EndoTODAY | EndoATLAS | OPD

Parasite | Eso | Sto | Cancer | ESD

Boxim | DEX | Sono | Schedule

Home | Recent | Blog | Links


[2018 À»Áöº´¿ø ¼ÒÈ­±â³»°ú ¿¬¼ö°­ÁÂ]

³»½Ã°æ ÁúÁöÇ¥¿¡ ½Ã°£ °³³äÀÌ µé¾î°¡¾ß ÇÑ´Ù°í ÁÖÀåÇÏ¿´½À´Ï´Ù.


1. À§, ´ëÀå³»½Ã°æ°Ë»ç ¼ö°¡°ü¸® ÇÙ½É »çÇ× Á¤¸® - ¹æ½ÉÇÏ¸é ¸ø¹Þ´Â ºñ¿ë ³õÄ¡Áö ¾Ê±â - ±¸¼±¹Ì (À»Áöº´¿ø ½É»çÆÀ)

³»½Ã°æ ¼ö°¡ °ü¸®. PDF 10M (2018³â 12¿ù ±âÁØ)

´ëÀå³»½Ã°æ ¿ëÁ¾ÀýÁ¦¼ú ÈÄ ÃâÇ÷ÀÌ ¹ß»ýÇÏ¿© clip ÁöÇ÷¼úÀ» ÇÑ °æ¿ì clip 4°³ ÀÌ»ó »ç¿ëÇÏ¿´À» ¶§¿¡´Â ±Þ¿©°¡ µÇ°í, clipÀ» ±× ÀÌÇÏ·Î »ç¿ëÇÏ¸é ±Þ¿©°¡ µÇÁö ¾Ê´Â´Ù´Â À̾߱⸦ µé¾ú½À´Ï´Ù. ìéÛ¡ù±ñéÀ¸·Î Ŭ¸³ Çϳª·Î ÁöÇ÷ÀÌ µÇ¸é '°¡º­¿î ÃâÇ÷'·Î ºÐ·ùµÇ¾î µ·À» ÁÖÁö ¾Ê°í, ìéÛ¡ù±ñé¿¡ ½ÇÆÐÇÏ¿© Ŭ¸³À» ¿Õâ »ç¿ëÇϸé 'ÁßÇÑ ÃâÇ÷'·Î ºÐ·ùµÇ¾î µ·À» Áشٴ °ÍÀÌ´Ï ¾ÕµÚ°¡ ¹Ù²î¾îµµ ³Ê¹« ½ÉÇÏ´Ù´Â »ý°¢ÀÌ µé¾ú½À´Ï´Ù.


2. ´Ù¾çÇÑ ½Äµµ¿° ¹× Á¶±â ½Äµµ¾Ï ³»½Ã°æ Áø´Ü - ¿ø±¤´ëÇб³ ±è¿ë¼º

±è¿ë¼º ¼±»ý´Ô²²¼­´Â tuberculous esophagitis ÈÄ °æ°ú°üÂûÀ» ÇÏ´Â °úÁ¤¿¡¼­ óÀ½¿¡´Â ¾à°£ À¶±âµÈ º´¼Ò¿´´Âµ¥ ¼ö ³â ÈÄ¿¡´Â ÀüÇüÀûÀÎ traction diverticulitis°¡ ¹ß»ýÇÑ Áõ·Ê¸¦ º¸¿©Áּ̽À´Ï´Ù. ÀÏÀü¿¡ Traction diverticulum ¹Ù´ÚÀÇ anthracotic pigmentationÁõ·Ê¸¦ º¸¿©µå¸° ¹Ù Àִµ¥ ¸ðµÎ °áÇÙ¿¡ ÀÇÇÑ °ÍÀÔ´Ï´Ù.

EndoTODAY ½ÄµµÁúȯ 043

º£Ã¼ ½Äµµ ±Ë¾ç Áõ·Êµµ ¼Ò°³µÇ¾ú½À´Ï´Ù (¼ÒÈ­±â³»½Ã°æÇÐȸ ±³À°ÀÚ·á º£Ã¼Æ® º´¿¡ ÀÇÇÑ ½Äµµ º´º¯).

