Treatment of Peptic ulcer
I. Treatment of Duodenal ulcer
1. ¼·Ð
Duodenal ulcer¿¡´Â HP°¡ Áß½ÉÀû ¿ªÇÒÀ» ÇϹǷΠġ·á¿ª½Ã HP eradication¿¡ ÃÊÁ¡À»
¸ÂÃá´Ù. bleeding°ú °°Àº complicated ulcer°¡ ¾Æ´Ï¶ó¸é HP eradicationÈÄ maintenance
´Â ÇÊ¿äÄ¡ ¾Ê´Ù.
* HP Tx¸¦ À§ÇÑ ¾àÁ¦µé
: bisthmus compounds, amoxicillin, TC
clarithromycin, metronidazole,
omeprazole, H2-blocker
´ÜÀÏ È¤Àº Á¶ÇÕÇØ¼ »ç¿ëÇÏ¸ç ´ÜÀÏ ¾àÁ¦·Î´Â È¿°ú°¡ ¾ø´Ù.
1) H. pyloriÄ¡·á
¨ç Bisthmuth compounds : ¼ö¼¼±âµ¿¾È »ç¿ëµÇ¾î ¿È
ÀÛ¿ë±âÀüÀº È®½ÇÄ¡´Â ¾ÊÀ¸³ª
i) ulcer base¿¡ °áÇÕÇÏ¿© mucus & PG»ý¼ºÀ» ÀÚ±ØÇÏ´Â cytoprotective effect
ii) antibactericidal effect
Bisthmus monotherapy : HP eradication rate = 20%
Bisthmus + antibiotics : 95%
¨è ÇöÀç °¡Àå ¼º°øÀûÀÎ Ä¡·á¹ý : Triple therapy
Bisthmus compounds 2T qid
metronidazole 500mg tid
amoxicillin or TC 500mg qid X 2ÁÖ = 90%
TC´Â amoxicillin(500mg qid)À¸·Î ´ëü°¡´ÉÇϳª
ºñ¿ëÀÌ ¾à°£ ´õ ºñ½Î°í È¿°ú´Â ¾à°£ ³·´Ù.
* triple thrapy 2ÁÖ + H2 blocker 6ÁÖ
-> ulcer healing rate¡è, ulcer recurrence¡é(15%¡é/1³â)
* omeprazoleÀ» triple tx¿¡ Æ÷ÇԽà HP eradication rate = 98%
* Áß¿ä¾àÁ¦ÀÇ side effects
bisthmuth : dark stool, dark tongue, constipation
amoxicillin : antibiotic-associated diarrhea(PMCÆ÷ÇÔ), N/V, skin rash,
allergic reaction
TC : skin rash, rarely anaphylaxis, hepatotoxicity
Metronidazole : Àå±â »ç¿ë½Ã paresthesia, µå¹°°Ô seizure
´Ü±â »ç¿ë½Ã N/V, diarrhea, altered taste sensation
* Metronidazole resisance°¡ ¹®Á¦°¡ µÇ°í Àִµ¥ ¹Ì±¹¿¡¼± 30%
metronidazole-resistant strainÀ̶ó°í ÇØ¼
¸ðµÎ HP eradication¿¡ ½ÇÆÐÇÏ´Â °ÍÀº ¾Æ´Ï´Ù.
metronidazole-susceptable strain : 91%
metronidazle -resistant strain : 63%
¨é Clarithromycin : newer macrolide antibiotics
metronidazole¿¡ ´ë½ÅÇØ¼ 250mg qid(=500 mg tid¿Í È¿°úµ¿ÀÏ)
triple regimenÀ¸·Î »ç¿ë: 90%È¿°ú
* Omeprazole(or lansoprazole)
+ Clarithromycin
+ metronidazole or amoxicillin X 1ÁÖÀÇ simple triple regimenµµ ÀÖ´Ù.
