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HEPATITIS

Dr. Leonardo B Dairi SpPD KGEH

Many causes of hepatitis


Infectious Bacterial Leptospirosis Syphillis Tuberculosis Toxoplasmosis Amebiasis

Parasitic

Viral

Epstein Barr Herpes Simplex Varicella Zoster Coxsackievirus Rubella Yellow Fever
Alcohol Drugs

Noninfectious

Viral agents that primarily or exclusively infect the liver


Hepatitis A virus Hepatitis B virus Hepatitis C virus Infectious hepatitis Serum hepatitis Parenterally transmitted

Hepatitis E virus
Hepatitis D virus Hepatitis G virus

Enterically transmitted
Coinfection with HBV Parenterally transmitted

Viral Hepatitis - Historical Perspective


Infectious

A
NANB

Enterically E transmitted

Viral hepatitis Serum

B D
F, G, ? other

Parenterally C transmitted

Viral Hepatitis - Overview


Type of Hepatitis

A
Source of virus Route of transmission Chronic infection feces

E
feces

blood/ blood/ blood/ blood-derivedblood-derived blood-derived body fluids body fluids body fluids

fecal-oral no

percutaneouspercutaneous percutaneous fecal-oral permucosal permucosal permucosal yes yes yes no

Prevention

pre/postpre/post- blood donor pre/post- ensure safe exposure exposure screening; exposure drinking immunization immunization risk behavior immunization; water modification risk behavior modification

Initial laboratory evaluation of jaundiced patient


TEST PERFORMED Urine bilirubin MEASUREMENT Conjugated bilirubin

Serum bilirubin
Alanine aminotransferase (ALT) Aspartate aminotransferase (AST) Alkaline phosphatase Prothrombin time, partial thromboplastin time, platelet count, bleeding Blood count with blood smear exam

Conjugated and unconjugated bilirubin


Hepatocellular damage Hepatocellular damage Intrahepatic or extrahepatic obstruction Clotting mechanism

Red blood cell morphology, parasites, atypical lymphocytes

HEPATITIS A

RNA Picornavirus
Single serotype worldwide Acute disease and asymptomatic infection

No chronic infection
Protective antibodies develop in response to infection - confers lifelong immunity

ACUTE HEPATITIS A CASE DEFINITION FOR SURVEILLANCE


Clinical criteria

An acute :
discrete onset of symptoms (e.g. fatigue, abdominal pain, loss of appetite, nausea, vomiting), and jaundice or elevated serum aminotransferase levels
Laboratory criteria

IgM antibody to hepatitis A virus (anti-HAV) positive

HEPATITIS A - CLINICAL FEATURES


Jaundice by

age group:
Rare complications:

<6 yrs 6-14 yrs >14 yrs

<10% 40%-50% 70%-80%

Fulminant hepatitis Cholestatic hepatitis Relapsing hepatitis Average 30 days Range 15-50 days

Incubation period:

Chronic sequelae:

None

EVENTS IN HEPATITIS A VIRUS INFECTION


Clinical illness

Infection

ALT IgM IgG

Response

Viremia

HAV in stool

10

11

12

13

Week

CONCENTRATION OF HEPATITIS A VIRUS IN VARIOUS BODY FLUIDS


Feces

Body Fluids

Serum Saliva

Urine

100
Source:

102

104

106

108

1010

Infectious Doses per mL


Viral Hepatitis and Liver Disease 1984;9-22 J Infect Dis 1989;160:887-890

GLOBAL PATTERNS OF HEPATITIS A VIRUS TRANSMISSION


Endemiciy Hi Moderate Rate Diseas es Low to high High Peak Age of Infection Early childhood Late childhood/ young adults Young adults Adult Transmission Patterns Person to person; outbreaks uncommon Person to person; food and waterborne outbreaks Person to person; food and waterborne outbreaks Travelers; outbreaks uncommon

Low Very low

Low

Very low

GEOGRAPHIC DISTRIBUTION OF HEPATITIS A VIRUS INFECTION

HEPATITIS A VIRUS TRANSMISSION


Close personal contact (e.g., household contact, sex contact, child day-care centers) Contaminated food, water (e.g., infected food handlers) Blood exposure (rare) (e.g., injection drug use, rarely by transfusion)

