¼±Åà - È­»ìǥŰ/¿£ÅÍŰ ´Ý±â - ESC

 

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¸¸)