* HP eradicationµÈ °æ¿ì endoscopy c Bx´Â ÀϹÝÀûÀ¸·Î ÇÊ¿ä¾øÀ¸¸ç
serologic test´Â Ab levelÀÌ ¼¼È÷ ¶³¾îÁö°í 0±îÁö ¶³¾îÁöÁö ¾Ê±â ¶§¹®¿¡
unreliable!
* Ä¡·á Á¾°á 1°³¿ùÈÄ HP eradicationÀÌ È®ÀεǸé reinfectionÀº µå¹°¸ç ¼±¸¿¡¼
ºóµµ´Â ¸Å³â 1%Á¤µµ·Î ³·´Ù.
* UBT°¡ HP eradicationÀ» È®ÀÎÇÏ´Â °¡Àå °£ÆíÇÏ°í ½Ñ ¹æ¹ýÀÌ´Ù.
2. Antiulcer drug
1) Antacids: neutralize HCl
Al hydroxide Cx= constipation, systemic phosphate depletion
-> phosphate poor dietȯÀÚ¿¡¼
weakness, malaise, anorexia¾ß±â
Mg hydroxide = loose stool
Ca carbonate : 10%°¡ Èí¼ö -> milk-alkali syndromeÀ¯¹ß°¡´É
(Ca, P, BUN, Cr, bicarbonate¡è)
2) H2 blocker
triple Tx + 4-6ÁÖ H2 blocker°¡ ÇöÀç º¸ÆíÀûÀ¸·Î ¾²ÀÌ´Â ¹æ¹ý
¨ç Cimetidine : 300mg = basal acid secretion¾ïÁ¦(1T=200mg)
300mg qid(½Ä»ç¶§ & Ãëħ½Ã)
= 400mg tid = 800mg qd hs¿Í È¿°úµ¿ÀÏ
* S/E : AST/ALT, Cr, Prolactin»ó½Â
cytochrome P450 inhibition -> Ç÷Á߳󵵡è
tender gynecomastia
¨è Ranitidine : cimetidineº¸´Ù 6¹è potent
150mg(1T) bid = 300 mg qd hs
* S/E : AST/ALT, ALP level¡è, No antiandrogenic effect
¨é Famotidine(40mg qd hs) and Nizatidine(300mg qd hs)
* S/E : blood dyscrasia, µå¹°°Ô hepatotoxicity(ranitidineÀ̳ª cimetidine°ú À¯»ç)
3) Anticholingergic agent : Pirenzepine
parietal cellÀÇ Ach receptor block -> gastric acid secretion¡é
±×·¯³ª H2 blocker¸¸Å È¿°úÀûÀÌÁö ¾Ê°í ´Ù¾çÇÑ ºÎÀÛ¿ëÀÌ ÀÖ´Ù.
* S/E : blurred vision, dry mouth
4) Coating agent
¨ç Sucralfate : polyaluminum hydroxide salt of sucrose sulfate
1g ½Ä»ç 1½Ã°£Àü + ÃëħÀü
i) acid pH¿¡¼ highly polar, 12½Ã°£µ¿¾È ulcer bed¿¡ °áÇÕ
ii) intact gastric or duodenal mucosa¿¡´Â °áÇÕX
iii) ulcer base¿¡ H+ diffusionÀ» ¹æÇØ
iv) bile aicd, pepsin°ú °áÇÕÇÏ¿© injurious effect¸¦ ÁÙÀÓ
v) endogenous tissue PG level¡è
==> mucosal defense°È
ÃÖ¼Ò·®ÀÌ Èí¼öµÇ¾î ¼Òº¯¹èÃâÀº 5%¹Ì¸¸ÀÌ´Ù.
* DU Ä¡·á ¹× Àç¹ßÀÇ ¿¹¹æ¿¡¼ H2 blocker³ª antacid¿Í È¿°ú°¡ ºñ½ÁÇÏ´Ù.