PREVENTING HEPATITIS A Hygiene (e.g., hand washing) Sanitation (e.g., clean water sources) Hepatitis A vaccine (pre-exposure) Immune globulin (pre- and post-exposure)

HEPATITIS A VACCINES

Highly immunogenic 97%-100% of children, adolescents, and adults have

protective levels of antibody within 1 month of receiving first dose; essentially 100% have protective levels after second dose
Highly efficacious In published studies, 94%-100% of children protected

against clinical hepatitis A after equivalent of one dose

HEPATITIS A VACCINE EFFICACY STUDIES


Vaccine Site/ Age Group N Vaccine Efficacy (95 % Cl)

HAVRIX (GSK) 2 doses 360 EL.U. VAQTA (Merck) 1 dose 25 units

Thailand 1-16 yrs

38,157

94% (79%-99%)

New York
2-16 yrs

1,037

100%
(85%-100%)

JAMA 1994;271:1363-4; N Engl J Med 1992;327:453-7

DURATION OF PROTECTION AFTER HEPATITIS A VACCINATION


Persistence of antibody

At least 5-8 years among adults and children No cases in vaccinated children at 5-6 years of follow-up

Efficacy

Mathematical models of antibody decline suggest protective antibody levels persist for at least 20 years Other mechanisms, such as cellular memory, may contribute

COMBINED HEPATITIS A HEPATITIS B VACCINE


Approved by the FDA in United States for persons >18 years old Contains 720 EL.U. hepatitis A antigen and 20 g. HBsAg Vaccination schedule: 0,1,6 months Immunogenicity similar to single-antigen vaccines given separately Can be used in persons > 18 years old who need vaccination against both hepatitis A and B

Formulation for children available in many other countries

HEPATITIS A PREVENTION IMMUNE GLOBULIN


Pre-exposure

travelers to intermediate and high HAV-endemic regions

Post-exposure (within 14 days)


Routine household and other intimate contacts Selected situations institutions (e.g., day-care centers) common source exposure (e.g., food prepared by infected food handler)

SAFETY OF HEPATITIS A VACCINE


Most common side effects Soreness/tenderness at injection site - 50% Headache - 15% Malaise - 7% No severe adverse reactions attributed to vaccine Safety in pregnancy not determined risk likely low Contraindications - severe adverse reaction to previous dose or allergy to a vaccine component No special precautions for immunocompromised persons

HEPATITIS B

HBV

1/3 worlds population infected 350 million chronic infected.

HBV

Acute / fulminant Inactive carrier state Chronic Hepatits Liver cirrhosis Hepatocellular Carcinoma.

HBV A Global Health Problem


HBsAg Positif, % Taiwan Vietnam China Africa Philippines Thailand Japan Indonesia 10.0-13.8 5.7-10.0 5.3-12.0 5.0-19.0 5.0-16.0 4.6-8.0 4.4-13.0 4.0 2.6-5.1 2.4-4.7 1.4-8.0

Prevalensi HBsAg
High ( 8%) Intermediate (2% to 8%) Low (< 2%) Mast EE, et al. MMWR Recomm Rep. 2006;55:1-33. Custer B, et al. J Clin Gastroenterol. 2004;38(10 suppl):S158-S168.

South Korea India Russia

US

0.2-0.5

8 genotypes (A-H) :

and

More advanced liver disease Lower response rate to interferon Greater risk of HCC development.

HBV nomenclature
HBV: hepatitis B virus HBsAg: hepatitis B virus surface antigen HBcAg: hepatitis B virus core antigen

Hepatitis B Virus (HBV)


4 overlapping open reading frames
polymerase
EcoRI 3221, 1

Domain Reverse transcriptase/ DNA polymerase mengalami overlap dengan gen permukaan Ditemukan dalam darah dan cairan tubuh cccDNA

(+) (-)
1622

MMWR. 2003;52:1-33. Ott MJ and Aruda M. J Pediatr Health Care. 1999;13:211-216. Ribeiro RM, et al. Microbes and Infection. 2002;4:829-835.

