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DR. WAQAR MBBS, MRCP ASST. PROFESSOR HEPATITIS It means inflammation of the liver. There is hepatocyte necrosis & inflammatory cell infiltration in the liver. There are many causes of hepatitis : 1) Viruses: Most common cause 2) Drugs ( panadol, some TB drugs) 3) Ischemia of liver( ischemic hepatitis) 4) Autoimmune 5) Alcohol 5) Poisons (carbon tetrachloride) VIRAL HEPATITIS A, B, C, D, E ( more common) * Epstein Barr virus(EBV) * Cytomegalovirus(CMV) * Other rare viruses ( less common) Viral hepatitis is of concern because of burden of illness, potential for outbreaks & death. Chronic HepB & C have a huge economic burden also. Many cases are preventable. Hepatitis can be acute or chronic. 1) Acute: Duration of the disease is less than 6 months. 2) Chronic: Duration is more than 6 months (clinical S/S or abnormal blood tests) *Hep A causeS only acute hepatitis *Hep B,C,D &E can cause both, acute & chronic. Chronic hepatitis B & C is the principal cause of chronic liver disease, cirrhosis & hepatic cancer HEPATITIS A 1) It is an RNA virus. Most common cause of acute viral hepatitis. 2) More common in Asia, Africa, Mid.East, South America. 3) Only acute hepatitis. No carrier state or chronic hepatitis.Usually,does not happen twice. Mode of transmission: * Fecal-oral route( contamination of food & water due to poor hygiene by food handlers) * Saliva Hep A contd. Incubation Period: avg. is 28 days( time from getting the virus till the onset of S/S) Period of greatest infectivity: • From 2 wks before onset of symptoms till 1-2 wks after onset of symptoms. In this period of infectivity, the virus is shed in the stools of the patient in high amounts. Hep A contd. Clinical Features: Prodromal Phase ( first 1 -2 wks) * Anorexia,nausea, malaise, bad taste, fever *Jaundice is absent initially Icteric Phase (next 3-6 wks) * Above symptoms may improve * Jaundice, pain in right upper quandrant, dark urine, pale stools, tender hepatomegaly Hep A contd. Severity of disease: Usually mild to moderate S/S but can be asymptomatic ( specially in children & young ppl) or very severe disease called Fulminant hepatic failure (F.H.F.) which is fatal. INVESTIGATIONS 1) L.F.T.s: * High bilirubin * AST & ALT are high ( 10 to 100 times) * Alk. Phosphatase slightly high 2) Urine : Contains bilirubin & urobilinogen 3) Hep A antibody: Anti HAV ab. * During acute infection: IgM type ( Diagnostic) * After recovery: IgG type ab. appears in blood TREATMENT There is no special drug treatment. Disease is self limited and recovers in 3-6 wks. 1) 2) 3) 4) 5) Good nutrition( whatever can be tolerated) Vitamin supplements Avoid alcohol, panadol and some other drugs Symptomatic treatment for complaints FHF needs liver transplant. PREVENTION General Measures Immunization * Good hygiene * Hep.A vaccine * Drink bottled water * HepA immunoin high risk areas -globulins * Avoid risky foods 1) Vaccine ( active immunization): Given to * Travellers to high risk areas( Asia etc) * Patients wth. chronic liver disease * People working with sewage (toilet drains) 2) HepA Ig. ( passive immunization) * Immunoglobulins are given to close contacts of Hep A patients ( to prevent infection) HEPATITIS B Epidemiology: * World wide problem( specially Africa, MidEast, S.America) * 1/3rd of the world population has serological evidence of past or present infection. * About 1 million deaths occur per year due to Hep B related liver disease & carcinoma Structure of Hep B virus 1) Outer covering has surface antigen( s ag.) 2) Inner center has: * “e” ag.(antigen) * HepB DNA * “c” ag. (so, 3 ag. plus DNA) It is a DNA virus ( hep A & hep C are RNA viruses) SEROLOGIC MARKERS 1) After infection wth HepB, “s” antigen, “e” ag. & HepB DNA appear in the blood. 2) “c” antigen never appears in the blood. Antibodies which appear in the blood: * Anti HB s ( against “s” ag.) * Anti HB“e”( against“e” ag.) * AntiHB “c” ( against “c” ag.) Note that “c” antigen does not appear in blood but c antibody appears. Routes of Transmission VERTICAL (mother to fetus) * Most common route worldwide. PARENTERAL * Transmission by body fluids (blood, semen etc) Modes of parenteral transfer 1) i.v. drug use : Coz drug abusers share needles 2) Transfusion of infected blood & blood products: V. rare in developed countries coz of blood screening. 3) Contaminated syringes 4) Needle stick injuries ( doctors &nurses at high risk) 5) Sexual transmission 6) Direct contact with blood of HepB patient ( even minor abrasions are risky) SPECTRUM OF HEP.B INFECTION Hep. B can cause any of the following: 1) Acute hepatitis ( may lead to fulminant hepatic failure in some cases) 2) Chronic hepatitis: Infection persists for more than 6 months. May lead to cirrhosis & hepatocellular cancer. 