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Acute viral hepatitis

1. Virology & Etiology

1) Hepatitis A

- nonenveloped 27-nm, heat, acid, ether-resistant RNA virus

- picornavirus familyÀÇ hepatovirus genus¿¡ ¼ÓÇÔ.

- incubation period : 4ÁÖ

- ¿ÀÁ÷ °£¿¡¼­¸¸ Áõ½ÄÇÏÁö¸¸ liver, bile, stool, blood¿¡¼­ Á¸ÀçÇÒ¼ö ÀÖ´Ù.

- Ȳ´ÞÀÌ ¹ß»ýÇÑÈÄ °¨¿°¼ºÀº °¨¼ÒÇÑ´Ù.

- IgM anti HAV´Â ¼ö°³¿ù°£ Áö¼ÓÇÒ¼ö ÀÖÀ¸³ª 6-12°³¿ù ÀÌ»óÁö¼ÓÀº µå¹°´Ù.

ȸº¹±â¿¡´Â IgG anti HAV°¡ ¿ì¼¼ÇØÁö¹Ç·Î hepatitis AÀÇ Áø´ÜÀº

IgM anti HAV·Î ÇÏ¸ç ±Þ¼º±â ÀÌÈÄ¿¡´Â IgG anti HAV°¡ °è¼Ó °ËÃâµÈ´Ù.

- anti-HAV´Â Àç°¨¿°¿¡ ´ëÇÑ ¸é¿ª¼ºÀ» °¡Áö´Â neutralizing AbÀÌ´Ù.

2) Hepatitis B : hepadnavirus type 1

- small, circular, 3200-basepair sizeÀÇ complex, multiparticle structure¸¦ °¡Áø DNA virus

- S, C, P, XÀÇ 4°³ geneÀÌ °ãÃļ­ ´Ü¹éÁúÀ» encodingÇϵµ·Ï ÇÏ´Â °æÁ¦ÀûÀ̰í È¿°úÀûÀÎ

Àü·«À» ±¸»çÇÑ´Ù.

- °£¿¡¼­ Áõ½ÄÇÏÁö¸¸ extrahepatic site¿¡µµ Á¸ÀçÇϸç endogenous DNA polymerase¸¦

°®°í ÀÖ´Ù.

- ºÎºÐÀûÀ¸·Î´Â double-stranded, ¶Ç ºÎºÐÀûÀ¸·Î´Â single-stranded genomeÀ» °®°íÀÖ°í,

acute & chronic hepatitis & HCC¸¦ ÀÏÀ¸Å²´Ù.

- Áõ½ÄÇÏ´Â ¹æ½ÄÀº DNA virus¿¡ ÀÇÇÏÁö ¾Ê°í retrovirusÀÇ Áõ½Ä¹æ½ÄÀ» µû¸¥´Ù.

Áï, DNA template¿¡¼­ Á÷Á¢ ÇÏÁö¾Ê°í DNA polymerase¿¡ ÀÇÇØ munus-strand DNAÀÇ

reverse transcription¿¡ ÀÇÇÏ¿© Áõ½ÄÇÑ´Ù..

plus-strand DNA´Â DNA-dependent DNA polymerase¿¡ ÀÇÇØ minus-strand DNA

template¿¡¼­ transcriptionµÈ´Ù.

minus-strand DNA template -----> plus-strand DNA

¡è

DNA dependent DNA polymerase

(1) Viral protein & particles

22 nm particle : spherical or long filamentous form

42 nm, double-shelled, spherical particle = hepatitis B virion

¨ç HBs Ag : S gene product

¸¹Àº HBsAg subdeterminant°¡ Àִµ¥ ÈçÇÑ group-reactive Ag = a

subtype d or y, w or r

±×·¯³ª ÀÓ»ó°æ°ú´Â subtype or genotype¿¡ »ó°ü¾ø´Ù.

S gene = preS1 + preS2 + S

S = major protein, S + preS2 = middle protein, S + preS2 + preS1 = large protein

¨è HBeAg : highly infectious

HBeAg(+) mother : 90%ÀÌ»ó žƿ¡°Ô ÀüÆÄ

HBeAg(-) : 10-15%

acute hepatitis B¿¡¼­ HBe AgÀÌ 3°³¿ùÀÌ»ó Áö¼ÓÇÏ¸é ¸¸¼º°£¿°À¸·Î ÀÌÇàÇÔÀ» ¿¹ÃøÇÒ¼ö

ÀÖÀ¸¸ç ongoing viral replication, infectivity, inflammatory liver injury¸¦ ÀǹÌÇÑ´Ù.

¨é P gene : DNA polymerase

DNA-dependent DNA polymerase¿Í RNA-dependent reverse transcriptase activity

¸ðµÎ¸¦ °¡Áø´Ù.

¨ê X gene : HBx Ag expression

i) severe chronic hepatitis B, HCC¸¦ ÀÏÀ¸Å²´Ù.

ii) ´Ù¸¥ virusÀÇ transcription, replication¡è

iii) human IFN-¥ã, MHC class I gene activation

=> HBV-infected hepatocyte°¡ cytotoxic T cell¿¡ ´ëÇØ °¨¼ö¼ºÀÌ ¿¹¹ÎÇϵµ·Ï ÇÑ´Ù.

iv) programmed cell death(apoptosis)¿Í °ü·ÃÀÖ´Ù.

v) ºñÆ÷À¯µ¿¹°ÀÇ hepadnavirus¿£ Á¸ÀçÇÏÁö ¾Ê´Â´Ù.

±×·¯¹Ç·Î X°¡ hepadnavirus replication¿¡ ÇʼöÀûÀÎ °ÍÀº ¾Æ´Ï´Ù.

(2) Serologic & viral markers

ALT°¡ Áõ°¡Çϱâ Àü¿¡ ¸ÕÀú HBsAgÀÌ ÃâÇöÇϱ⠶§¹®¿¡ Ȳ´ÞÀÌ ÀÖ´Â Àü±¸°£ ¹×

ÀÓ»óÁõ»óÀÌ ÀÖÀ» ¶§ HBsAgÀÌ ¹ß°ßµÈ´Ù.

HBs Ag¼Ò½ÇÈÄ anti-HBs°¡ ¹ß°ßµÈ´Ù.

anti HBc´Â HBsAgÀÌ ÃâÇöÇÑÈÄ 1-2ÁÖ³»¿¡ ¹ß°ßµÇ´Âµ¥ anti HBsº¸´Ù ¼öÁÖ-¼ö°³¿ù

ºü¸£´Ù.

¨ç "Gap" or "Window" period

HBsAg¼Ò½Ç°ú anti HBsÃâÇö»çÀÌ¿¡ ¼öÁÖ ÀÌ»óÀÇ gapÀÌ Àִµ¥ ÀÌ ±â°£À»

"gap" or "window" period¶ó ÇÑ´Ù. À̶§´Â HBV infectionÀÇ Ç÷ûÇÐÀûÀΠǥÁöÀÚ·Î

anti HBc(IgM)ÀÌ ³ªÅ¸³­´Ù.