¨è Colloidal bisthmuth(DeNol)
i) bisthmuth-protein coagulantÇü¼º -> acid, pepsinÀ¸·ÎºÎÅÍ ulcer protect
ii) little neutralizing effect
iii) gastric acid secretionÀ» ÁÙÀÌÁö ¸øÇÑ´Ù.
iv) pepsin activity¾ïÁ¦
v) gastric mucus gel layer¿¡ °áÇÕ -> H+ diffusion¹æÁö
vi) PG, bicarbonate, glycoprotein mucusºÐºñ¸¦ ÃËÁø
5) PG
¨ç low dose exogenous PGE : mucosal defense¸¦ ÃËÁø½Ã۴µ¥ Áß¿äÇÏ´Ù.
i) gastric mucus secretion¡è
ii) gastric & duodenal bicarbonate secretion¡è
iii) gastric mucosal blood flow¡è
iv) gastric mucosa barrier to diffusion of H+
iv) mucosal cell replacement¡è
¨è S/E : diarrhea, uterine contraction
* ´Üµ¶À¸·Î´Â DU Ä¡·á¿¡ »ç¿ëÄ¡ ¾Ê°í ¹Ì±¹¿¡¼ misoprostol(PGE analogue,
cytotec)ÀÌ NSAID-induced ulcer¿¹¹æÀ§ÇØ »ç¿ëÇÑ´Ù.
6) PPI
H+ secretionÀÇ ¸¶Áö¸· ´Ü°èÀÎ H+, K+-APTase(proton pump)ÀÇ inhibitor
omeprazole & lansoprazoleÀÌ
DU, erosive esophagitis, gastric acid hypersecretory state(ZES µî)¿¡ Áõ¸íµÇ¾ú´Ù.
II. Gastric Ulcer Treatment
DU Tx¿Í µ¿ÀÏÇϸç HP¿Í ¿¬°üµÈ °æ¿ì triple Tx + acid-suppressive agent¸¦ »ç¿ëÇÑ´Ù.
GUȯÀÚ¿¡¼ gastric acid secretionÀÌ Á¤»óÀ̰ųª °¨¼ÒµÇ¾î ÀÖÁö¸¸ acid-inhibiting
agent°¡ ulcer healing¿¡ È¿°úÀûÀÌ´Ù.
1) Diet
salicylate, NSAID stop
milk, creamÀº µµ¿òÀÌ µÇÁö ¾Ê´Â´Ù.
coffee(caffeine-containing or caffeine-fee), alcoholÀ» Áß´ÜÇϵµ·Ï ÇÑ´Ù.
2) Carbenoxolone(derived from licorice)
Áõ»óÀ» °¨¼Ò½Ã۸ç GU healingÀ» ÃËÁø½ÃŲ´Ù.
¹Ì±¹¿¡¼± »ç¿ëÇÏÁö ¾Ê´Â´Ù.
3) Ä¡·á±â°£
2-3°³¿ù³» ¿ÏÀüÈ÷ healingµÈ´Ù.
ulcer size°¡ ÃæºÐÈ÷ °¨¼ÒÇÏÁö ¾ÊÀ» ¶§ ¹Ýµå½Ã malignancy°¡´É¼ºÀ» »ý°¢ÇØ¾ß ÇÑ´Ù.
¡Å Ä¡·áÈÄ ¹Ýµå½Ã ³»½Ã°æÀ» ½ÃÇàÇÏ¿© ulcer healingÀÌ ¾ÈµÇ¾úÀ»¶© cytology & biopsy¸¦
½ÃÇàÇÏ¿©¾ß ÇÑ´Ù.
* complete healingµÇ¾ú´Ù°í ÇØ¼ ¹Ýµå½Ã benignÀÎ °ÍÀº ¾Æ´Ï´Ù.
¿Ö³ÄÇϸé malignancy·Î ÆÇ¸íµÈ ulcerÀÇ 70%´Â Ä¡·áÇϸé significant healingÀ» º¸À̱â
¶§¹®ÀÌ´Ù.(º¸Åë incomplete healingÀ» º¸À̱ä ÇÏÁö¸¸)