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Flashcards in Chronic Hepatitis Deck (5)
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1
Q

What is the serological definition of chronic HBV infection

A

HBs persistence beyond 6 months.

AntiHBc appears before HBsAg (may mark gap period) and IgG anti HBc persists years after antiHBs, may represent oaccult HBV infection

HBeAg shortly after HBsAg, marks viral replication, presence of circulating intact virions and viral DNA. Disappears after peak TA levels and antiHBe appeaerance. Immune clearance represented by seroconversion to antiHbe (10%/year) to become inactive carrier but can still mutate to progress to cirrhosis by precore mutation (viral replication without HBeAg production)

2
Q

How are infants infected with HBV differently from adults?

A

At birth: clinically silent and 90% become chronic

Becomes immune active (HBsAg+ and Anti-HBc+)

Adults: Clinically apparent and only 1% chronic (most infected as infants)

If adults resolve the infection, the HBsAg goes away but can reccur because the virus DNA is within liver cells.

3
Q

Treatment of HBV

A

Won’t cure chronic disease, goal is to prevent symptoms by seroconverting HBe. Can stop treatment one year after seroconversion and follow up.

If elevated ALT and normal DNA do biopsy to rule out NAFLD and other underlying liver conditions. Also Asian origin or other immune tolerant need a biopsy because may not show liver serology.

  1. Pegylated IFN-alpha
    No resistance but slow. Can’t use for immunosuppressed or pregnant (works by stimulating immune system). Ideally: young male HBAg+.
  2. Nucleoside/Nucleotide analogues (NUCs)
    Faster suppression, few side effects, but long term treatment and resistance. (Can’t stop after 1 year even if seroconvert.) Lower resistanceand high potency: Entecavir and Tenofovir.
4
Q

Progression of HCV infection

A

Most (55-85%) of acute HCV patients develop chronic HCV.

Of those 75-95% are stable and 5-25% develop cirrhosis (especially if long term carrier).

Of cirrhotic HCV patients, 97-99% are stable but 1-3% develop hepatocellular carcinoma (HCC) or decompensate per year

Most common cause of chronic hepatitis, #1 cause of liver transplant

5
Q

Diagnosis and Treatment of HCV infection

What, who?

A

High liver enzymes

+Anti-HCV Ab
PCR-RNA (qualitative then quantitative)-6 months negative means cured

Goals:
Complete viral eradication-Sustained Virological Response (SVR)
Normalize ALT and prevent complications (cirrhosis)
Reach undetectable levels of HCV-RNA

Meds:
Pegylated interferons
Ribavirin (direct antiviral for RSV but not for HCV, synergy with PEG-IFN)

Genotype I has bad prognosis (<50%), II and III have high treatment (80-90% and half length). Either way beneficial phenotype (CC) has 90% SVR chance with treatment.

For genotype I: can add Bocepravir and Telaprevir to increase success to 70-80%

Advanced fibrosis has little chance for cirrhosis development

If positive serology for over 6 months of treatment stop treatment because recovery is <1%

Can’t treat:
Uncontrolled depression, organ transplant (treat before), uncontrolled autoimmune conditions (exacerbated by tx), pregnant, chronic cardiovascular condition, <2yo

Side effects:
Anemia (treat)
Maintain Hb, neutrophil high, serum creatinine low