ÇöÀç immunoassay¹Î°¨µµ°¡ ¹ß´ÞÇÏ¿© window period´Â µå¹°´Ù.

¨è Isolated anti HBc(IgG)

i) ´ëºÎºÐ remote past infectionÀ» ÀǹÌÇÑ´Ù.

ii) ±×·¯³ª µå¹°°Ô low-level hepatitis B viremia¸¦ ÀǹÌÇÏ´Â ¼öµµ ÀÖ´Ù.

(HBs AgÀÌ detection threshold ÀÌÇÏ levelÀÏ ¶§)

¨é anti HBc : 6°³¿ù À̳»´Â IgM, 6°³¿ù ÀÌÈÄ´Â IgG

¨ê chronic hepatitis BÀÇ 10-20%°¡ low-level, low-affinity anti HBsÀÌ´Ù.

¨ë natural seroconversion of HBe Ag(HBe Ag -> anti HBe)

¸Å³â 10%, À̶§ ÀϽÃÀûÀÎ acute hepatitis-like ALT elevationÀÌ ÀϾ´Âµ¥

cell-mediated clearance of virus-infected hepatocyteµÇ±â ¶§¹®ÀÌ´Ù.

¨ì °¡²û nonreplicative HBV infectionÀÌ replicative infectionÀ¸·Î ÀüȯÇϴµ¥

ÀÌ·± spontaneous reactivation¶§ HBeAg, HBV DNA°¡ Àç¹ßÇöµÇ¸ç

¶§·Î´Â IgM anti HBc(+), liver injury exacerbationµÈ´Ù.

(3) Molecular variant

¨ç precore mutant

preC geneÀÇ last codonÀÇ µÎ¹øÂ°¿¡¼­ G->A´ëÄ¡(TGG->TAG)

=> HBe Ag translation¹æÇØ

severe liver disease, cirrhosis·Î »¡¸® ÁøÇà

antiviral tx¿¡ Àß ¹ÝÀÀ¡¿

fulminant hepatitis B¿Í °ü·Ã

Wild type°ú °øÁ¸Çϰųª mutant HBV°¡ wild-type infectionµ¿¾È ¹ß»ýÇÒ¼öµµ ÀÖ´Ù.

¨è escape mutant(G->A, HBV/a mutant)

HBsAg all subtype¿¡¼­ ÈçÇÑ immunodominant a determinantÀÇ 145¹ø À§Ä¡¿¡¼­

¹ß»ý(Glycine-> Arginine)

=> neutralizing anti-HBs activity loss

µÎ°¡Áö »óȲ(active & passive immunization)¿¡¼­ °üÂû°¡´É

: humoral immunologic pressure¿¡ ´ëÇØ virus°¡ evolutionary change(escape)ÇÔ.

(4) Extrahepatic sites

HBsAg, HBV DNA°¡ extrahepatic site¿¡¼­µµ ¹ß°ßµÈ´Ù.

: LN, BM, circulating lymphocyte, spleen, pancreas

extrahepatic site¿¡ tissue injury¸¦ ÀÏÀ¸Å°Áö´Â ¾ÊÀ¸³ª orthotopic liver transplantation

ÈÄ Àç¹ßÀÇ source°¡ µÈ´Ù(="remote" reservoirs)

3) Hepatitis D(¥ä-agent or HDV)

Áõ½Ä°ú ¹ßÇöÀ» À§Çؼ­´Â HBV(ȤÀº ´Ù¸¥ hepadnavirus)¿Í coinfect³»Áö´Â µµ¿òÀ» ÇÊ¿ä·Î

ÇÏ´Â defective RNA virus·Î HBVº¸´Ù´Â Å©±â°¡ ¾à°£ ´õ ÀÛ´Ù.

HBV¿Í antigenic homololy°¡ ¾øÀ¸¸ç ¥ä-core´Â ¿ÜºÎ¿¡ HBsAgÀÇ envelope¿¡ ÀÇÇØ

" encapsidated"µÇ¾î ÀÖ¾î HBV¿Í ±¸º°ÇÒ¼ö ¾ø´Ù.

- HDV RNA : small, 1700-nucleotide, circular, single stranded RNA(minor strand)·Î

polymerase geneÀϺθ¦ Á¦¿ÜÇϰí´Â HBV DNA¿Í °°Àº ºÎºÐÀÌ ¾øÀ¸¸ç

RNA directed RNA synthesis·Î Áõ½ÄÇÑ´Ù.

- HBV¿Í µ¿½Ã¿¡ °¨¿°(coinfection)µÇ°Å³ª HBV°¨¿°È¯ÀÚ¿¡¼­ superinfectionµÈ´Ù.

- HBV¿¡ Àý´ëÀûÀ¸·Î ÀÇÁ¸ÇϹǷΠHDV°¨¿°±â°£Àº HBV°¨¿°±â°£¿¡ ÀÇÇØ °áÁ¤µÈ´Ù.

4) Hepatitis C

- linear, single-stranded, positive-sense, 9400-nucleotide RNA virus

- Flaviriridae and pestivirus¿Í À¯»ç

- 5¡Çend¿¡ untranslated regionÀ¸·Î ±¸¼ºµÈ genomeÀÌ ÀÖ´Ù

: nucleocapsid core protein°ú 2°³ÀÇ envelope glycoproteins(=E1 and E2/ES1)

- 5¡Çuntranslated region & core gene : highly conserved.

envelope protein : hypervariable region¿¡ ÀÇÇØ codeµÊ

= virus host immunologic containment(¼÷Áָ鿪)À» ÇÇÇϵµ·Ï ÇÔ.

- 3¡Çend : nonstructural(NS) proteinÀ» À§ÇÑ gene

C100-3(NS4) = 1st immunoassay

NS5 : RNA dependent RNA polymerase, À̰ÍÀ» ÅëÇØ HCV°¡ Áõ½ÄÇÔ.

¢¼ Quasispecies(=intragenotypic difference)

HCV´Â Àû¾îµµ ¿©¼¸ °³ÀÇ genotypeÀÌ ÀÖÀ¸¸ç genotype¼Ó¿¡´Â ¸¹Àº subtypeÀÌ ÀÖ´Ù.

genotype ȤÀº subtype³»¿¡¼­, ±×¸®°í °°Àº ¼÷ÁÖ³»¿¡¼­ HCV divergence°¡ Àֱ⠶§¹®¿¡

genotypeÀ» ºÐ¸íÈ÷ Á¤Çϱâ´Â ¾î·Æ´Ù. ÀÌó·³ genotype³»¿¡¼­ º¸ÀÌ´Â sequenceÀÇ

´Ù¾ç¼ºÀ» quasispecies¶ó ÇÑ´Ù.

- genotypic & quasispecies diversityÀÇ ¿ªÇÒ

= high mutation rate, effective humoral immunity¹æÇØ

- 1¼¼´ë(C100-3=NS4) °¨¿° 1-3°³¿ùÈÄ detect°¡´É

2¼¼´ë(C22-3 & NS3 region=C33c) -20%´õ sensitive, 30-90ÀÏ ´õ ÀÏÂï detect

* most sensitive indicator = HCV RNA(PCR)

anti-HCV°¡ ÃâÇöÇϱâÀü ¼öÀϳ» detect°¡´ÉÇÏ´Ù.

