Hello everyone,
In a previous discussion, @cscoffin suggested I talk to my specialist about considering treatment. I was excited to see your name referenced in the CASL guidelines, which gave me a reassuring feeling knowing that you contribute your expertise to this wonderful forum. Thank you so much for your valuable insights!
I have some questions about how to ask the right questions to communicate effectively with my specialist, so I wanted to create a new post to ensure this is in the correct category for feedback and guidance.
I am currently an e-antigen negative Hepatitis B patient with a viral load of 97,500 IU/mL. My most recent Shear Wave Elastography showed a liver stiffness measurement of 8.53 kPa, which suggests F2 fibrosis. I have had fluctuations in my viral load over the past year, and my ALT/AST levels have remained consistently low.
I’m working with an internal specialist who is currently recommending that we wait to initiate treatment until my fibrosis progresses to F3 or F4. I have also been told that Hepatitis B tends to progress slowly, so rapid liver liver disease progression is not a major concern. However, after reading the CASL guidelines, I understand that Hepatitis B is considered a dynamic disease that can evolve gradually or rapidly, and that the progression risk may vary.
My understanding of these guidelines is that patients with a high viral load and significant fibrosis, especially those who are e-antigen negative, could be at increased risk of severe liver injury, cirrhosis, or HCC. I’ve also read that women of Asian descent, particularly those with genotype C, may face higher risks of cirrhosis and HCC.
My concern is that, by waiting until fibrosis worsens, we may be underestimating the risks, especially since I might be in a higher-risk group. I want to ensure we are accurately assessing the benefits and risks of treating versus delaying treatment.
My goal is not to push for treatment prematurely, but rather to ensure that we are scoring the risks correctly and developing a clear plan based on my individual situation. I also find that communication with my specialist has been challenging, as some of my questions have left me feeling more confused than reassured.
I would really appreciate any advice on how to effectively discuss this with my specialist, what questions I should be asking, and whether there are specific factors I should emphasize during these discussions. How can I better communicate my concerns about balancing the risks of waiting versus starting treatment now?
I have included some questions I am considering and would greatly appreciate you insights on but not limited to the following:
- Possible misunderstandings in my current understanding
- Better ways to communicate my concerns
- Additional points to consider that may be beneficial
- Anything I should consider emphasizing
- Anything I should consider omitting
Background:
- Gender: Female, 42 years old
- Hepatitis B likely contracted at birth (from South China)
- Hepatitis B GenoType: Unknown (possibly B or C based on origin)
- e-Antigen status: Negative
HBV DNA, ALT, and AST Over Time
| Date | HBV DNA (IU/mL) | ALT (U/L) | AST (U/L) |
|---|---|---|---|
| Aug/2024 | 97,500 | 15 | 19 |
| Jan/2024 | 284,000 | 21 | 22 |
| Sep/2023 | 458,000 | 20 | 19 |
| Jun/2023 | 280,000 | 32 | 28 |
| Mar/2023 | 131,000 | 17 | 21 |
| