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General Characteristics a. Hepatitis = inflamm of liver b. Non-infectious types: alcoholic, drug-induced, autoimmune, hereditary diseases that cause c. Causes: hepatitis virus, EBV, CMV, HSV (EBV-HSV not assoc. w/immunocompetent pts) d. Transmission i. HAV & HEV fecal-oral route ii. HEV is common in India, Pakistan, SE Asia, parts of Africa iii. HBV parenteral, sexual, perinatal (Africa, Asia) iv. HDV needs outer envelope of HbsAg for replication so can only be transmitted as coinfection w/HBV or superinfection in chronic HBV carrier v. HCV parenteral so more common in IVDA vi. Progress to chronic disease: HBV, HCV, HDV Clinical Features a. Either acute (< 6 mos inflamm) or chronic (> 6 mos inflamm) b. Acute i. Jaundice, esp in sclera ii. Dark-colored urine (conjugated hyperbilirubinemia) iii. RUQ pain, N/V, fever & malaise, hepatomegaly iv. If severe liver failure = fulminant hepatitis (HBV, HDV, HEV) 1. Complications: hepatic encephalopathy (asterixis, palmar erythema), hepatorenal syndrome, bleeding diathesis v. Can present w/only transient flu-like sx (fever, myalgias, malaise) vi. Acute HBV can present w/serum sickness-like illness vii. No acute HCV illness c. Chronic i. Some can be asx (chronic carriers) & only present w/late complications (cirrhosis, hepatic cell carcinoma) ii. Most commonly in pts w/HCV iii. Categorized based on grade of inflamm, stage of fibrosis, etiology of disease iv. Risk of developing cirrhosis or HCC is higher in HBV than HCV d. Course of HBV i. Subclinical acute infection in 70% 1. Most will resolve 2. 5-10% will have chronic hepatitis cirrhosis or HCC 3. 1% will have fulminant hepatitis transplant or death 4. < 5% will be chronic carriers HCC ii. Assoc. w/PAN e. Course of HCV i. Subclinical acute infection in 75% 1. 10-15% resolve 2. Majority get chronic hepatitis cirrhosis, HCC

3. < 1% get fulminant hepatitis transplant or death ii. Assoc. w/cryoglobulinemia III. Dx a. Serum serology most important factor; help determine if acute or chronic & if there is adequate immunity i. Hepatitis A 1. Anti-HAV: detectable during acute infection & persists for life so this does NOT distinguish btwn active disease & immunity; IgM = acute ii. Hepatitis B 1. HBsAg: in acute or chronic (will persist even if asx) & seen as early as 1-2 wks after infection; CANT BE SEEN IF VIRUS IS CLEARED 2. HBeAg: active viral replication & infectivity, appears shortly after HBsAg 3. Anti-HBs: after vaccine or after clearance of HBsAg & seen 1-3 mos after infection; PRESENCE = IMMUNITY TO HBV 4. Anti-HBc: combined IgM & IgG; only marker during window period (HBsAg is disappearing but anti-HBs cant yet be seen); does NOT distinguish btwn acute & chronic & doesnt indicate immunity 5. Viral load: HBV DNA measured by PCR; if > 6 wks, likely to develop chronic disease iii. Hepatitis C 1. Hepatitis C Ab: marker of infection but sometimes not seen until months later so absence does NOT R/O infection 2. Viral load: HCV RNA measured by PCR & seen 1-2 wks after infection (more sensitive) iv. Hepatitis D 1. Anti-HDV: indicates HDV superinfection but may not be there in acute so might have to do repeat testing b. LFTs i. ALT > AST (alcoholic AST > ALT) ii. Acute: ALT > 1000 iii. Chronic HBV: ALT > 1000 but can vary (chronic HCV, ALT is lower than 1000) Tx a. Active (vaccine) & passive (IG) immunization for HAV & HBV b. Infants & HCW must be vaccinated for HBV c. Travelers get vaccinations for HAV; passive immunization can be given if exposed d. HAV, HEV supportive care e. Chronic HBV IFN-a or lamivudine (nucleoside analog) or tenofovir f. Chronic HCV pegylated IFN-a & ribavirin g. Liver transplant in advanced disease although recurrence can still occur after transplantation