Fig 295-6

1¼¼´ë : C100-3

2¼¼´ë : C22-3 + C200(C33c + C100-3)

3¼¼´ë : C22-3 + C200(C33c + C100-3), NS5

RIBA : 5-1-1, C100-3, C33c, C22-3, NS5 - false positive°¡ ¹®Á¦

5) Hepatitis E

HAV¿Í À¯»ç,

32-34 nm, nonenveloped, HAV-like virus with 7600-nucleotide, single stranded

positive-sense RNA genome

active infectionÈÄ ±Þ°ÝÈ÷ ¶³¾îÁ® 9-12°³¿ù³»¿¡ low level¿¡ µµ´ÞÇÑ´Ù.

ÇöÀç HEV¸¦ °ËÃâÇϱâ À§Çؼ­ À¯¿ëÇÏ°Ô »ç¿ëÇÒ¼ö ÀÖ´Â serologic test´Â ¾ø´Â ½ÇÁ¤ÀÌ´Ù.

2. Pathogenesis

1) Hepatitis B : hepatitis B carrier°¡ ¹«Áõ»óÀ̸鼭 normal liver histology & function

À» º¸ÀÌ´Â °ÍÀº virus°¡ Á÷Á¢ cytopathicÇÏÁö´Â ¾Ê´Ù´Â °ÍÀ» ÀǹÌÇÑ´Ù.

cellular immune response°¡ hepatitis B related liver injuryÀÇ pathogenesis¿¡ °ü¿©ÇÑ´Ù.

Áï, °£¼¼Æ÷¸·¿¡ host & hepatitis B viral Ag(nucleocapsid protein, HBcAg, possibly

HBeAg)ÀÌ ¼Ò·® ¹ßÇöÇϸé cytolytic T cellÀÌ À̸¦ ÀÎÁöÇÏ¿© cytokineÀ» ºÐºñÇϰí

°á±¹ HBV infected hepatocyte°¡ ÆÄ±«µÈ´Ù.

* inflammatory cytokines

: cytopathic antiviral mechanism°ú º°°³·Î early viral clearance¿¡ ±â¿©ÇÑ´Ù.

2) Hepatitis C

lymphoid cell¿¡ ´ëÇÑ HCV infectionÀÌ ¹ÙÀÌ·¯½º¿¡ ´ëÇÑ ¸é¿ª¹ÝÀÀÀ» Á¶ÀýÇϴµ¥ Áß¿äÇÑ

¿ªÇÒÀ» ÇÏ´Â °ÍÀ¸·Î »ý°¢µÈ´Ù.

virus-specific cytolytic T cell response°¡ liver injuryÁ¤µµ¿Í ºñ·ÊÇÏÁø ¾Ê´Â´Ù.

3) Extrahepatic manifestations

¨ç HBV

immune complex-mediated tissue damage - acute hepatitis B

ex> prodromal serum sickness-like syndrome

( urticarial rash, angioedema, fever, arthritis)

´Ù¸¥ immune-complex diseaseµµ ¹ß°ß

: GN with nephrotic syndrome, polyarteritis nodosa, EMC..

¨è HCV

HCV RNA¸¦ Æ÷ÇÔÇÏ´Â circulating immune complex

: EMC pathogenesis¿¡ ¹ÙÀÌ·¯½º°¡ 1Â÷Àû ¿ªÇÒÀ» ÇÔ.

3. Pathology

- large hepatocyte with a ground glass appearance of the cytoplasm

: chronic¿¡¼­ º¸ÀÌ´Â ¼Ò°ß(acute HBV infection¿¡¼± ¾Èº¸ÀÓ)

ÀÌ·¯ÇÑ ¼¼Æ÷µé¿¡ HBsAgÀÌ ÇÔÀ¯µÇ¾î ÀÖÀ¸¸ç orcein or aldehyde fuchsin¿°»öÀ» ÇÏ¿©

Á¶Á÷ÇÐÀûÀ¸·Î Áõ¸íÇÒ¼ö ÀÖ´Ù.

- uncomplicated viral hepatitis¿¡¼­ reticulum framework´Â preserved

- acute hepatitis ȯÀÚ ÀϺο¡¼­ bridging necrosis(=subacute or confluent necrosis)°¡

°üÂûµÇ´Âµ¥ lobule»çÀÌ¿¡ "bridging"Çü¼º -> reticulum framework collapse

°ú°Å¿¡ ¿¹ÈÄ¿Í °ü·ÃÇÏ¿© Áß¿äÇÏ°Ô »ý°¢ÇÏ¿´À¸³ª ÃÖ±ÙÀÇ ¿¬±¸´Â acute hepatitis¿¡¼­

bridging nerosis¿Í poor Px»çÀÌ¿¡´Â °ü·ÃÀÌ ¾øÀ½À¸·Î ³ªÅ¸³µ´Ù.

chronic hepatitis¿¡¼­´Â ¿¹ÈÄ¿Í °ü·ÃÀ¸³ª acute hepatitis¿¡¼­´Â ±× Àǹ̰¡ Àû´Ù. µû¶ó¼­ ÀÌ

º´º¯À» È®ÀÎÇϱâ À§ÇØ ´õ ÀÌ»ó routineÀ¸·Î liver biopsy¸¦ ½ÃÇàÇÏÁö ¾Ê´Â´Ù.

4. Epidemiology

1) Hepatitis A : fecal-oral route

- poor personal hygiene & overcrowdingȯ°æ¿¡¼­ large break

: contaminated food, water, milk, forzen reapberries, strawberries, shellfish..

- Intrafamily & intrainstitutional spreadµµ ¶ÇÇÑ ÈçÇÏ´Ù.

- ´Ê°¡À», Ãʰܿ£ ÁÖ·Î ¹ß»ýÇÑ´Ù.

- ¼ºÀο¡¼­ °¨¿°ºóµµ´Â °¨¼ÒÇÏÁö¸¸ more symptomatic.

2) Hepatitis B

i) percutaneous inoculation - major route

ii) ¸ðµç ü¾×(ƯÈ÷ semen & saliva)¿¡ HBsAgÁ¸Àç

iii) intimate contact(especially sexual)

iv) perinatal transmission

HBeAg-positive mother : 90%

anti-HBeAg postive mother : 10-15%

3) Hepatitis D

i) endemic area(ºÏ¹Ì, ³²À¯·´, Áßµ¿) : nonpercutaneous(close personal contact)

ii) nonendemic area(¹Ì±¹, ºÏÀ¯·´) : blood & blood product¿¡ ÈçÈ÷ ³ëÃâµÇ´Â »ç¶÷

(injection drug users & hemophilias)

4) Hepatitis C

* transmission mode

i) bloodborne infection

- hemodialysis, organ transplantation, cancer CTx¶§ transfusionÀÌ ÇÊ¿äÇÑ °æ¿ì

ii) sexually & perinatally(5%) : HIV³ª HBVº¸´Ù ³·´Ù.

sexual transmissionÀº multiple sexual partner, STDȯÀÚ¿¡ ±¹ÇѵǸç

stable, monogamous sexual partner¿¡¼± µå¹°´Ù.

breast feedingÀ¸·Î Àü¿° À§ÇèÀÌ Áõ°¡ÇÏÁö ¾ÊÀ¸¸ç health worker´Â accidental needle

puncture¸¦ ÅëÇÑ À§ÇèÀÌ Áõ°¡ÇÑ´Ù(3-10%).

household contactÀ» ÅëÇÑ ÀüÆÄ´Â µå¹°´Ù.