·ç°ñ »ö¼Ò ³»½Ã°æÀÇ ´ÜÁ¡


3. The paradigm shift in the treatment of Helicobacter pylori infection: from antibiotics to acid inhibition - ÇѾç´ëÇб³ ¹ÚÂùÇõ

P-CABÀº parietal cell¿¡¼­ Á» ´õ ¿À·¡ stableÇϹǷΠÅõ¾à ÈÄ ¸¸µé¾îÁø acid pump¿¡µµ ÀÛ¿ëÇÒ ¼ö ÀÖ½À´Ï´Ù.

Figure 1. Simplified schematic description: differences between ¡®conventional¡¯ proton-pump inhibitors (PPIs) (a) and vonoprazan (b). (a) The H+/K+-ATPase is located on the secretary membrane of parietal cells and maintains the acidity in the stomach. The enzyme is responsible for pumping H+ ions out of the cells into the canaliculi, in exchange for K+ ions. Conventional PPIs are absorbed in the small intestine and subsequently reach the gastric parietal cells where they are converted to their active forms upon acid exposure, and covalently bind to the H+/K+-ATPase. Since conventional PPIs are unstable in canaliculi and are rapidly degraded, they are not able to inhibit new proton pumps (PPs) that surface after administration of the drug. Thus they require a few days to reach their maximum effect. (b) Vonoprazan, a potassium-competitive acid blocker, does not require acid activation. Vonoprazan is rapidly absorbed in the small intestine and accumulates in the canalicular membranes of parietal cells, binding to H+/K+-ATPase in a K+-competitive manner. Vonoprazan is more stable than conventional PPIs in the canaliculi, allowing fast and stable inhibition of gastric acid secretion. (Therap Adv Gastroenterol. 2016)

Potassium-competitive acid blockers (PCABs) inhibit acid secretion in gastric parietal cells by competitively inhibiting the binding of potassium ion to H+/K+-ATPase. Vonoprazan is a new PCAB that has been clinically available since 2015 in Japan. Vonoprazan is a basic compound with pKa 9.06-9.3, which is significantly higher than the pKas of conventional PPIs (lansoprazole, pKa 3.8) and previously developed PCABs (SCH28080l, pKa 5.6). The higher basicity of vonoprazan compared with that of conventional PPIs enables its concentration in low pH-secretory canaliculi. In addition, vonoprazan dissociates slowly from the H+/K+-ATPase. Other advantages of vonoprazan are that it does not require acid activation, is rapidly absorbed in the intestine, and leads to fast inhibition of acid secretion. In addition, vonoprazan is more stable at neutral pH compared with conventional PPIs: the half maximal inhibitory concentration (IC50) values at pH 7.5 were 66 and 0.028 ¥ìM for a conventional PPI and vonoprazan, respectively, in a study employing porcine H+/K+-ATPase. Plasma half life of 5.7 and 7 h was reported for vonoprazan (20 mg) after a single dose and on the seventh day of administration in humans, respectively, longer than the half life of conventional PPIs (<2 h). Importantly, as vonoprazan is mainly metabolized by CYP3A4, its acid inhibitory effect is least influenced by CYP2C19 haplotypes. These features allow vonoprazan to exert rapid, strong, and stable inhibition of H+/K+-ATPase. Vonoprazan increased intragastric pH to over 4.0 within 4 h after the first administration in humans, creating conditions in which amoxicillin and clarithromycin are stable. In addition, amoxicillin and clarithromycin are growth-dependent antibiotics, exerting optimal effects against H. pylori at pH 6-7. However, lower pH values suppresses growth of H. pylori, leading to antibiotic resistance. A recent study in humans showed that intragastric pH greater than 5 holding time ratio was 99% with vonoprazan at 20 mg twice daily and 84% with esomeprazole at 20 mg twice daily when administered for 7 days. In the same study, the acid inhibitory effect of vonoprazan was superior to that of esomeprazole. As expected, the effect of vonoprazan was not influenced by the CP2C19 genotype. Further, a single administration of vonoprazan raised the gastric pH to over 6 for several hours. Taken together, these observations imply the improved potential of vonoprazan for eradicating H. pylori compared with that of conventional PPIs, as discussed in the next section. (Therap Adv Gastroenterol. 2016)

