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[±â´É¼º ¼ÒÈ­ºÒ·®Áõ. Functional dyspepsia] - ðû

1. Symptoms

2. Helicobacter associated dyspepsia

3. Duodenal inflammation

4. Treatment

5. Symposiums

6. FAQs

7. References

2022-8-10. ±â´É¼º ¼ÒÈ­ºÒ·®Áõ (È«ÁöÅà ±³¼ö´Ô)

2023-5-4. ¼øõÇâÀÇ´ë ÀÌÅÂÈñ ±³¼ö. ´ÚÅͺô log-in é©

¼³¸í¸¸ Àß Çصå·Áµµ ÁÁ¾ÆÁö´Â ȯÀÚ°¡ ¸¹½À´Ï´Ù.

°æ»óµµ¿¡¼­ ¿À¼Ì´Âµ¥ °Ë»çÇغ¸±â ÀüºÎÅÍ ÁÁ¾ÆÁ³½À´Ï´Ù. ¼³¸íÀÇ ÈûÀÔ´Ï´Ù.

¾à°£ÀÇ Æ®¸§Àº º´ÀÌ ¾Æ´Ò ¼ö ÀÖ½À´Ï´Ù.


1. Symptoms

SubtypeSymptoms
PDSpostprandial fullness, early satiation
EPSepigastric pain, epigastric burning

2020-10-29 ÀÌdz·Ä ±³¼ö´Ô comment: Satiety¿Í satiationÀº ´Ù¸¥ ÀǹÌÀÔ´Ï´Ù. Satiety´Â ¹èºÎ¸¥ »óÅÂÀÌ°í satiationÀº ¹°¸®´Â °Í, ´õ ¸ø ¸Ô°Ú´Ù´Â ´À³¦ÀÔ´Ï´Ù.


2. Helicobacter associated dyspepsia

NNT = 14


3. Duodenal inflammation


4. Treatment

Ç︮ÄÚ¹ÚÅÍ Á¦±ÕÄ¡·á NNT = 14

Áõ»ó cure¿¡ ´ëÇؼ­´Â 14ÀÌÁö¸¸ Áõ»ó È£Àü¿¡ ´ëÇؼ­´Â 9, Á¦±Õ ¼º°øÇÑ »ç¶÷ÀÇ Áõ»ó ¼º°øÀº 4.5¿´½À´Ï´Ù.

PPI NNT=10

Prokinetics D2 antagonist NNT = 12 (Metoclo, motiliumÀº ½ÉÀå ºÎÀÛ¿ë, ½Å°æ ºÎÀÛ¿ë ¿ì·Á°¡ À־ mosapride°¡ ¸¹ÀÌ »ç¿ëµÇ°í ÀÖ½À´Ï´Ù.)

Acotiamide (Z-338) fundus relaxing and gastroprokinetic properties. NNT=6·Î cisapride¿Í ºñ½ÁÇÑ ¼öÁØÀÎ °ÍÀ¸·Î »ý°¢µÊ.

* Âü°í: Clin Gastroenterol Hepatol 2018 ¸®ºä


5. Symposiums

[2013-12-15] ±â´É¼º ¼ÒÈ­ºÒ·®Áõ Áý´ãȸ

2013-12-15. ±â´É¼º ¼ÒÈ­ºÒ·®Áõ Áý´ãȸ

2013-12-15. ±â´É¼º ¼ÒÈ­ºÒ·®Áõ Áý´ãȸ


[2017-6-17] ¿¬¼¼´ëÇб³ °­³²¼¼ºê¶õ½º ½ÉÆ÷Áö¾ö. Recent update of pathogenesis of functional dyspepsia. Hiroto Miwa (Hyogo, Japan)

¼Ò°³ÀÇ ¸»: It's great honor to introduce the next speaker professor Hiroto Miwa. After graduating Kagoshima University, he has been working as one of the best researchers in the field of functional gastrointestinal disorders. He is now the professor of Medicine, Hyogo College of Medicine and has been serving as the Vice president of Japanese Society of Gastroenterology. His topic today is funtional dyspepsia.