¸é¿ª¾ïÁ¦È¯ÀÚ¿¡¼­´Â anti-HCV°¡ °ËÃâÀÌ µÇÁö ¾Ê´Â °æ¿ì°¡ ÈçÇϹǷΠÀ̶§´Â HCV RNA·Î

Áø´ÜÇÑ´Ù.

5 . Clinical & Lab features

1) Sx & signs

¨ç incubation period A : 15ÀÏ-45ÀÏ(Æò±Õ 4ÁÖ)

B : 30-180ÀÏ(Æò±Õ 4-12ÁÖ)

C : 15-160ÀÏ(Æò±Õ 7ÁÖ)

E : 14-60ÀÏ(Æò±Õ 5-6ÁÖ)

¨è prodromal sx : Àü½ÅÀûÀÌ¸ç ¸Å¿ì ´Ù¾çÇÏ´Ù.

anorexia, N/V = ³¿»õ, ¸ÀÀÇ º¯È­¶§¹®

fatigue, malaise, arthralgia, myalgia, headache, photophobia, paryngitis, cough,

coryza

- jaundice¹ß»ý 1-2ÁÖ Àü¿¡ ¼±Çà

- low-grade fever(38-39¡É) = A ,E > B, C

- B : serum sickness-like syndrome

- clinical jaundice¹ß»ýÈÄ Àü±¸Áõ»óÀº ¼Ò½ÇµÇÁö¸¸ mild wt loss(2.5-5kg)°¡ ÈçÇÏ´Ù.

¨é liver enlargement & tenderness -> RUQ pain & discomfort

¨ê splenomegaly, cervical lymphadenopathy(10-20%)

ȸº¹±â¶§ Áõ»óÀº ¼Ò½ÇµÇÁö¸¸ liver enlargement & LFT abnormality´Â ¿©ÀüÈ÷ Áö¼ÓµÈ´Ù.

¨ë posticteric phase±â°£Àº ´Ù¾çÇϸç(2-12ÁÖ) B, C¿¡¼­ ´õ ¿À·¡ Áö¼ÓÇÑ´Ù.

¿ÏÀüÇÑ È¸º¹Àº A, E´Â 1-2°³¿ù, B, C´Â 3-4°³¿ù(3/4¿¡¼­) °É¸°´Ù. ³ª¸ÓÁö´Â ´õ ¿À·¡ Áö¿¬.

¨ì HDV infection

acute & chronic HBV infection»óÅ¿¡¼­ »ý±æ¼ö ÀÖÀ¸¸ç HBV infection±â°£ÀÌ HDV

infection±â°£ÀÌ´Ù.

LabÀº coinfection½Ã ´õ ½ÉÇÒÁö¶óµµ ÈçÈ÷ HBV infection´Üµ¶°ú ±¸º°ÇÒ¼ö ¾ø´Ù.

¨í HBVȯÀÚ¿¡¼­ acute hepatitis-like clinical event°¡ »ý±æ¼ö ÀÖ´Ù.

i) spontaneous HBeAg-to-anti-HBe seroconversion

ii) spontaneous reactivation

Áï, nonreplicative -> replicative infectionÀ¸·Î reversionµÉ ¶§

iii) precore mutantÃâÇö½Ã

chronic hepatitis BÀÇ acute clinical exacerbationÀº precore mutantÃâÇöÀ» ³ªÅ¸³»±âµµ

ÇÑ´Ù.

2) Lab features

¨ç AST/ALT : liver cell damageÁ¤µµ¿Í ºñ·ÊÇÏÁö ¾Ê´Â´Ù.

clinically ictericÇÒ ¶§ peak level¿¡ µµ´ÞÇÏ¿´´Ù°¡ ȸº¹±â¶§ Á¡Â÷ °¨¼ÒÇÑ´Ù.

¨è Bil : 2.5 mg/dLÀÌ»óÀÏ ¶§ sclera or skin¿¡¼­ jaundice¸¦ È®ÀÎÇÒ¼ö Àִµ¥

jaundice°¡ ¹ß»ýÇϸé s-Bil levelÀº º¸Åë 5-20 mg/dLÁ¤µµ µÇ¸ç AST/ALT levelÀÌ ¶³¾î

Á®µµ °è¼Ó Áõ°¡ÇÑ´Ù.

20 mg/dLÀÌ»óÀÏ ¶§ viral hepatitisÀÇ °æ°ú°¡ ¿À·¡°¡¸ç severe disease¸¦ ÀǹÌÇÑ´Ù.

¿¹¿Ü> glucose-6-phosphate dehydrogenase deficiency, sickle cell anemiaȯÀÚ¿Í °°ÀÌ

underlying hemolytic anemia°¡ ÀÖ´Â °æ¿ì¿¡ high s-Bil levelÀÌ ÈçÇÏ´Ù.

±×·± ȯÀÚµéÀº bil levelÀÌ 30ÀÌ»ó ¿Ã¶ó°¡±âµµ ÇϹǷΠ¹Ýµå½Ã poor Px¿Í °ü·ÃÀÌ

ÀÖ´Â °ÍÀº ¾Æ´Ï´Ù.

¨é Neutropenia & lymphopenia

ÀϽÃÀûÀ̸ç ÀÌÈÄ relative lymphocytosis°¡ »ý±ä´Ù.

atypical lymphocyte(2-20%)µµ acute phase¶§ ÈçÇÏ´Ù. À̶§´Â I.M¿Í °¨º°ÇÏ±â ¾î·Æ´Ù.

¨ê PT¡è : severe synthetic defect, extensive hepatocellular necrosis¸¦ ÀǹÌÇϸç

worse Px¿Í °ü·ÃÀÖ´Ù.

¨ë Glu¡é : severe viral hepatitis

¨ì ALP : normal or mild ¡è

¨í s-Alb¡é : uncomplicatedÀÇ °æ¿ì¿£ µå¹°´Ù.

¨î microscopic hematuria & minimal proteinuria

¨ï diffuse, mild ¥ã-globulin fraction¡è : ÈçÇÏ´Ù.

1/3¿¡¼­ IgG, IgMÀÌ Áõ°¡µÇ¸ç ƯÈ÷ IgMÀº hepatitis A¿¡¼­ Áõ°¡µÈ´Ù.

¨ð AutoAb

smooth m. Ab, RF low titer, ANA, heterophil Ab°¡ °¡²û ¹ß°ßµÈ´Ù.

Hepatitis C, D : anti LKM Ab(+)

À̶§ C, DÀÇ Ab typeÀº ¼­·Î ´Ù¸£´Ù(C = LKM1, D=LKM3 Ab)

3) Serologic test: Áø´Ü¿¡ À¯¿ëÇÏ´Ù.