Clarithromycin sensitivie strainÀº vonoprazanÀ̳ª PPI ¸ðµÎ È¿°úÀûÀ̳ª, clarithromycin resistant strain¿¡¼­´Â vonoprazanÀ» »ç¿ëÇÏ¿´À» ¶§ PPI¸¦ »ç¿ëÇÏ¿´À» ¶§¿¡ ºñÇÏ¿© ³ôÀº Á¦±Õ ¼º°ø·üÀ» º¸¿´½À´Ï´Ù (80%´ë 40%). (Murakami. Gut 2016)

ÀϺ»¿¡´Â clarithromycin resistance°¡ 30% Á¤µµÀÌÁö¸¸ P-CABÀ» »ç¿ëÇÑ °æ¿ì Á¦±ÕÀ²ÀÌ ³ôÀ¸¹Ç·Î clarithromycin resistance°¡ ³ôÀº Áö¿ª¿¡¼­´Â ´Ù¸¥ ¾àÁ¦¸¦ »ç¿ëÇ϶ó´Â ¼­±¸ÀÇ Áöħ°ú ´Þ¸® ÀÏ´Ü P-CAB + clarithromycin + amoxicillin 3Á¦¿ä¹ýÀ» »ç¿ëÇÏ´Â °æÇâÀÔ´Ï´Ù.

Áß±¹¿¡¼­ vonoprazan + amoxicillin 2Á¦¿ä¹ý¿¡ ´ëÇÑ ¿¬±¸°¡ ÁøÇàµÇ°í ÀÖÀ¸³ª ¹ÚÂùÇõ ±³¼ö´ÔÀº P-CABÀ» »ç¿ëÇÑ quadruple therapy, sequantial therpay, ¶Ç´Â concomitant therapy¿Í °°Àº alternative therapy¸¦ ½ÃµµÇÏ´Â °ÍÀÌ ÁÁÁö ¾ÊÀ»±î¶ó´Â ÀÇ°ßÀ» ¸»¾¸ÇØ Áּ̽À´Ï´Ù.


4. Áß°£ ´ëÀå¾ÏÀÇ ¿øÀΰú ¿¹¹æ - µ¿±¹´ë Àϻ꺴¿ø °­Çö¿ì

´ëÀå³»½Ã°æ 13°³¿ù ÈÄ splenic flexureÀÇ mass°¡ obstructionÀ» ÀÏÀ¸Å² Áõ·Ê°¡ ¼Ò°³µÇ¾ú½À´Ï´Ù.

Áß°£¾Ï ¿øÀÎÀº missed lesionÀÌ 50%, incomplete resectionÀÌ 20%, new lesionÀÌ 30% Á¤µµ·Î ÃßÁ¤µË´Ï´Ù (Adler J & Robertson DJ. Am J Gastroenterol 2015).

Áß°£¾Ï ¹ß»ý·üÀº index colonoscopy¸¦ GP³ª family physicianÀÌ ½ÃÇàÇÑ °æ¿ì´Â 1.53¹è, surgeonÀÌ ½ÃÇàÇÑ °æ¿ì´Â 1.15¹è ³ô½À´Ï´Ù. Manitoba study¿¡ ÀÇÇϸé general physicianÀÌ ½ÃÇàÇÑ °æ¿ì Áß°£¾Ï ¹ß»ý·üÀÌ 60% ´õ ³ô¾Ò½À´Ï´Ù.

Adenoma detection rate (ADR)ÀÇ targetÀº Á¡Á¡ ³ô¾ÆÁ®¼­ ÃÖ±Ù ¿µ±¹ °¡À̵å¶óÀο¡¼­´Â 35-40%¸¦ Á¦½ÃÇÏ°í ÀÖ½À´Ï´Ù.

* Âü°í: EndoTODAY interval cancer


5. À§¾Ï ³»½Ã°æ Áø´Ü°ú Ä¡·á update 2018 - ¼º±Õ°üÀÇ´ë ÀÌÁØÇà

1. ÀûÁ¤ ³»½Ã°æ °Ë»ç ½Ã°£Àº ¸î ºÐÀԴϱî?

