Liver· Chapter 18

Viral Hepatitis

HBV serology phases and the entecavir versus tenofovir choice, reactivation prophylaxis around rituximab and other immunosuppression, HBV in pregnancy with TDF for high viral load, HCV pan-genotypic DAAs in 8 versus 12 weeks, HDV bulevirtide, and the HEV mortality risk in pregnancy.

44 MCQs3 podcast episodes
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What this chapter covers

  • Section 18.1: Acute viral hepatitis phases and differential

    Acute viral hepatitis has the same clinical envelope regardless of the offending virus, which is why the serologic panel, not the symptoms, identifies the virus.

  • Section 18.2: HBV serology

    Each HBV serologic marker reflects a specific part of the virus or the immune response, and the combination determines management.

  • Section 18.3: HBV treatment and reactivation prevention

    The decision to treat chronic HBV is a multifactorial integration of HBV DNA, ALT, fibrosis stage, and clinical context, not a single threshold.

  • Section 18.4: HBV in pregnancy and vertical transmission

    Vertical transmission of HBV is the dominant route by which chronic HBV is acquired worldwide because perinatal infection produces the highest chronicity rate of any age window: 90 percent of neonates infected at birth become chronic carriers, compared with 30 percent of children infected between ages 1 and 5 and only 1 to 5 percent of immunocompetent adults.

  • Section 18.5: HCV diagnosis and DAA regimens

    Chronic HCV is now a curable disease, which is the single most consequential change in hepatology over the past decade.

  • Section 18.6: HCV special populations and post-SVR

    Special populations modify DAA selection because protease inhibitors are hepatically cleared and unsafe in decompensated liver disease, while nucleotide and NS5A inhibitors have distinct renal and drug-interaction profiles.

  • Section 18.7: HDV and bulevirtide

    Hepatitis D is a defective negative-stranded RNA virus that requires HBsAg from HBV as its envelope protein, which is why HDV exists only in patients who are also infected with HBV.

  • Section 18.8: HAV and HEV

    Hepatitis A is a fecal-orally transmitted picornavirus that produces an acute self-limited illness with an incubation period averaging 28 days, with a typical acute presentation and a few atypical ones.

Podcast episodes

  1. 01

    Viral Hepatitis: Acute Hepatitis A and E

    Acute viral hepatitis looks the same whatever the virus, so the serologic panel, not the history, decides the diagnosis. The episode starts with the first panel and how to read it, then shows why a negative hepatitis C antibody can miss acute infection and why acute hepatitis C is treated promptly. It moves to acute hepatitis B, which is treated only if fulminant or protracted, and to core IgM in a chronic flare. Hepatitis E follows, as a mimic of drug injury, as chronic infection in transplant recipients, and as a danger in pregnancy. Hepatitis A closes the episode, with its unusual courses, vaccination, and postexposure prophylaxis.

    Read the transcript →
  2. 02

    Viral Hepatitis: Hepatitis B and D

    Hepatitis B decisions follow from reading the markers correctly and asking what is about to happen to the liver or the patient. The episode starts with surface, core, and e markers and the phases of chronic infection, then the isolated core antibody. It moves to treatment criteria, the three first-line drugs, and why therapy is usually indefinite. Reactivation under immunosuppression comes next, with prophylaxis timing, followed by pregnancy: newborn prophylaxis, maternal tenofovir, and the postpartum flare. It ends with hepatitis D, which needs hepatitis B, with testing, coinfection versus superinfection, and bulevirtide, then the common board traps.

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  3. 03

    Viral Hepatitis: Hepatitis C Screening to Cure

    Hepatitis C is now curable with pills, so the episode follows one pathway and then shows where it bends. It starts with universal screening and confirming infection with antibody and reflex RNA. Next come the pretreatment workup, the two preferred regimens, and SVR twelve as the test of cure. Salvage after relapse follows. Then three patients leave the standard pathway: a woman with decompensated cirrhosis awaiting transplant, who also shows who needs surveillance after cure, a man on dialysis, and a pregnant woman. The episode closes with the traps the boards set.

    Read the transcript →

Key topics

  • Course of acute viral hepatitis
  • First serologic panel and its readings
  • Acute hepatitis C and antibody lag
  • Pretreatment workup and vaccination
  • Acute hepatitis B management
  • Core IgM in a chronic hepatitis B flare
  • Hepatitis E mistaken for drug injury
  • Chronic hepatitis E in transplant recipients
  • Hepatitis E in pregnancy
  • Hepatitis A courses, vaccine, and prophylaxis
  • Hepatitis B serologic markers
  • Phases of chronic infection
  • Isolated core antibody
  • Treatment criteria and drug choice
  • Duration of therapy and cure
  • Reactivation and prophylaxis
  • Pregnancy and newborn prophylaxis
  • Postpartum flare
  • Hepatitis D testing and diagnosis
  • Bulevirtide and peginterferon
  • Direct-acting antiviral classes
  • Universal screening and risk factors
  • Antibody with reflex RNA
  • Pretreatment workup
  • Preferred regimens and interactions
  • SVR twelve and benefits of cure
  • Salvage after relapse
  • Decompensated cirrhosis and transplant timing
  • Cancer surveillance after cure
  • Dialysis and pregnancy

Sources

Guidelines, consensus statements, and validated instruments this chapter draws on. Named here because the chapter applies them directly.

Professional society guidelines

  • American Association for the Study of Liver Diseases (AASLD)
  • European Association for the Study of the Liver (EASL)
  • Infectious Diseases Society of America (IDSA)

Scoring systems

  • MELD score
  • Child-Pugh score
  • FIB-4 index