¨ç IgM anti HAV : RF°¡ fase (+)À¯¹ß

¨è HBV

i) HBsAg

µå¹°°Ô HBs Ag levelÀÌ ³Ê¹« ³·Àº °æ¿ì°¡ Àִµ¥ ÀÌ·²¶§ Áø´ÜÀº IgM anti HBc·Î ÇÑ´Ù.

HBsAg titer¿Í severity»çÀÌ¿£ °ü°è°¡ ¾ø´Ù. ¹Ý´ë·Î liver cell damage¿Í ¿ª°ü°è°¡ ÀÖ´Ù.

¿¹> ¸é¿ª¾ïÁ¦È¯ÀÚ¿¡¼­ titer°¡ °¡Àå ³ô´Ù.

CLD¿¡¼­´Â levelÀÌ ³·´Ù(severeº¸´Ù mild CLD¿¡¼­ ´õ ³ô´Ù)

acute fulminant hepatitis¿¡¼± ¾ÆÁÖ ³·´Ù.

=> liver cell damageÁ¤µµ¿Í ÀÓ»ó°æ°ú´Â circulating HBsAgÀÇ ¾çº¸´Ù´Â HBV¿¡ ´ëÇÑ

ȯÀÚÀÇ ¸é¿ª¹ÝÀÀ°ú °ü·ÃÀÖ´Ù.

±×·¯³ª ¸é¿ªÀÌ Á¤»óÀÎ »ç¶÷¿¡¼± HBV replication marker¿Í liver injury»çÀÌ¿¡ ºñ·Ê°ü°è°¡

ÀÖ´Ù.

ii) HBe Ag : relative infectivity marker

iii) IgM anti HBc : high-titer rheumatic factorȯÀÚ¿¡¼­ »ý±æ¼ö ÀÖ´Ù.

iv) Anti-HBs

acute hepatitis B¿¡¼± µå¹°´Ù.

chronic HBV infectionÀÇ 10-20%¿¡¼­ low level anti HBs°¡ Á¸Àç.

ÀÌ Ab´Â common group determinant a¿¡ ´ëÇÑ Ç×ü°¡ ¾Æ´Ï¶ó

heterotypic subtype determinantÀÌ´Ù.

¿¹> HBsAg of subtype ad with anti HBs of subtype y

ÀÌ Ab´Â ÀÓ»óÀû Á߿伺ÀÌ ¾ø´Ù.

* Tab 295-3 Hepatitis B infectionÀÇ serologic patterns

v) HBV DNA : HBeAg°ú ÇÔ²² HBV replicationÀÇ indicator

HBe Agº¸´Ù ´õ ¹Î°¨Çϰí Á¤·®Àû.

Hybridization assay : 105-106 virions/mL sensitivity

ÇöÀç insensitive hybridization assay¿¡¼­ amplification assay(PCR : 100-1000

virions/mL)·Î ¿Å°ÜÁö°í ÀÖ´Â Ãß¼¼.

* HBV replication marker(HBV DNA)

: antiviral chemotherapy(interferon or lamivudine)¹Þ´Â ȯÀÚ¿¡¼­ HBV replication°æ°ú

¸¦ ÃßÀûÇϴµ¥ À¯¿ëÇÏ´Ù.

immunocompetent person¿¡¼± HBV replication level(=HBV DNA level)°ú liver injury

Á¤µµ°¡ ´ëü·Î ºñ·ÊÇÑ´Ù.

¨é HCV

i) anti-HCV

acute hepatitis CÀÇ 5-10%¿¡¼­ detect¡¿, ȸº¹ÈÄ¿£ undetectable

chronic hepatitis C¿¡¼± 95%À̻󿡼­ detect

volunteer blood donor³ª rheumtic factor(+)ÀÎ »ç¶÷°ú °°ÀÌ infection°¡´É¼ºÀÌ ³·Àº

»ç¶÷¿¡¼­ anti-HCV´Â ƯÀ̵µ°¡ ³·´Ù.

-> Ãß°¡ÀûÀÎ RIBA½ÃÇà. ±×·± RIBA´Â blood donor¿¡¼­ anti-HCV reactivity¸¦ È®Á¤Áþ±â

À§ÇØ routineÀ¸·Î »ç¿ëÇÏÁö¸¸ ÀÓ»ó¿¡¼­´Â HCV RNA°¡ RIBA¸¦ ´ë½ÅÇÑ´Ù.

ii) HCV RNA

HCV°¨¿°À» Áø´ÜÇϴµ¥ °¡Àå ¹Î°¨ÇÑ °Ë»çÀ̸ç Hepatitis C¸¦ Áø´ÜÇÏ´Â

" gold standard"ÀÌ´Ù.

AST/ALT°¡ ±Þ°ÝÈ÷ »ó½ÂÇϱâ Àü¿¡µµ °ËÃâÇÒ¼ö ÀÖÀ¸¸ç, anti-HCV°¡ ÃâÇöÇϱâ Àü¿¡µµ

°ËÃâ°¡´ÉÇÏ´Ù.

HCV RNA¸¦ °ËÃâÇϱâ À§ÇØ 2°¡Áö À¯¿ëÇÑ amplification techniqueÀÌ ÇÊ¿äÇѵ¥

¤¡. branched-chain complementary DNA(bDNA) assay

¤¤. PCR assay

µÑ´Ù Á¤·®ÀûÀ¸·Î »ç¿ëÇÒ¼ö ÀÖ°í »ó´ëÀûÀÎ "viral load"ÃøÁ¤À» À§ÇØ »ç¿ëÇÒ¼ö ÀÖ´Ù.

PCR(102-103 virions/mL)ÀÌ bDNA(2¡¿105)º¸´Ù ´õ sensitiveÇÏ´Ù.

viral load°¡ disease severity³ª prognosis marker·Î¼­´Â À¯¿ëÇÏÁö ¾ÊÁö¸¸

antiviral tx¿¡ ´ëÇÑ ¹ÝÀÀÀ» ¿¹ÃøÇϴµ¥ µµ¿òÀÌ µÈ´Ù.

¸¶Âù°¡Áö·Î HCV genotypeµµ °°Àº ÀǹÌÀÌ´Ù.

4) Liver biopsy

chronic hepatitis°¡ ÀÇ½ÉµÉ ¶§ ¸»°í´Â °ÅÀÇ ÇÊ¿äÄ¡ ¾Ê´Ù.

<¿ä¾à>

¨ç Acute heaptitis¸¦ Áø´ÜÇϱâ À§ÇÑ 4 serologic tests(Tab 295-4)

: HBsAg, IgM anti-HAV, IgM anti HBc, anti HCV

¨è Chronic hepatitis¸¦ Áø´ÜÇϱâ À§ÇÑ initial serologic test

: HBsAg, anti HCV

-> HBsAg(+)À̸é HBeAg, anti HBe, HBV DNAÁ¶»ç

¨é Hepatitis BȯÀÚ¿¡¼­ anti HDV test°¡ À¯¿ëÇÑ °æ¿ì

i) severe & fulminant disease

ii) severe chronic disease

iii) acute hepatitis-like exacerbation

iv) frequent percutaneous exposure

v) HDV infectionÀ¯ÇàÁö¿ª¿¡ »ç´Â »ç¶÷

6. Prognosis

Hepatitis A : ¿ÏÀüÈ÷ ȸº¹

Hepatitis B : 95-99%¿¡¼­ ¿ÏÀüÈ÷ ȸº¹µÇÁö¸¸

advanced age, underlying medical disorder°¡ ÀÖ´Â °æ¿ì¿£ °æ°ú°¡ ¿À·¡°¡¸ç

severe hepatitis¸¦ °æÇèÇÑ´Ù.