NATURAL COURSE OF CHRONIC HBV INFECTIONS


The HBV three detectable antigens : 1. HBsAg Surface antigen 2. HbcAg Core antigen 3. HBeAg e antigen Chronic infection HBsag persistence for more than 6 months HBsAg non infectious HBcAg represents the nucleocapsid of the virus presence indicates infectivity, found in the liver not in the serum. HBeAg found in the serum a. Viral replication b. Infectivity

Modes of Transmission
Transfusion (blood, blood products) Fluids (blood, semen) Tattoos; Body piercing Mother to infant

Hepatitis B

Shared needles & syringes

Organs & tissue transplantation

Child to child

HBV CLINICAL SYNDROMES


ACUTE INFECTION
Incubation phase: long (6weeks-6month) Prodromal phase: insidious
Flu-like: malaise, fatigue, anorexia, nausea, abdominal discomfort, chills

Icteric phase: liver damage: jaundice, dark urine, pale stools Recovery: decline in fever; renewed appetite

Fase Infeksi Kronik Hepatitis B


Increasing age HBeAg+/antiHBe HBeAg - / anti-HBe +

HBV DNA ALT


FASE IMMUNE TOLERANCE
FASE IMMUNE CLEARANCE

FASE INACTIVE CARRIER HBsAg

FASE REACTIVATION

Monitor HBV DNA and ALT/ 3-6 month No to treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

Fase Infeksi Kronik Hepatitis B


Increasing age HBeAg+/antiHBe HBeAg - / anti-HBe +

HBV DNA ALT


FASE IMMUNE TOLERANCE
FASE IMMUNE CLEARANCE

FASE INACTIVE CARRIER HBsAg

FASE REACTIVATION

Rekomendation to treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

Fase Infeksi Kronik Hepatitis B


Increasing age HBeAg+/antiHBe HBeAg - / anti-HBe +

HBV DNA ALT


FASE IMMUNE TOLERANCE
FASE IMMUNE CLEARANCE

FASE INACTIVE CARRIER HBsAg

FASE REACTIVATION

Monitor HBV DNA and ALT/3-6 month No to treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

Fase Infeksi Kronik Hepatitis B


Increasing age HBeAg+/antiHBe HBeAg - / anti-HBe +

HBV DNA ALT


FASE IMMUNE TOLERANCE
FASE IMMUNE CLEARANCE

FASE INACTIVE CARRIER HBsAg

FASE REACTIVATION

Rekomendation to treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

39

HBV DIAGNOSIS
CLINICALL LABORATORY Liver enzymes Serology HBeAg, HBcAg, virus: active infection Anti-HBc IgM: acute active infection Anti-HBe IgG: acute infection

Healthy Liver

Hepatic Fibrosis

Cirrhosis

Liver Cancer

Healthy Liver

Hepatic Fibrosis

Cirrhosis

Liver Cancer

HBV Complications
Chronic HBsAg antigenemia

Chronic persistent hepatitis (CPH)


Chronic active hepatitis (CAH)

Chronic lobular hepatitis (CLH)


Liver cirrhosis

Hepatocellular carcinoma

MANAGEMENT HBV: PREVENTION OF LIVER CIRRHOSIS,HEPATOMA AND MORTALITY

Supretion replikation of HBV

MANAGEMENT
--1. Evaluation of the disease 2. Non-specific/specific therapy 3. Monitoring and surveillance The diagnosis of CHB infection HBsAg at least 6 month HBeAg and Anti-HBe Viral replication and thus infectivity. ALT/AST measured inflammation Liver Biopsy is more accurate USG/Fibro Scan parenchymal impairment, fibrosis Early cirrhosis ussually not detected by ultrasound