[Abstract] Dyspepsia is one of most common symptom and approximately 10% of general population has chronic dyspeptic symptoms without apparent organic causes, which is functional dyspepsia. Although FD is one of most important functional GI disorders, its pathogenesis is highly complicated. Possible pathogenic factors for FD includes, acid, H.pylori infection, motility disorders, gastric hypersensitivity and so on. Among those, it is well recognized that motility disorders and gastric hypersensitivity are the factors that directly induce GI symptom manifestation. However, what brings these physiological impairment has remained to be addressed.

Recently the importance of duodenum as a pathogenic center of functional dyspepsia has been gradually and widely recognized. Stimulus or inflammation to duodenum may bring the physiological impairment of the stomach. In fact, early reports demonstrated that intraduodenal application of lipid and acid alter visceromotor function of the stomach. These data suggest that stimulation to duodenum causes motility and sensory dysfunction of the stomach which result in generation of dyspeptic symptoms even in normal subjects. However, unlike the normal subjects, FD patients have dyspeptic symptoms chronically. What is the difference between duodenum of FD patients and that of normal subjects?

I assume duodenum of FD patients is primed, in other words, the duodenum of FD patients is ready to be activated. Two factors, which is presence of low grade inflammation and increased mucosal permeability may be responsible for this phenomenon. There are many reports describing low grade inflammation in FD patients, and the consensus seems to be made recently that both mast cells and eosinophils were increased especially in the second portion of the duodenum. One of the factors that brings the infiltration of eosinophils or mast cells in duodenal mucosa may be severe GI infection, which is known as ¡°post-infectious FD¡±. Low grade inflammation must be a remaining of severe inflammation, however other clear causes for low grade infiltration is not known. The increased permeability of duodenal mucosa in FD patients was first reported recently by Belgium group, which was proven using biopsy specimens from duodenum mucosa and Ussing chamber. Regarding the factors that makes mucosal permeability increased in duodenal mucosa, much is not known. However, there is a recent report demonstrating that small intestinal permeability is increased in psychological stress condition, which is inhibited by pre-administration of mast cell stabilizer, suggesting that the psychological stress increases intestinal permeability by a mast cell-dependent mechanism possibly through CRH axis.

Very recently, the data have been presented suggesting the important role of bile in pathogenesis of functional dyspepsia. The researchers have shown that the bile was associated with increased mucosal permeability and especially secondary bile is correlated with the permeability in FD patients. Furthermore, they showed that one of several bile salt receptor in duodenum is increase in FD patients. It is a future matter of debate that ¡°what¡¯s happening in duodenum of FD patients?¡± Luminal factors or luminal antigens must play some roles in duodenum, which include acid, bile, nutrients including lipid, microbiome and product of microbiome. It would be possible that interaction of such factors with duodenum may explain pathogenesis of functional dyspepsia.

[ÀÌÁØÇà Áú¹®] You emphasized the role of low grade inflammation and increased mucosal permeability of the duodenum in the pathogenesis of FD symptom development. I wonder what is the role of Helicobacter pylori in the development of chronic low grade inflammation or permeability change of the duodenal mucosa. After eradication treatment, could you tell me what kind of histological or functional changes happen?

[Miwa ¼±»ý´Ô ´äº¯] Ç︮ÄÚ¹ÚÅÍ ¾ç¼º FD ȯÀÚ¿Í À½¼º FD ȯÀÚ »çÀÌ¿¡¼­ ½ÊÀÌÁöÀå ¿°ÁõÀ̳ª permeability´Â Â÷ÀÌ°¡ ¾ø½À´Ï´Ù. Ç︮ÄÚ¹ÚÅÍ Á¦±ÕÄ¡·á°¡ Å©°Ô È¿°úÀûÀÌÁö ¾ÊÀº °ÍÀº ÀÌ°Í ¶§¹®ÀÎ °ÍÀ¸·Î »ý°¢ÇÕ´Ï´Ù.

[À̵¿È£ ±³¼ö´Ô Áú¹®] Ç׿°ÁõÁ¦³ª probioticsÀÇ È¿°ú´Â ¾î¶°Çմϱî?

[Miwa ¼±»ý´Ô ´äº¯] Rebamipide´Â ¿©·¯ Àӻ󿬱¸¿¡¼­ È¿°ú°¡ ¾ø¾ú½À´Ï´Ù. Probiotics¿¡ ´ëÇؼ­´Â Èñ¸ÁÀÌ ÀÖÁö¸¸ ÀÚ·á°¡ ºÎÁ·ÇÕ´Ï´Ù. ¿¬±¸°¡ ÇÊ¿äÇÕ´Ï´Ù.