* Poor Px

initial ascites(+), peripheral edema(+), hepatic encephalopathy sx(+)

PT¡è, Alb¡é, Glu¡é, Bil¡è¡è ==> severe hepatocellular disease¸¦ ÀǹÌ.

* fatality´Â A,B µÑ´Ù 0.1%Á¤µµ·Î ³·Áö¸¸ »ó±â¿Í °°ÀÌ advanced age, underlying disorder

°¡ ÀÖÀ»¶§´Â Áõ°¡ÇÑ´Ù.

ÀÔ¿øÈ¯ÀÚ¿¡¼± 1%Á¤µµ

Hepatitis C(posttransfusion) less severe

Hepatitis E(waterborne outbreak in Asia, India)

fatality 1-2%(Àӽſ©¼º¿¡¼± 10-20%±îÁö)

Hepatitis D : simultaneous B + D°¡ B´Üµ¶º¸´Ù ´õ ³ôÁö´Â ¾Ê´Ù.

±×·¯³ª HDV superinfectionÀÇ °æ¿ì¿¡ fulminant hepatitisÀÇ °¡´É¼ºÀÌ Áõ°¡ÇÑ´Ù.

HDVÀÇ case-fatality rate°¡ Á¤È®È÷ ¾Ë·ÁÁöÁø ¾Ê¾ÒÁö¸¸ high hepatitis B carrier rate¸¦

°¡Áö´Â Áý´Ü¿¡¼­ severe HDV superinfection outbreakÈÄ mortality°¡ 20%¸¦ ³Ñ¾ú´Ù°í

±â·ÏµÇ¾î ÀÖ´Ù.

7. Complications & Sequalae

1) Relapsing hepatitis

ÀϺÎȯÀÚ°¡ ±Þ¼º°£¿°¿¡¼­ ȸº¹µÈÈÄ ¼öÁÖ-¼ö°³¿ùÈÄ °£¿°ÀÌ Àç¹ßÇÑ´Ù.

À̶§ Áõ»óÀÌ ´Ù½Ã »ý±â°í AST/ALT°¡ »ó½ÂÇÏ¸ç °¡²û Ȳ´ÞÀÌ »ý±â±âµµ ÇÑ´Ù.

´ëº¯¿¡¼­ HAV°¡ ¹èÃâµÈ´Ù.

2) Cholestatic hepatitis

unusual variant of acute hepatitis A

cholestatic jaundice, pruritus»ý±è.

3) Liver function abnormalityÁö¼Ó

µå¹°°Ô ¼ö°³¿ùÀÌ»ó Áö¼ÓÇÏ´Â °æ¿ì°¡ ÀÖ´Ù. ±×·¯³ª 1³âÀÌ»ó Áö¼ÓÇÏ´õ¶óµµ hepatitis A´Â

ÀÚ¿¬È¸º¹µÇ¸ç ¸¸¼º°£ÁúȯÀ¸·Î ÀÌÇàÇÏÁö ¾Ê´Â´Ù.

4) serum sickness-like syndrome

acute hepatitis BÀÇ prodromal phase¶§ arthritis, rash, angioedema, µå¹°°Ô´Â

hematuria, proteinuria¹ß»ý(5-10%)

Ȳ´ÞÀÌ ¹ß»ýÇϱâ Àü¿¡ »ý±â¸ç rheumatologic disease·Î ¿ÀÀÎÇϱ⠽±´Ù.

Áø´ÜÀº AST/ALT»ó½Â°ú HBsAg(+)·Î ÇÒ¼ö ÀÖ´Ù.

5) EMC(Essential Mixed Cryoglobulinemia)

Hepatitis C¿¡¼­ ÇÕº´µÇ´Â immune-complex disease

cf. Hepatitis C : cutaneous disorders(prophyria cutanea tarda, lichen planus)¿Í Àß

µ¿¹ÝµÇ´Âµ¥ ±âÀüÀº Àß ¸ð¸¥´Ù.

6) Fulminant hepatitis(massive hepatic necrosis)

hepatitis B, D, E¿¡¼­ ÁÖ·Î »ý±â°í A¿¡¼± µå¹°´Ù.

A¿¡¼± older adults, underlying CLDÀÖ´Â »ç¶÷¿¡°Ô¼­ ÁÖ·Î »ý±ä´Ù.

50%ÀÌ»óÀÌ HBV(¡¾HDV)À̸ç HCV¿¡¼± µå¹°´Ù.

HEV¿¡¼­´Â 1-2%¿¡¼­ »ý±ä´Ù(pregnant woman = 20%)

*Áõ»ó : hepatic failure & encephalopathy

cerebral edema, brainstem compression, GI bleeding, sepsis, resp. failure,

cardiovascular collapse, renal failure

mortality = 80%

»ýÁ¸ÇÑ °æ¿ì complete biochemical & histological recovery¸¦ º¸ÀδÙ.

7) Chronic hepatitis

¨ç HBV : 10%

ÀÌÁß ¹ÝÀº ¼ö³âµ¿¾È HBsAg cleared, ´Ù¸¥ ¹ÝÀº Áö¼ÓÀûÀ¸·Î HBsAg(+)

* HBV infectionÈÄ HBsAg carrier·Î ³²À» À§ÇèÀÌ Áõ°¡ÇÏ´Â °æ¿ì

i) neonate

ii) Down's syndrome

iii) hemodialyzed pt

iv) immunosuppressed pt(HIV Æ÷ÇÔ)

¸¸¼º °£¿°Àº ±Þ¼º Áúȯ¾øÀÌ »ý±â´Â °æ¿ì°¡ ´õ ÈçÇÏ´Ù.

±Þ¼º°£¿°ÀÌ ¸¸¼ºÈ­ÇÏ´Â °ÍÀ» ½Ã»çÇÏ´Â ÀÓ»óÀû ¹× °Ë»ç¼Ò°ßÀº

i) sx resolution¡¿ (anorexia, wt loss, fatigue, hepatomegaly)

ii) bridging or multilobular hepatic necrosis(Bx»ó)

iii) 6-12°³¿ù³» AST/ALT, Bil, globulinÀÌ Á¤»óÈ­¡¿

iv) HBeAgÀÌ 3°³¿ùÀÌ»ó Áö¼ÓÇϰųª HBsAgÀÌ 6°³¿ùÀÌ»ó Áö¼ÓÇÏ´Â °æ¿ì

¨è HDV

acute hepatitis B chronicity¸¦ Áõ°¡½ÃŰÁö ¾ÊÀ¸³ª severity´Â Áõ°¡½ÃŲ´Ù.

superinfectionµÇ¸é asymptomatic, mild chronic hepatitis

-> severe, progressive chronic hepatitis, cirrhosis·Î ÁøÇà½Ãų¼ö ÀÖ´Ù.