MANAGEMENT
Non-spesific advice General advice
CHB infection potentially infectious should not share toothbrushes or shaving equipment Household contacts and sexual partners should have their hepatitis serology determined and should be immunized if found negative for HBsAg, anti-HBs and anti HBc When a woman becomes pregnant inform her gynecologist about her HBV status appropriate steps can be taken to immunize her baby at birth A Baby born to HBeAg-positive mother should be given hepatitis B immune-globulin at the same time

MANAGEMENT
Diet

Nutritious diet to maintain normal body weight May be needed protein, salt and water restriction
Exercise Subjects with asymptomatic infection should continue their regular form of exercise With cirrhosis should avoid strenuous jogging and heavy weight lifting

MANAGEMENT
Alcohol and Drugs Should be avoided Potentially hepatotoxic agents or regular alcohol intake, steroids and immunosuppressive agents In Endemic countries patients need steroids or immunosuppressive drugs,HBV status checked to prevent HBV flares.

Suggested management of chronic HBV infection

54

Phases of Chronic HBV Infection: Candidates for Therapy


Phases of Chronic HBV Infection Immune Tolerance HBV DNA, IU/mL 105 - 1010 Immune Clearance/ HBeAg-Positive CHB 104 - 1010 Nonreplicative (Inactive Carrier) < 104 Reactivation/ HBeAg-Negative CHB 103 - 108

HBeAg
ALT Other

HBeAg+
Normal --

HBeAg+
High or fluctuating Active inflammation on liver biopsy Yes

HBeAgNormal HBsAg may become undetectable No

HBeAgHigh or fluctuating Active inflammation on liver biopsy Yes

Candidates for therapy?

No

Yim HJ, et al. Hepatology. 2006;43:S173-S181.

Treatment of Chronic Hepatitis B


Drugs for Chronic HBV inf
1. 2. 3. 4. 5. 6. 7. 8. Interferon Alfa 2b ( 1992) Peginterferon Alfa 2a ( 5/2005 ) Lamivudin ( 1998 ) Adifovir dipivoxil ( 2002 ) Entecavir ( 3/ 2005 ) Tenofovir Telbivudine ( 2/2007) Emtricitabine

Pemberian terapi imunomodulator atau nucleoside analog b ergantung kepada : 1. Genotipe HBV 2. Kadar ALT 3. Kadar serum HBV DNA 4. Sirosis kompensasi atau dekompensasi 5. Resistensi Obat 6. Cost effective

Rekomendation treatment patient with HBeAg (+) /(APASL 2008)

Rekomendation Treatment Patient With HBeAg (-) / (APASL 2008)

Rekomendation Treatment Pasient Cirrhosis (APASL 2008)

Yun FL et al Liver Int 2005;25:472 Yun FL.et al Guidelines for HBV management, APASL 2008

60

Rekomendasi terapi dari EASL (European Association for the Study of the Liver) 2009
Indikasi terapi sama untuk pasien HBeAg (+) dan HBeAg (-). Memenuhi 3 kriteria : kadar serum HBV DNA, kadar serum aminotransferase & grade/tingkat histologi. Pasien dapat diterapi bila kadar HBV DNA > 2000 IU/ml (10.000 kopi/ml) dan atau kadar ALT diatas BANN, dan biopsi hati menunjukkan moderate sampai severe necroinflammation dan atau fibrosis memakai sistim skor standar (contoh paling sedikit grade A2 atau tingkat F2 skor METAVIR.
61

ALGORITMA PENATALAKSANAAN HBV KRONIK ( PPHI )


HBsAg (+)

Periksa HBeAg dan ALT


HBe Ag (+) HBe Ag (-)

ALT <BANN

ALT >BANN

<2X Monitor/3 bulan Monitor/1-2 bulan

>2X

ALT > BANN

ALT < BANN

Dekompensasi hati

Monitoring/ 6 bln HBV DNA

Ya

Tidak ada Pos Neg

AN

AN atau IFN AntiVirus -

Respoms Tidak Respons MONITORING Strategi lain??? Kombinasi IFN dan AN Kombinasi AN Terapi alternatif

HBV Prevention
Screen blood products Sterilization of needles, etc. Avoiding intimate contact, e.g., household or sexual contacts Vaccination