ÀÇ·á¿¡¼­ÀÇ ÁúÁöÇ¥´Â (1) structure ÁöÇ¥, (2) process ÁöÇ¥, (3) outcome ÁöÇ¥°¡ ÀÖ½À´Ï´Ù. °¡Àå Á÷°üÀûÀÎ °ÍÀº outcome ÁöÇ¥ÀÌ°í, ´ÙÀ½Àº outcome°ú °ü·Ã¼ºÀÌ ÀÔÁõµÈ process ÁöÇ¥ÀÔ´Ï´Ù. ´ëÀå³»½Ã°æ ¿µ¿ª¿¡´Â outcome ÁöÇ¥ÀÎ adenoma detection rate³ª process ÁöÇ¥ÀÎ colonoscopy withdrawal timeÀÌ ³Î¸® ¾²ÀÌ°í ÀÖ½À´Ï´Ù. Colonoscopy withdrawal time°ú adenoma detection rateÀÇ °ü°è´Â ¸í¹éÇÏ°í, adenoma detection rate¿Í interval cancer ¹ß»ý·ü »çÀÌÀÇ ¿¬°ü°ü°èµµ ÀÔÁõµÇ¾ú½À´Ï´Ù. À̵éÀº Á÷°üÀûÀÌ°í ÃøÁ¤ÀÌ ¿ëÀÌÇϹǷΠ´©±¸³ª µ¿ÀÇÇÏ°í ½±°Ô ¹Þ¾ÆµéÀÌ°Ô µÇ¾ú½À´Ï´Ù. ±×·¯³ª À§³»½Ã°æ ºÐ¾ß¿¡¼­´Â Á÷°üÀûÀÌ°í ÀÔÁõ°¡´ÉÇÑ ÁúÁöÇ¥°¡ ¾ÆÁ÷ °³¹ßµÇÁö ¾Ê¾Ò½À´Ï´Ù.

¿ì¸®³ª¶ó¿¡¼­ Á¦¾ÈµÈ ±¹°¡¾Ï°ËÁø À§³»½Ã°æ Áú Æò°¡ Ç׸ñÀº ºñ±³Àû Ÿ´çÇÏÁö¸¸ ³Ê¹« º¹ÀâÇÕ´Ï´Ù. À¯¿ë¼ºÀ» ³ôÀ̱â À§Çؼ­´Â ´ÜÀÏÇÑ °´°üÀû ÁöÇ¥°¡ ÇÊ¿äÇÕ´Ï´Ù. ¿¹¸¦ µé¸é °Ë»ç½Ã°£ °°Àº °Í ¸»ÀÔ´Ï´Ù. ¼­¿ï¼º¸ðº´¿øÀÇ ¹ÚÀç¸í ±³¼ö²²¼­´Â À§³»½Ã°æ °Ë»ç½Ã°£°ú Á¾¾ç ¹ß°ßÀ²¿¡ À¯ÀÇÇÑ »ó°ü°ü°è°¡ ÀÖÀ½À» º¸¿©ÁØ ¹Ù ÀÖ½À´Ï´Ù. À¯·´¿¡¼­´Â 7ºÐ °Ë»ç½Ã°£À» Á¦¾ÈÇÏ°í ÀÖÀ¸³ª, ¸¹Àº °Ë»ç¸¦ ¼ÒÈ­ÇØ¾ß ÇÏ´Â ¿ì¸®³ª¶ó¿¡¼­´Â Çö½ÇÀûÀÌÁö ¾Ê´Ù´Â ÀÇ°ßÀÌ ¸¹½À´Ï´Ù.