¶ÇÇÑ chronic hepatitis B°æ°ú¸¦ °¡¼ÓÈ­½Ã۸ç, fulminant hepatitis¸¦ À¯¹ßÇÒ¼öµµ ÀÖ´Ù.

¨é HCV : remaining chronically infected approach(85-90%)

cirrhosis = 20%(10-20³â³»)

mortality, mortality : 20³â³»¿£ limited

* Progression¿¡ ¿µÇâÀ» ¹ÌÄ¡´Â ÀÎÀÚ

i) genotype

ii) °¨¿°µÈ ³ªÀÌ

iii) duration

iv) immunosuppression

v) coexisting excessive alcohol use

vi) other hepatitis virus infection

8) Rare complication

pancreatitis, myocarditis, aypical pneumonia, aplastic anemia

transverse myelitis, peripheral neuropathy

9) HCC : HBsAg carrier - infancy, early childhood¶§ °¨¿°½Ã À§ÇèÀÌ Áõ°¡ÇÑ´Ù.

8. °¨º°Áø´Ü

1) Viral disease : infectious mononucleosis, CMV, herpes simplex, coxsackievirus,

toxoplasmosis

-> AST/ALT¡è(less commonly bilirubin)

HBsAg, anti HBc, IgM anti HAV, anti HCV°¡ À½¼ºÀ̸é heterophil Ab & À̵é virus¿¡ ´ëÇÑ

serologic test°¡ µµ¿òÀÌ µÈ´Ù.

2) Infection : Leptospira, candida, Brucella, Mycobacteria, Pneumocystis

3) Drug : Hx°¡ Áß¿ä

4) Alcoholic hepatitis : liver Bx»ó fatty infiltration, neutrophilic inflammatory reaction, "

alcoholic hyaline"ÀÌ Áø´Ü¿¡ µµ¿òÀÌ µÈ´Ù.

5) obstructive jaundice d/t CBD stone or pancreatic ca

6) Rt heart failure with passive hepatic congestion

or hypoperfusion syndrome(shock, severe hypotension, servere LV failure)

7) Vascular disorder(hepatic vein occlusion, venoocclusive disorder)

8) acute fatty liver of pregnancy, cholestasis of pregnancy, eclampsia, HELLP syndrome

-À̵é ÁúȯÀº ÀÓ½ÅÁß ¹ß»ýÇÏ´Â viral hepatitis¿Í È¥µ¿µÈ´Ù.

9) metastatic liver cancer

10) genetic or metabolic liver disorder(Wilson's disease, ¥á1-AT deficiency)

9. Ä¡·á

1) Acute attack

¨ç acute hepatitis B

99%¿¡¼­ ȸº¹µÇ¹Ç·Î Ä¡·á°¡ ÇÊ¿ä¾ø´Ù.

¨è acute hepatitis C

ȸº¹ÀÌ µå¹°°í 85-90%¿¡¼­ chronic hepatitis·Î ÁøÇàÇϹǷÎ

IFN-¥á(300¸¸ U SC ¡¿ 3ȸ/ÁÖ) Ä¡·á¸¦ Çϸé chronicity°¡ °¨¼ÒÇϰí sustained response´Â

40%Á¤µµ µÈ´Ù.

Ä¡·á±â°£°ú nucleoside analogue RibavirinÃß°¡¿©ºÎ¸¦ °áÁ¤ÇØ¾ß ÇÏÁö¸¸ ´ëºÎºÐ chronic

hepatitis C recommendationÀ» µû¸¥´Ù.

¨é Supportive Care

i) ´ëºÎºÐ ÀÔ¿øÄ¡·áÇÒ Çʿ䰡 ¾øÀ¸¸ç physical activity¸¦ Á¦ÇÑÇÒ Çʿ䰡 ¾øÀ¸³ª bed rest¸¦

Çϸé ȯÀÚ ±âºÐÀÌ ÁÁ´Ù.

ii) high calorie diet

iii) liver·Î ´ë»çµÇ´Â ¾à¹°Àº ÇÇÇÒ °Í

iv) severe pruritus - bile salt-sequestering resin(cholestyramine) : Áõ»ó¿ÏÈ­

v) Glucocorticoid - no value, ¿ÀÈ÷·Á ÇØ·Ó´Ù.

vi) °Ý¸®ÇÒ ÇÊ¿ä´Â ¾ø´Ù.

¿¹¿Ü> fecal incontinence¸¦ º¸ÀÌ´Â hepatitis A, E

¨ê Fulminant hepatitis

i) fluid balance, circulation & respiration support, bleeding control, hypoglycemia

correction

ii) complication Tx(comatous status¿Í °°Àº)

protein restriction, oral lactulose or neomycin

iii) Glucocorticoid - ineffective

iv) exchange transfusion, plamapheresis, human cross-circulation,

porcine liver cross-perfusion, hemoperfusion - survivalÇâ»ó¡¿

v) meticulous intensive care - survivalÇâ»ó

vi) orthotopic liver transplantation - excellent result

10. Prophylaxis

1) Hepatitis A

passive immunization(IG), active immunization(killed vaccine)ÀÌ À¯¿ëÇÏ°Ô »ç¿ëµÈ´Ù.

¨ç Immune globulin(IG) - plasma-derived IGÀ¸·Î ¾ÈÀüÇÏ´Ù.

- preexposure or early incubation period : IG is effective

( infectionÀ» ¾ø¾Ù¼ö´Â ¾øÀ¸³ª ºÒÇö¼º °¨¿°À¸·Î ¸¸µé ¼ö ÀÖ´Ù.)

- postexposure prophylaxis

AÇü °£¿°È¯ÀÚ¿Í Á¢ÃËÇÑ °æ¿ì(household, institutional) °¡´ÉÇÑ »¡¸® IG 0.02 mL/kg¸¦ Åõ¿©

ÇÑ´Ù. ±×·¯³ª 2ÁÖÈıîÁö Åõ¿©Çصµ È¿°ú°¡ ÀÖ´Ù.

i) ÀÏ»óÀûÀÎ Á¢ÃË(»ç¹«½Ç, °øÀå, Çб³, º´¿ø), ³ëÀÎ, ¸é¿ªÀÌ ÀÖ´Â »ç¶÷, anti-HAV(+)

: prophylaxis°¡ ÇÊ¿ä¾ø´Ù.

ii) Ź¾Æ¼Ò¿¡ ÀÖ´Â ¾ÆÀ̳ª ±Ù¹«ÀÚ°¡ AÇü °£¿°¿¡ °É¸®¸é immunoprophylaxisÇØ¾ß ÇÏ¸ç ¾ÆÀÌ

°¡Á·µéµµ ÇØ¾ß ÇÑ´Ù.

iii) À¯ÇàÁö¿ª, ¹Ì°³¹ß±¹, Á¤½Ä¿©Çà·Î°¡ ¾Æ´Ñ °÷À¸·Î ¿©ÇàÇÏ´Â »ç¶÷Àº IG prophylaxis°¡

ÇÊ¿äÇÏ´Ù.