HEPATITIS C

Progression of liver disease in chronic hepatitis C


Chronic hepatitis mild moderate severe fibrosis

Liver cirrhosis
End-stage liver disease HCC

10

20 Time after infection

30

40

HCV Risk Factors


received blood, blood products, or an organ transplant prior to 1992 ever, even once, shared drug paraphernalia ever been stuck by a used blood needle been on kidney dialysis had a tattoo or body piercing had multiple sex partners, or sexual activity that involved contact with blood shared personal care items (razors, tooth brushes, etc.) with other people combat veteran

Chronic hepatitis C infection


HCV affects about 2 % of the world population and approximately 300 million people are infected. The majority transmitted parenterally Up to 80 % will develop chronic infection Patients with chronic disease will develop cirrhosis over 20 to 30 years proportion of them will develop PHC. Co infection with HBV and HCV increases the risk of developing PHC.

Factors Promoting Progression of severity CHC


Increased alcohol intake Age > 40 years at time of infection HIV co-infection Other
Male gender Chronic HBV co-infection

Serologic Pattern of Acute HCV Infection with Recovery


Symptoms +/-

antiHCV

HCV RNA

Titer

ALT

Normal 0 1 2 3 4 Months 5 6 1 2 3 Years 4

Time after exposure

HCV Prevention and Control

Reduce or Eliminate Risks for Acquiring HCV Infection


Screen and test donors Virus inactivation of plasma-derived products Risk-reduction counseling and services Obtain history of high-risk drug & sex behaviors Provide information on minimizing risky behavior, including referral to other services Vaccinate against hepatitis A and/or hepatitis B Safe injection and infection control practices

HCV Counseling

Preventing HCV Transmission to Others


Avoid Direct Exposure to Blood

Do not donate blood, body organs, other tissue or semen Do not share items that might have blood on them
personal care (e.g., razor, toothbrush) home therapy (e.g., needles)

Cover cuts and sores on the skin

HCV Counseling

Other Transmission Issues


HCV not spread by kissing, hugging, sneezing, coughing, food or water, sharing eating utensils or drinking glasses, or casual contact Do not exclude from work, school, play, childcare or other settings based on HCV infection status

Chronic hepatitis C infection


Recent studies indicate a slow disease progression in patients with persistently normal ALT levels show minimal inflammation and low fibrosis scores in their liver histology. To diagnose anti-HCV HCV-RNA by PCR highly sensitive molecular Six genotypes (strains) of HCV Genotypes does not seem to influence the progression of the disiase sensitivities to therapeutic.

HCV Diagnosis
Most patients asymptomatic Abnormal liver function tests; AST/ALT Hepatitis C antibody (EIA) RIBA HCV RNA levels Liver biopsy: grade and stage damage

Diagnosis of Chronic Viral Hepatitis: Serologic Testing


Patients should be tested for HCV and HBV if they:
have known risk factors for viral hepatitis indicate possible risk factors for hepatitis have elevated liver enzymes express a desire to know their HCV and/or HBV status

Management of Hepatitis C NH Consensus Statement, 1997.

Diagnosing Chronic HCV Elevated ALT


All persons with chronic ALT elevation should undergo HCV testing.

elevated ALT level + risk factor(s) for hepatitis C

anti-HCV (EIA) testing


<5% chance of hepatitis C

diagnosis of hepatitis C >95% certain


Confirm with HCV RNA testing. Refer to specialist for evaluation and treatment.

Chronic HCV Infection : Recommended pretreatment evaluation


Test
HCV-RNA by PCR Serum albumin, bilirubin, PT Iron, transferrin, ferritin Antinuclear antibody

Purpose
Confirm viremia. Assess liver function. Assess for iron overload. Detect autoimmune hepatitis.

1- Antitrypsin phenotype
Ceruloplasmin (age<45 years) HBsAg, HIV antibody test Hepatitis C genotype

Detect 1- antitrypsin deficiency.


Detect Wilson disease. Detect viral coinfection. Assess likelihood of response to therapy.