Àú´Â ¼ø¼øÇÑ À§³»½Ã°æ °Ë»ç½Ã°£ÀÌ 5ºÐÀº µÇ¾î¾ß ÇÑ´Ù°í »ý°¢ÇÕ´Ï´Ù. °Ë»ç Àü ȯÀÚ¿¡°Ô Áõ»óÀ» ¹°¾îº¸°í, ÁøÁ¤Á¦¸¦ Åõ¿©ÇÑ ÈÄ Àá½Ã ±â´Ù¸®°í, °Ë»ç ÈÄ °á°ú¸¦ ±â·ÏÇÏ´Â µî ±âŸ ½Ã°£À» °í·ÁÇϸé 10ºÐ¿¡ 1¸íÀ» °Ë»çÇÏ´Â °Íµµ ¸Å¿ì ¹Ù»Û ÀÏÀÔ´Ï´Ù. ÃÖ¼ÒÇÑÀÇ Áú°ü¸®¸¦ À§Çؼ­´Â ÇÑ ¸íÀÇ ³»½Ã°æ Àǻ簡 1½Ã°£¿¡ 5¸í ȤÀº ±× ÀÌÇϸ¦ °Ë»çÇÏ´Â °ÍÀÌ ¹Ù¶÷Á÷ÇÕ´Ï´Ù. À̸¦ À§ÇÑ È¯°æ¸¶·ÃÀÌ ÇÊ¿äÇѵ¥, ¼ö°¡ Á¤»óÈ­°¡ °¡Àå Áß¿äÇÑ ¿ä¼ÒÀÔ´Ï´Ù. ½Î°í ÁÁÀº °Ë»ç´Â ¾ø½À´Ï´Ù. ÀûÀýÇÑ ÁúÇâ»óÀ» À§Çؼ­´Â ¼ö°¡ ÀλóÀÌ ÇʼöÀÔ´Ï´Ù. ¼ö°¡ Á¤»óÈ­¸¦ ÅëÇÏ¿© °Ë»ç Á¤»óÈ­°¡ ÀÌ·ç¾îÁö±â¸¦ ±â´ëÇÕ´Ï´Ù. Çѽ𣿡 3-5¸í °Ë»çÇÏ´Â °ÍÀÌ Á¤»óÀÔ´Ï´Ù.

2. Á¶Á÷°Ë»ç°¡ ÇÊ¿äÇÑ °æ¿ì´Â ¾ðÁ¦ÀÌ°í ¸î °³¸¦ ÇØ¾ß Çմϱî?

À°¾È¼Ò°ßÀÌ °¡Àå Áß¿äÇÕ´Ï´Ù. ÀÚ¼¼ÇÑ °üÂûÀ» ÅëÇÏ¿© impressionÀ» Àâ°í, À̸¦ È®ÀÎÇϱâ À§ÇÑ Á¶Á÷°Ë»ç°¡ µÇ¾î¾ß ÇÕ´Ï´Ù. ¿äÁòÀº impression ¾ø´Â Á¶Á÷°Ë»ç ³Ê¹« ¸¹½À´Ï´Ù. ±×³É ´Ã ¹Ì¶õÀÎ °æ¿ì°¡ ³Ê¹« ¸¹½À´Ï´Ù.

Á¶Á÷°Ë»ç°¡ ÇÊ¿äÇÒ ¶§¿¡´Â ´Ã ÇØ¾ß ÇÕ´Ï´Ù. Çΰ谡 ¸¹À¸¸é °ï¶õÇÕ´Ï´Ù. ¾Æ½ºÇǸ°À» µå½Ã°í ÀÖ´Ù°í, clopidogrelÀ» µå½Ã°í ÀÖ´Ù°í, ¾î·Á¿î À§Ä¡¶ó´Â ÀÌÀ¯·Î Á¶Á÷°Ë»ç¸¦ ÇÏÁö ¾ÊÀ¸¸é ȯÀÚ¿¡°Ô Çظ¦ Áֱ⠽±½À´Ï´Ù.

Á¶Á÷°Ë»ç °¹¼ö´Â ±×¸® Áß¿äÇÏÁö ¾Ê½À´Ï´Ù. Á¤¹ÐÇÑ target biopsy°¡ ÇÙ½ÉÀÔ´Ï´Ù. Ãʺ¸ÀÚ¸¦ À§ÇÏ¿© ´ë°­ÀÇ °¡À̵带 ¿ä±¸ÇÏ´Â °æ¿ì°¡ ¸¹¾Æ¼­ °³ÀÎÀûÀ¸·Î´Â ¾ç¼º À§±Ë¾ç¿¡¼­´Â 3°³, Á¶±âÀ§¾Ï¿¡¼­´Â 3°³, ÁøÇ༺ À§¾Ï¿¡¼­´Â 6°³, Á¡¸·ÇÏ Á¾¾ç¿¡¼­´Â 2°³¶ó´Â ´ë°­ÀÇ ÁöħÀ» ¸¸µé¾î °¡¸£Ä¡°í ÀÖ½À´Ï´Ù.

3. À§ÁÖ¸§ ºñÈÄ´Â ¾î¶»°Ô Áø´ÜÇմϱî?