3°³¿ù¹Ì¸¸ ¿©Çà : 0.02 mL/kg

±× ÀÌ»ó : 0.06 mL/kg q 4-6 Mo Ãß°¡

¨è Formalin-inactivated vaccine

Àû¾îµµ 2»ìÀ̻󿡼­ »ç¿ëÇϵµ·Ï ÇÑ´Ù.

Á¢Á¾ÈÄ 4ÁÖÈÄ¿¡ ¹æ¾îÈ¿°ú°¡ ³ªÅ¸³ª¹Ç·Î 4ÁÖ³» Æø·Î°¡ ¿¹»óµÇ¸é(¿©Çà µî) preexposure

immunoprophylaxis°¡ ´õ ³´´Ù.

* ¿©ÇàÀÌ ´õ ±æ¾îÁø´Ù¸é?

IG(0.02 mL/kg)¸¦ ´Ù¸¥ ÆÈ¿¡ ±ÙÁÖ

* long-standing protection(20³âÀÌ»ó)À» °¡Áö¹Ç·Î À¯ÇàÁö¿ª¿¡ ÀÚÁÖ ¿©ÇàÇÏ´Â »ç¶÷Àº ²À

vaccinationÇϵµ·Ï ÇÑ´Ù.

* ´Ù¸¥ vaccination´ë»ó±º

i) military personnel

ii) hepatitis AÀÇ cyclic outbreaksÁö¿ª(Alaska natives)

iii) Ź¾Æ¼Ò ±Ù¹«ÀÚ(day-care center employee)

iv) primate handler(¿µÀå·ù »çÀ°»ç)

v) hepatitis A, fecal specimen¿¡ Æø·ÎµÇ´Â °Ë»ç½Ç Á¾»çÀÚ

vi) hepatitis Aºóµµ°¡ ³ôÀº°÷ÀÇ ¾ÆÀÌ

vii) chronic liver diseaseȯÀÚ(chronic hepatitis C)

viii) homosexual

ix) injection drug user

x) clotting factor concentrateÀÚÁÖ ¸Â´Â »ç¶÷

* ¸ðµç injectionÀº IM

2) Hepatitis B

(1) Preexposure prophylaxis

frequent exposureµÇ´Â »ç¶÷À» ´ë»óÀ¸·Î vaccination½ÃÇà

: health workers exposed to blood, hemodialysis pt

custodial institutionÀÇ resident & staff

injection drug user, long-term correctional facilities inmates,

hemosexual men, hemophilia, HBsAg ptÀÇ sexual contact

18¼¼ ¹Ì¸¸ unvaccinated children, Alaskan natives childrenµîµî..

3ȸ IM(Deltoid), gluteal injectionÀº ÇÇÇÑ´Ù(¡ñÇ×ü»ý¼ºÈ¿°ú°¡ ¶³¾îÁö¹Ç·Î)

ÀӽŽÿ¡µµ ¶È°°ÀÌ vaccinationÇÏ¸é µÈ´Ù.

¹Ì±¹°ú °°ÀÌ ³·Àº À¯º´Áö¿ª¿¡¼­ high-risk group¿¡ ´ëÇØ¼­¸¸ vaccinationÇÏ´ø Àü·«Àº

È¿°úÀûÀÌÁö ¸øÇß´Ù.

i) vaccineµµÀÔÀÌÈÄ hepatitis B¹ß»ýÀÌ Áõ°¡Çϰí ÀÖ´Ù.

ii) high risk groupȯÀÚÁß 10%¹Ì¸¸¸¸ÀÌ vaccinationÇϰí ÀÖ´Ù.

iii) sporadic acute hepatitis BȯÀÚÀÇ 30%°¡ high-risk group category¿¡ ¼ÓÇÏÁö ¾Ê´Â

ȯÀÚ¿´´Ù.

=> ±×·¯¹Ç·Î ¾ÆÀ̶§ universal hepatitis B vaccinationÀÌ ÃßõµÈ´Ù.

* 2 available recombinant hepatitis B vaccine

HBsAg 10ugÇÔÀ¯ÇÑ Recombivax-HB

20 ug(Engerix-B)

(2) Postexposure prophylaxis

HBIG + HB vaccineÀÌ ÃßõµÈ´Ù. (µ¿½Ã Á¢Á¾½Ã ´Ù¸¥ ÆÈ¿¡ ±ÙÁÖ)

i) perinatal exposure

HBIG 0.5 mL IM(Ãâ»ýÁï½Ã) + HB vaccine 3ȸ(12½Ã°£³»)

ii) ÁÖ»ç¹Ù´Ã ¶Ç´Â transmucosal exposure

HBIG 0.06 mL/kg IM(Áï½Ã) + HB vaccine(1ÁÖ³»)

iii) sexual contact

HBIG 0.06 mL/kg(2ÁÖ³») + HB vaccine

immunocompetent vaccinesÀÇ 80-90%°¡ ÃÖ¼Ò 5³â°£ protectiveÇϰí 10³âµ¿¾ÈÀº 60-80%

¿¡¼­ protectiveÇÏ´Ù. ±× ÀÌÈÄ¿¡ anti HBs°¡ ¹ß°ßµÇÁö ¾Ê´õ¶óµµ º¸È£È¿°ú´Â Áö¼ÓµÈ´Ù. µû¶ó¼­

ÇöÀç booster´Â routineÀ¸·Î ÃßõµÇÁö´Â¾Ê´Â´Ù.

* Booster¸¦ ÃßõÇÏ´Â °æ¿ì

i) immunosuppressed person

ii) Áö¼ÓÀûÀ¸·Î HBsAg(+) inoculationÀ§ÇèÀÌ ÀÖ´Â °æ¿ì

iii) hemodialysis pt => anti HBs ¸Å³â check

=> 10 mIU/mLÀÌÇϰ¡ µÇ¸é boosterÇÑ´Ù.

3) Hepatitis C

¨ç IG - ineffective

¡Å perinatal, needle stick or sexual exposure¿¡ ´ëÇØ postexposure prophylaxis´Â Ãßõ

µÇÁö ¾Ê´Â´Ù.

¨è transfusion-associated hepatitis CÀÇ ¿¹¹æ

commercial blood donor¸¦ Á¦¿ÜÇϰí risk groupÀÇ Ç÷¾×À» Á¦¿ÜÇÑ´Ù.

anti HIV screening test, anti-HCV°Ë»ç¸¦ ½ÃÇàÇÑ´Ù.

¨é monogamous sexual partner : ÀüÆÄÀ§ÇèÀÌ ¾ÆÁÖ µå¹°´Ù. ÁÖÀÇÇÒ ÇÊ¿ä¾ø´Ù.

multiple sexual partner, STD - barrier precaution(latex comdom)ÀÌ ÃßõµÈ´Ù.

¨ê perinatal, breast feeding : Ưº°È÷ ÁÖÀÇÇÒ ÇÊ¿ä¾ø´Ù.