Liver biopsy
Hepatitis B surface antibody Hepatitis A antibody (total)

Determine severity of disease and urgency for therapy.


Determine need for hepatitis B vaccination. Determine need for hepatitis A vaccination.

Peter R.McNally:GI/Liver Secret plus 4th ed.2010

HCV TESTING

EIA Negative Positive Measure HCV RNA by PCR

Negative Low risk High risk RIBA Negative

Positive

Consider treatment for HCV infection Positive

No further workup

Previous infection and clearance

Chronic hepatitis C infection


The progression of fibrosis determines the ultimate prognosis and urgency therapy. Liver biopsy remains the gold standard to access fibrosis. The major factors known to be associated with fibrosis progression : 1. Older age at infection 2. Male gender 3. Excessive alcohol consumption Alcohol to enhance the risk of developing PHC Co-infection with the HIV shown to worsen the course of chronic HCV infection Cirrhosis develops more frequently in those infected through blood transfusion than intravenous drug usage.

Chronic hepatitis C infection


The general management of patients with chronic hepatitis C is similar to that for chronic hepatitis B infection. Alcohol should be avoided as this has been shown to accelerate liver damage. Reducing the number of patients with HCV viraemia : 1. Screening of blood donors for anti-HCV 2. Active treatment of viraemic patients with Interferon and/or Ribavirin

Therapeutic goals in CHC


Eradication of the viral infection Diminution of viremia and infectivity Diminution of the severity of hepatitis

Diminution of fibrogenesis and progression


Prevention of complications of cirrhosis

Delay in development of HCC

Management of chronic HCV Infection

HCV Therapy
Pegylated Interferon injections weekly AND Ribavirin pills (or liquid) twice daily

HEPATITIS FULMINANT

HEPATITIS FULMINANT
Hepatic failure with in 2-3 weeks. Reactivation of chronic or acute hepatitis Massive necrosis, shrinkage, wrinkled Collapsed reticulin network Only portal tracts visible Little or massive inflammation More than a week regenerative activity Complete recovery or - cirrhosis.

ACUTE LIVER FAILURE acute liver disease with prothrombin time less than 50% of normal FULMINANT HEPATIC FAILURE acute liver failure with hepatic encephalopathy,develoving less than 2 weeks or 8 weeks after onset jaundice SUBFULMINANT HEPATIC FAILURE acute liver disease with hepatic encepalopathy,develoving from 2/8 weeks to 3/6 month onset jaundice

OGRADY and colleagus/:


Based liver failure,onset of jaundice,encepalopathy HYPERACUTE LIVER FAILURE,interval less than 7 days ACUTE LIVER FAILURE,interval 8 and 28 days SUBACUTE LIVER FAILURE,interval between 5 and 12 weeks

Clinical features
ICKTERUS PROGRESIF BILIRUBIN > 20mg % NAUSEA,MALAISE,VOMITING,FEVER.LIVER SIZE SMALL.COMA MAY RAPIDLY (FEWDAYS). TACHYCARDIA,HYPOTENSION,HYPERVENTILAT ION ,CEREBERAL OEDEME ARE LATER FEATURES

PROLONG PROTROMBIN TIME,ALT/AST INCREASE

IMUNOPATOGENESE DARI FULMINAN HEPATITIS

E ETIOLOGI
VIRAL HEMORAGIC FEVER VIRUS HEPATITIS VIRUS SITOMEGALOVIRUS HEPATITIS A HERPES SIMPLEX VIRUS HEPATITIS B EPSTEIN BARR VIRUS HEPATITIS C PARAMIXOVIRUS HEPATITS E ADENOVIRUS HEPATITIS G DRUG/ TOXIN, HALOTHANE ISCHEMIC ACETAMINOFEN ISCHEMIC HEPATITIS ISONIAZID-RIFAMPICIN SURGICAL SHOCK ANTIDEPRESANT ACUTE BUCCHIARY SYNDROME NSAID VALPROIC ACID MISCELLANEUS (RARE) MUSHROOM POISONING HEAT STROKR HERBAL REMEDIES SEVERE BACTERIAL INFECTION AMANITA POISONING MASSIVE MALIGNANT INFILT. YELLOW PHOSPORUS BACILLUS CEREUS EMETIC TOXIN