À§ÁÖ¸§ÀÌ µÎ²¨¿öÁ³´Ù°í ÆÇ´ÜµÇ¸é º¸¸¸ 4Çü ÁøÇ༺À§¾ÏºÎÅÍ °í·ÁÇØ¾ß ÇÕ´Ï´Ù. ºñÈļº À§¿°, ¸²ÇÁÁ¾, Menetrier º´ µîÀº º¸¸¸ 4Çü ÁøÇ༺À§¾Ïº¸´Ù ÈξÀ µå¹® ÁúȯÀÔ´Ï´Ù. º¸¸¸ 4Çü ÁøÇ༺ À§¾ÏÀÌ Áß¿äÇÑ ÀÌÀ¯´Â ¾Æ·¡¿Í °°½À´Ï´Ù.

1) ³õÄ¡±â ½±´Ù.
2) Àǻ糪 ȯÀÚ ¸ðµÎ ¹æ½ÉÇϱ⠽¬¿î ÀþÀº ¿©¼º¿¡ ¸¹´Ù.
3) À帷 ÀüÀÌ°¡ ÈçÇÏ´Ù.
4) Á¶Á÷ °Ë»ç À½¼ºÀÌ ¸¹´Ù.
5) °Ç°­°ËÁø ¼öÁøÀڵ鿡°Ôµµ ¹ß°ßµÈ´Ù.
6) ½ÅÀü ¿©ºÎ·Î °¨º° Áø´ÜÇϱâ Èûµé´Ù.
7) °úÁõ½Ä¼º À§¿°°ú ±¸ºÐÀÌ ¾î·Æ´Ù.

4. Blind area´Â ¾î´À ºÎÀ§¸¦ Á¶½ÉÇØ¾ß Çմϱî?

ÀڽŸ¸ÀÇ routineÀ» °¡Áö°í ±¸¼®±¸¼® »ó¼¼È÷ »ìÆì¾ßÇÕ´Ï´Ù. Çѹø È× º¸´Â °ÍÀº ºÎÁ·ÇÑ ÀÏÀ̸ç, ÇÑ ºÎÀ§¸¦ Àû¾îµµ 3¹ø º»´Ù´Â »ý°¢À» °®±â ¹Ù¶ø´Ï´Ù. °ËÁø ³»½Ã°æÀÇ °£°ÝÀº º¸Åë 2³âÀÔ´Ï´Ù. ȯÀÚÀÇ 2³âÀ» Ã¥ÀÓÁø´Ù´Â »ý°¢À¸·Î ³»½Ã°æÀ» Àâ±â ¹Ù¶ø´Ï´Ù. À§Ã¼ºÎ Èĺ®°ú ºÐ¹®ºÎ°¡ °¡Àå À¯¸íÇÑ blind areaÀÔ´Ï´Ù.

5. ESD ÀûÀÀÁõÀº ¾î¶»°Ô ¹Ù²î¾ú½À´Ï±î?

2018³â 11¿ù 1ÀϺÎÅÍ Àû¿ëµÇ´Â ±Þ¿© ´ë»óÀº ¾Æ·¡¿Í °°½À´Ï´Ù. Á¤ºÎ¿¡¼­ Á¤ÇÑ ±Þ¿© ´ë»óÀÌ °ð¹Ù·Î ÀûÀÀÁõÀº ¾Æ´Ï¶ó´Â Á¡¿¡ À¯ÀÇÇϽñ⠹ٶø´Ï´Ù. ºñ±Þ¿©¸¦ ¾ø¾Ø´Ù´Â Á¤Ã¥¹æÇâ¿¡ µû¶ó ȯÀÚ°¡ 80%¸¦ ºÎ´ãÇÏ´Â ¼±º°±Þ¿©°¡ ¸¹¾ÆÁ³½À´Ï´Ù. ´Ü¼øÇÏ°í ÀÌÇØÇϱ⠽¬¿î ÅëÀÏµÈ ±Þ¿©Á¤Ã¥À» ±â´ëÇÏ´Â Àú·Î¼­´Â ½Ç¸Á½º·´±â ±×Áö¾ø´Â º¯È­ÀÌÁö¸¸, 20% Á¤µµ Àú·ÅÇØÁø Ãø¸éµµ À־ ȯÀÚµéÀº ȯ¿µÇÒ °Í °°½À´Ï´Ù.

