç÷º¯(hematochezia)À¸·Î »óÇϺΠ³»½Ã°æÀ» ½ÃÇàÇÏ¿´½À´Ï´Ù. »óºÎÀ§Àå°ü¿¡´Â ÃâÇ÷º´¼Ò·Î º¸ÀÌ´Â ºÎºÐÀº ¾ø¾úÀ¸¸ç, ¸»´ÜȸÀå¿¡ 1.5-2cmÅ©±âÀÇ ulcer°¡ 2°³ ÀÖ¾î Á¶Á÷°Ë»çÇÏ°í °Ë»ç¸¦ ¸¶ÃƽÀ´Ï´Ù. ´ëÀå¿¡´Â ÃâÇ÷ÇÒ ¸¸ÇÑ º´¼Ò´Â ¾ø¾ú½À´Ï´Ù.

Aspirin-induced enteropathy³ª CMV ileitis µîÀ» »ý°¢ÇÏ°í Á¶Á÷°Ë»ç¸¦ Çߴµ¥, "Section shows moderate infiltration by lymphoplasma cells, neutrophils and eosinophils in the lamina propria. Active granulation tissue with heavy neutrophilic infiltration and necrotic ulcer detritus are noted. Granulomatous change or viral inclusion are not seen. Ther is no evidence of malignancy."·Î ³ª¿Ô½À´Ï´Ù. CMV PCR, Tuberculous PCR µµ ½ÃÇàÇߴµ¥ ¾ÆÁ÷ °á°ú´Â ¾È ³ª¿Â »óÅÂÀÔ´Ï´Ù.

¾Æ½ºÇǸ°À̳ª NSAID-induced enteropathy´Â ³»½Ã°æÀû Ư¡ÀÌ ÀÖ´ÂÁö, CMV enteritis³ª CMV colitisÀÇ ³»½Ã°æÀû Ư¡ÀÌ ÀÖ´ÂÁö ±Ã±ÝÇÕ´Ï´Ù. À§¿Í ½ÊÀÌÁöÀå¿¡ ±Ë¾çÀ̳ª ¹Ì¶õÀÌ ¾øÀÌ small bowel¿¡ ¾Æ½ºÇǸ°À̳ª NSAID·Î ÀÎÇÑ ±Ë¾çÀÌ »ý±æ ¼ö ÀÖ´ÂÁöµµ ±Ã±ÝÇÕ´Ï´Ù. ±Ã±ÝÇؼ­ ¿©ÂÞ¾î º¾´Ï´Ù. Ç×»ó °¨»çÇÕ´Ï´Ù.

[2016-6-24. Â÷Àç¸í ±³¼ö´Ô ´äº¯]

¾î·Á¿î Áú¹®ÀÎ °Í °°½À´Ï´Ù. 2012³â Clinical Endoscopy¿¡ ½Ç·È´ø NSAID-induced enteropathy¸¦ Âü°íÇÏ½Ã¸é µÉ °Í °°½À´Ï´Ù (Lim YJ. Clin Endosc 2012). À§Àå¿¡ »ý±â´Â NSAID Á¡¸· ¼Õ»ó°ú´Â ´Ù¸£°Ô NSAID ¼ÒÀå ¼Õ»óÀº ±×¶÷ À½¼º±Õ°ú ´ãÁó ¶§¹®¿¡ »ý±â¸ç, enterohepatic circulation¿¡ ÀÇÇØ ¾ÇÈ­µÉ ¼ö Àֱ⠶§¹®¿¡ »óºÎÀ§Àå°ü¿¡ º´º¯ ¾øÀÌ ¸»´Ü ȸÀå¿¡¸¸ º´º¯ÀÌ ¹ß»ýÇÒ ¼ö ÀÖ½À´Ï´Ù.

The pathogenesis of NSAID-induced enteropathy is distinct from that of NSAID-induced gastropathy. Unlike stomach, NSAID-induced lower GI injuries are not caused by sup-pression of prostaglandin synthesis due to inhibition of cyclo-oxygenase (COX) activity but, most of the time, by gram negative bacteria and bile. Bjarnason et al. proposed a "three hit" hypothesis. First, NSAIDs solubilize lipids of phospholipids on the mucosal surface, so the epithelial mitochondria are directly damaged. Second, the mitochondrial damage depletes intercellular energy and leads to calcium efflux and to induction of free radicals, a disruption of intercellular junctions occurs, and mucosal permeability increases in the small intestinal mucosa. Third, the mucosal barrier becomes weakened, so bile acid, proteolytic enzymes, intestinal bacteria, or toxins can easily penetrate into the epithelial cells, resulting in mucosal injury. NSAID-induced small intestinal injuries augment through the enterohepatic circulation of the NSAID. NSAIDs with no enterohepatic circulation did not cause significant intestinal damage in animal models.

Lim YJ. Clin Endosc 2012

Enteric-coated aspirinÀÇ °æ¿ì ¾Æ½ºÇǸ°ÀÇ ºÎÀÛ¿ëÀ» º°·Î ÁÙÀÌÁö ¸øÇÏ°í, ¿ÀÈ÷·Á ¼ÒÀå ¼Õ»óÀÌ ¸»´Ü ȸÀå ÂÊÀ¸·Î À̵¿µÇ´Â °æÇâÀ» º¸¿©, NSAID-induced enteropathy¿Í °ÅÀÇ À¯»çÇÏ°Ô °üÂûµÉ ¼ö ÀÖ½À´Ï´Ù. º´º¯ÀÇ ¸ð¾çÀº reddish erosion, multiple sharply demarcated ulcer, concentric stenosis µî ´Ù¾çÇÏ°Ô ¹ß»ýÇÒ ¼ö ÀÖ½À´Ï´Ù.


[References]

1) EsoTODAY - Esophageal diseases

2) SmallTODAY - Small bowel diseases

3) ColonTODAY - Colorectal diseases

© ÀÏ¿ø³»½Ã°æ±³½Ç ¹Ù¸¥³»½Ã°æ¿¬±¸¼Ò ÀÌÁØÇà. EndoTODAY Endoscopy Learning Center. Lee Jun Haeng.