PREGNANCY RELATED ACUTE FATTY LIVER OF PREGNANCY HELLP SINDROME

MANAGEMENT
FARMAKOLOGI

N-ASETIL SISTEIN
PROSTAGLANDIN HAEMOPERFUSI ARANG KOLOUMN HEPATOSIT

MOLEKULER

REGULASI SITOKIN REGULASI KASKADE KOAGULASI INHIBISI APOPTOSIS HEPATOSIT GROWTH FACTOR

HEPATOSIT TRANSPLANT
TRANSPLANTASI LIVER TRANSPLANT

HEPATITIS D

HEPATITIS AKUT - D
Terdeteksi bersamaan dengan virus Hepatitis B. Prevalensi HDV (+) berhubungan dengan

prevalensi infeksi HBV (+). HDV lebih dominan didaerah tropikal dan subtropik,di negara berkembang drpd negara maju (Barat).

Klinis bervariasi dr asimptomatis sampai berat

80% kasus kronik hepatitis D menjadi sirosis dalam 5-10 tahun.

Gold standard d/: HDV RNA (+) atau HDAg (+) liver.

Transmisisi ,Parenteral contant, seksual, transfusi,needle,Hemodyalisa


Prevalence, less than 5% carier HbsAg

Clinical finding, acute HBV-HDV coinfection, severe hepatitis withhepatocelluler necrosis and inflammation,Chronic. Chronic HBV-HDV infection,initial severe liver disesase,may be chronic healthy carrier state similar with HBV chronic
Diagnosa , Anti HDV (+) IgM /IgG,in the presence Hepatitis B patient Therapi ,is problematic, initial Interferron alpha result in clinical and biochemical respons,but relaps are common Prevention,dvaccination with Hepatitis B Vaccine

HEPATITIS E

HEPATITIS E
Nonenveloped spherical RNA virus Transmission fecal oral,main target hepatocyte Endemic in India,Southeast and Central Asia The largest affected in young adult (15-40 years) Incubation period 2 10 weeks Clinical same with HepatitisA,but generrally more severe Diagnosed presence anti HEV (+) / IgG or IgM,HEV RNA (+)

TREAEMENT,supportive and no effective vaccine available Prvention,improved sanitation,sanitary handling,food,water, boil of water

HEPATITIS G

HEPATITIS G


Termasuk Flava virus.

Terdistribusi secara luas. Ditularkan melalui parenteral, seksual dan perinatal. HGV RNA dideteksi dengan PCR. HGV tidak mempengaruhi respon untuk terapi antiviral.

DILD

Drug-induced chronic hepatitis


Many drugs including herbal products can cause acute hepatotoxicity will induce chronic hepatitis with prolonged administration. These include gold, isoniazid, ketoconazole, methyldopa, nitrofuratoin, phenylbutazone and silfonamides. Oxyphenisatin the first agent known to be associated with chronic hepatitis. Older females are affected more frequently.

Wilsons disease
It is important to exclude wilsons disease as a cause of chronic hepatitis when it apprears in patients younger than 35 years. Liver disease often precedes symptoms attributed to central nervous system involvement and the appearance of Kayser-Fleischer rings and may be the initial presentation in 50 % of cases. Elevated urinary and hepatic copper levels are diagnostic. Improvement may be achieved by early treatment with D-penicillamine.

Autoimmune chronic hepatitis


This condition is relatively rare locally and usually affects young woman. Lipoid hepatitis positive lupus erythematosus (LE) cell test 15 % This is not the same as classical systemic lupus erythematosus (SLE) as the liver is typically not involved in SLE. The etiology of autoimmune hepatitis is not fully understood but genetic factors influence susceptibility and multiple viruses (including hepatitis C) and drugs can trigger the disease. Extrahepatic manifestations are prominent : 1. Amenorhea 4. Acne 2. Striae 5. Hirsutism 3. Obesity 6. Cushingoid facies

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