[2022-4-23] °æÁÖ ½ÉÆ÷Áö¾ö. ±è¼öÁø ±³¼ö´Ô °­ÀÇ


[2022-6-8] µ¿¾ÆST web seminar ¿ÀÁ¤È¯ ±³¼ö´Ô °­ÀÇ

½ÅȯÀÇ organic disease´Â ³õÄ¡Áö ¾ÊÁö¸¸ ¿À·¡ ´Ù´Ï½Ã´ø ºÐÀÇ organic disease´Â °£°úµÉ ¼ö ÀÖ½À´Ï´Ù.

PDS : mixed : EPS = 4:4:2

TCA´Â EPS¿¡¼­ ´õ È¿°úÀûÀÌ´Ù.

"ÀÌ ¾àÀº TylenolÀÌ ¾Æ´Õ´Ï´Ù."

"¼ÒÈ­ÀÇ ½ÃÀÛÀº amylaseºÎÅÍÀÔ´Ï´Ù. Àß ¾Ã¾î µå½Ê½Ã¿À."


[2023-4-15] Á¦Ãµ ½ÉÆ÷Áö¾ö


[2023-6-4] ÀÎõ ½ÉÆ÷Áö¾ö. ¾Æ»êº´¿ø Á¤½Å°Ç°­ÀÇÇаú Á¤¼®ÈÄ ±³¼ö´Ô °­ÀÇ


[2023-7-12] ±×³àµéÀÇ ¼ö´Ù - ´ë¿õÁ¦¾à ´ÚÅͺô web-seminar

±×³àµéÀÇ ¼ö´Ù ´ë¿õÁ¦¾à ´ÚÅͺô log-in é©

±×³àµéÀÇ ¼ö´Ù ´ë¿õÁ¦¾à ´ÚÅͺô log-in é©


[2023-10-27] ¿ÀÁ¤È¯ ±³¼ö´Ô °­ÀÇ


[2024-1-14] ¹®Èñ¼® ±³¼ö´Ô °­ÀÇ


[FAQ]

[2018-9-16. ÀÌÁØÇà È¥À㸻]

FD ȤÀº GERD¶ó°í ¿À½Ã´Â ȯÀÚ Áß FD³ª GERD°¡ ¾Æ´Ñ ºÐµéÀÌ ¸¹½À´Ï´Ù. ¿ì¿ïÁõÀ̰ųª ºÒ¸éÁõÀε¥ ³»°ú¿¡¼­ ÀûÀýÇÏ°Ô Ä¡·á¹ÞÁö ¸øÇÑ °æ¿ìµµ ÀûÁö ¾Ê½À´Ï´Ù. ºÒ¸éÁõÀÌ ÁÖ ¿øÀÎÀ¸·Î »ý°¢µÇ¾î Á¤½Å°Ç°­ÀÇÇаú ºÒ¸éÁõ clinicÀ¸·Î ¾È³»ÇÏ¿´´Âµ¥ ȯÀÚ°¡ Å©°Ô ¸¸Á·ÇÏ°í °í¸¿´Ù°í ¸»¾¸Çϼ̽À´Ï´Ù.

ºÒ¸éÁõÀÌ Áø´ÜµÇÁö ¾Ê¾Æ¼­ ºÒÇÊ¿äÇÏ°Ô PPI¸¦ µå½Ã´Â ºÐÀÌ ¸¹½À´Ï´Ù. ȯÀÚ¿¡°Ô Àß ÁÖ¹«½Ã´ÂÁö ¹°¾îº¸¸é ¾î¶³±î¿ä?


[References]

1) Â÷Àç¸í ±³¼ö´Ô - ºñ¿ÂµÚ ÀÎÅͺä

YouTube

2) 2022-6-8. ±â´É¼º¼ÒÈ­ºÒ·®Áõ µ¿¾Æ ST °­ÀÇ. ¿ÀÁ¤È¯ ±³¼ö´Ô (°ü¸®ÀÚ¿ë)

3) 2023-2-14. ºñ¿ÂµÚ ÀÌÁØÇà ÀÎÅͺä

Youtube

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