Please enable JavaScript.
Coggle requires JavaScript to display documents.
Path: Liver 3 - Acute + Chronic Hepatitis (iv) (screening blood products,…
Path: Liver 3 - Acute + Chronic Hepatitis (iv)
Phases of chronic HBV infection
Replicative, immune tolerance
high viral rep, no immune response
characteristic of perianal/early childhood infection
explains why > 90% of such infections become chronic
consequence of in utero exposure to maternal antigens
persists for 20+ yrs, then immune response appears - "immune clearance"
reservoir of infection, highly infective
HBsAg +ve, HBeAg +ve, high level of HBV DNA, normal ALT
unresponsive to tx (no immune response to augment)
Replicative, immune clearance
when immune tolerance wanes or if in adult
viral rep but immune system is responding - necroinflamm damage, elevated ALT, high viral DNA
HBsAg +ve, HBeAg +ve
may cause sustained disappearance of HBeAg (10%/yr +/- seroconversion if anti-HBe appears)
may rarely cause clearance of HBsAg (apparent resolution)
can be ineffective (flares/exacerbations)
enhanced by IFNa
a/w damage, fibrosis, cirrhosis, HCC - so consider tx
Non-replicative, immune control
inactive HBV carrier
Chronic HBV infection
HBaAg +ve
a/w HBeAg clearance (seroconversion - anti-HBe +ve)
no/minimal replication
low/no HBV DNA
normal ALT
further disease progression halted
liver may have already sustained damage
not a fixed state - hence term 'healthy carrier' avoided
requires ongoing immune surveillance
reactivation may occur
Replicative, immune escape
reactivation
mutant strains develop (precore, basal core promotor)
abolished/reduced HBeAg expression - allows immune escape
can be due to host immunosuppression
replication resumes, variable level of HBV DNA
HBsAg +ve, HBeAg often -ve, ALT variable elevation
known as HBeAg -ve chronic HBV hepatitis
HBV Tx
aims
control viral rep
reduce HBV DNA
promote HBeAG clearance
reduce/prevent further damage/progression
pegylated IFNa
long but finite tx duration
injected
low tolerability
ILI
fatigue
depression
AI
cytopenias
response rate = 30-40%
responders have a durable response
nucleoside/nucleotide analogues (antivirals)
potentially long term tx
response not always durable
oral
resistant viral mutants can develop
better tolerated
tenofovir
entecavir replacing lamivudine
who to tx?
cirrhosis (+/- decompensation)
pregnant women
chronic HBV infection (HBeAg +ve or -ve)
assess HBV DNA load + ALT
possible do biopsy to judge grade/stage of disease
non-invasive fibrosis assessments
viral hep screen
IgM anti-HAV
IgM anti-HEV
HBsAg - if +ve, HBV DNA levels to confirm rep state, HBeAg, anti-HBe
anti-HCV - if +ve do virology to confirm (genotype + quanitfy HCV)
anti-HBs (immunity)
anti-HBc (has patients ever been exposed?) - used prior to immunosuppression even if HBsAg -ve
IgM anti-HBc (recent exposure)
screening blood products
HBV (HBsAg + anti-HBc)
HCV
HIV
HTLV-1
syphilis
CMV (to identify CMV -ve stock)
risk of transfusion associated hepatitis reduced
ALT (blood borne viral hep)
ask donor's risk factors