Hep B / HCC screening - ReachB

 https://www.youtube.com/watch?v=3cP2kvPq7iQ

m.c form of acquiring Hep B in Asia - Vertically

m.c form of acquiring Hep B in western coutnries: Parenterally (sexual / needles etc)

• Neonates have immature immune system, so they cant 'fight-off' vertically acquired virus. Over 90% of babies infected with Hep B, go on to have chronic Hep B infection
• 95% of adults if they acquire Hep B - fight it off!

• HBV is a DNA virus - replicates efficiently. But is error-prone. Plagued with mutants. 
• e-antigen negative mutant - tend to be in older patients, tend to be more aggressive.
• 30-50% of HCC in HBV occurs in absence of cirrhosis

Reveal study - 15 year follow-up study of untreated patients with HEp B. The only factor that was relevant in predicting risk of HCC was viral load at base-line!

Viral load more than 10*4 (2000 IU/ml) was predictive of risk of HCC or Cirrhosis (similar graph for Cirrhosis as for HCC)

Immune Tolerant Phase: typically after vertical infection. DNA remains very high, no inflammation, no fibrosis. Immune system is not trying to fight-off the virus.

Over time - 

The immune tolerant phase -> Active heaptitis B

Viral load comes down, inflammation in liver goes up, ALT goes up. 

Some patients will spontaneously lose e-Antigen, eantibody becomes positive. (IgM for core antibody becomes positive) - usually with an acute bout of hepatitis /jaundice. 

Rate of spontaneous seroconversion is few% per year. There is resolution / improvement of fibrosis to a certain degree. 

Patients with inactive / seroconversion  - have low ALT, low viral count (immune control phase).

E-negative Hep B:

E-gene is located in the pre-core region of HBV. Not necessary for replication. However is the target for immune response. 

If there is mutation in E-gene, it produces no detectable E-antigen, it prevents immune response. 

So basically, after the Immune Control phase - where e-antigen seroconversion has taken place, the virus 'Escapes' and moves in to 'Immune Escape' phase when e-antigen mutates. These patients still might have E-antibody

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*Criteria for Stratification of Hepatocellular Carcinoma (HCC) Risk in patients with Hepatitis B 

 

Not on Treatment 

REACH-B (adopted by Hepatitis Foundation) 

Score <10 (low risk) → 6 monthly AFP in primary care 

Score >10 (mod/high risk) → 6 monthly AFP/USS in secondary care 

(Reach-B score available from MD Calc)

REAL-B score (patients on Treatment)

 

NUC suppressed patients 

 

Parameter		Points	Patient Score
Gender	Female	0	0
	Male	1
Age	18-29	0
	30-39	1
	40-49	2	0
	50-59	3
	60-69	4
	70-79	5
	≥80	6
Alcohol	No alcohol	0	0
	Drinking	1
Cirrhosis at baseline	No cirrhosis	0	0
	Cirrhosis	2
Diabetes	No diabetes	0	0
	Diabetes	1
Platelet count	≥150	0	0
	<150	1
	<100	2
AFP	<10	0	0
	≥10	1
REAL-B Score			0

 

REAL B score 

Score ≤4 (low risk) → 6 monthly AFP in primary care 

Score >4 (mod/high risk) → 6 monthly AFP/USS in secondary care 

 

New Recommendations 

AFP + USS 6 monthly if at least one of the following: 

1. Severe fibrosis/cirrhosis (LSM >8.1kPa) 

2. Family history of HCC (one first degree relative or two second degree relatives) 

3. Not on NUC treatment and REACH B score >10 

4. Suppressed on NUCS and REAL B score >4