1) º»ÀÎÀϺκδãÇÏ´Â °æ¿ì

°¡) À§(Stomach)

(1) Á¡¸·¿¡ ±¹ÇÑµÈ ±Ë¾çÀÌ ¾ø´Â 2cm ÀÌÇÏÀÇ ºÐÈ­Çü Á¶±â¾Ï
(2) 1.5cm ÀÌ»óÀÎ ¼±Á¾,ÀÌÇü¼ºÁõ(adenoma, dysplasia)
(3) ¼¶À¯È­¸¦ µ¿¹ÝÇÑ ¼±Á¾(adenoma, dysplasia)
(4) Á¡¸·ÇÏ Á¾¾ç

³ª) ½Äµµ(Esophagus)

(1) Á¡¸·¿¡ ±¹ÇÑµÈ ±Ë¾çÀÌ ¾ø´Â ºÐÈ­Çü Á¶±â¾Ï(ÀýÁ¦µÈ Á¶Á÷ÀÌ ¿øÁÖ(circumference)ÀÇ 2/3ÀÌÇϸ¦ ħ¹üÇÏ´Â °æ¿ì)
(2) 1.5cm ÀÌ»óÀÎ ¼±Á¾ ¹× ÀÌÇü¼ºÁõ(adenoma, dysplasia)
(3) ¼¶À¯È­¸¦ µ¿¹ÝÇÑ ¼±Á¾(adenoma, dysplasia)

´Ù) °áÀå, Á÷Àå(Colon, Rectum)

(1) Á¡¸·¿¡ ±¹ÇÑµÈ ±Ë¾çÀÌ ¾ø´Â 5cm ÀÌÇÏÀÇ ºÐÈ­Çü Á¶±â¾Ï
(2) 2cm ÀÌ»óÀÇ Ãø¹æ¹ßÀ°ÇüÁ¾¾ç
(3) 2cm ÀÌ»óÀÇ ¹«°æ¼ºÀÇ ¿ëÁ¾
(4) ¼¶À¯È­¸¦ µ¿¹ÝÇÑ ¼±Á¾(adenoma, dysplasia)

2) ¡¸¼±º°±Þ¿© ÁöÁ¤ ¹× ½Ç½Ã µî¿¡ °üÇÑ ±âÁØ¡¹¿¡ µû¶ó º»Àκδã·üÀ» 80% Àû¿ëÇÏ´Â °æ¿ì

°¡) º»ÀÎÀϺκδ㠱޿©´ë»ó ÀÌ¿ÜÀÇ ¸²ÇÁÀý ÀüÀÌ°¡ ¾ø´Â ºÐÈ­Çü Á¶±â¾Ï: À§, ½Äµµ, °áÀå, Á÷Àå
³ª) Á¡¸·¿¡ ±¹ÇÑµÈ ±Ë¾çÀÌ ¾ø°í 2cm ÀÌÇÏÀÌ¸ç ¸²ÇÁÀý ÀüÀÌ°¡ ¾ø´Â ¹ÌºÐÈ­Çü Á¶±â À§¾Ï
´Ù) Á¡¸·ÇÏ Á¾¾ç: ½Äµµ, °áÀå, Á÷Àå

6. °á·Ð

Àú¼ö°¡ ȯ°æ¿¡¼­ ¸¹Àº ȯÀÚ¸¦ ºü¸£°Ô °Ë»çÇÏ´Â ¿­¾ÇÇÑ ¿ì¸®³ª¶ó ³»½Ã°æ½Ç¿¡¼­ Áúº´À» ³õÄ¡Áö ¾Ê´Â´Ù´Â °ÍÀº ½±Áö ¾ÊÀº ÀÏÀÔ´Ï´Ù. ±×·³¿¡µµ ºÒ±¸ÇÏ°í ȯÀÚ¸¦ À§ÇÏ¿© ÃÖ´ëÇÑ ÁýÁß·ÂÀ» ¹ßÈÖÇØ¾ß ÇÏ´Â °ÍÀÌ ¿ì¸® ÀÇ»çÀÇ »ç¸íÀ̱⵵ ÇÕ´Ï´Ù. ¿©·¯ºÐ. Èû³»½Ê½Ã¿À.

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