3) Carrier state: Virus is present in the body for more than 6 months but no active hepatitis & normal LFTs. ACUTE HEP. B 1) Incubation Period: Very variable. Avg. 6 wks 2) S/S : * Jaundice + all others like Hep A * May be asymptomatic * 1% cases develop fulminant hep.failure 1) Extrahepatic features: * Skin rash * Polyarthritis of small joints * Glomerulonephritis (Membranous type) 4) Blood Tests: a) LFTs: bili., AST & ALT (same like hepA) b) Hep B serology ( antigens & antibodies) contd. SEROLOGY IN ACUTE HEP B 1) Antigens which appear * “s”ag. * “e”ag. * HepB DNA levels( not measured in acute hep.) (all these disappear after infection is finished) 2) Antibodies which appear: • AntiHBs (means recovery) * Anti HBe * AntiHBc Treatment of Acute Hep B • Symptomatic • No specific treatment ( Thank God this slide is small ! ) Chronic Hep B 1) Def.: Persistence of abnormal serology for more than 6 months with or wthout S/S. 2) More chance of chronic infection in newborns ( by vertical transmission), children,& ppl. with poor immunity). 3) Serology: * “s” ag. + * “e” ag. + * DNA + 4) S/S may be mild or absent. Often found on routine tests.( LFTs & liver biopsy are abnormal) 5) Patient is highly infectious coz “e”ag. is present 6) If only “s” ag. is present & no “e”ag., it is chronic carrier state & patient is less infectious. (LFTs & liver biopsy are normal) SO, REMEMBER * IF “e” antigen is present in Hep B patient, he is highly infectious. • IF only “s” ag. is present , he is less infectious. SO: • Chr. Hep B: “s” ag. +, “e” ag. + , Abnormal LFTs • Chr.carrier state: Only “s” ag. +. No “e” ag & LFTS are normal. TREATMENT OF CHR.HEP B 1) Drugs used: * Nucleoside analogues: eg Entecavir oral * Nucleotide analogues: eg. Tenofovir drugs * Interferon ( Injections) 2) Treatment is 6 months to 1 yr. 3) Treatment is not given to chronic carriers(only “s” ag. positive with normal LFTs) PREVENTION OF HEP B. 1) Avoid risk factors ( iv drugs, needle sharing, sexual contact wth. unknown or HepB positive person, avoid direct contact wth blood, no sharing of razors etc. 2) Vaccine: Given routinely to everyone. * 3 doses: 0, I month,6 mnth(from the 1st dose) 3) Immune globulins: Given to a person if he has not received vaccine before, & now has a high risk exposure eg. needle stick injury from Hep.B patient, sexual exposure or newborns of ‘s’ ag. + mothers OUTCOME Untreated Hep B can lead to cirrhosis & hepatocellular cancer REMEMBER * Vaccine produces protective antibody over after time (wks to months) but lasts long. * Immunoglobulins provide immediate protection that lasts for a short time. HEP C 1) Epidemiology: Occurs worldwide but very common in Africa & Egypt. 2) Mode of Spread: (Parenteral) * i.v. drug use ( West) * Blood transfusion (developing countries) * Contaminated needles & instruments (surg., dental) * Sexual transmission is very less(<1%) *Perinatal : <1% * Contact with infected blood( razors, cuts) 3) There are 6 subtypes of HepC ( 1 to6) * Type 1 : More severe disease * Type 2 &3: Less severe disease & good response to treatment. WHAT HAPPENS AFTER INFECTION 1) Only 10-20% patients are able to clear the virus from their body. They may get mild S/S after infection. 1) Most patients develop chronic hepatitis 1) 2) 3) 4) CHRONIC HEP C Usually asymptomatic & detected by chance on routine blood tests(slightly high AST & ALT). LFTS often fluctuate. Often presents after many yrs., as cirrhosis Mild jaundice, fatigue may occur Extrahepatic features: GN, arthritis, cryoglobulins in the blood DIAGNOSIS (HEP C) 1) HepC antibody ( Anti HCV ab.): * It is the initial test done * Becomes positive about 2 months after infection * Antibody is not protective(opposite of Hep B) * False +ve & -ve may occur. 2) HepC RNA levels (by PCR): * This is actual virus level in the blood * Appears in blood in 1-2 wks of infection 3) Liver Biopsy: Not done for diagnosis, but only done before treatment to see fibrosis TREATMENT 1) Offered to most patients 2) Response to treatment depends on genotype & some other factors( type2 & 3 has very good response & can be cured). 3) Till recently, only the following combination was used: * Oral Ribavirin + * Interferon inj 4) Latest treatments are all oral & free of interferons. They are given for 3 months. ( Sofosbuvir, Simeprevir etc) ( CAN YOU REMEMBER THESE NAMES? ) OTHER THINGS IN MANAGEMENT 1) Patient counselling: * Don’t donate blood or tissue * No iv drugs, no needle/razor sharing * Explain that there is a risk of sexual transmiss-ion although small. * Avoid alcohol ( can worsen the disease) 2) Check for Hep B, Hep A and vaccinate if –ve. 3) Check for HIV VACCINE No vaccine or immunoglobulins are available as yet. OUTCOME Without treatment, Hep C can lead to cirrhosis and hepatocellular carcinoma ( liver cancer). HEP D 1) Hep D virus is unable to cause infection on its own.It requires the presence of HepB virus to replicate. 2) Infection can occur alongwith HepB ( coinfection) or occurs in a person who has HepB from before. 3) Risk factors, mode of spread & S/S are like Hep B. 4) Treatment of chronic Hep D: INTERFERON HEP E 1) 2) 3) 4) Mode of transmission is like HepA (fecal-oral) Infection is self limited. Occurs in developing countries Mortality is high if it occurs in pregnancy.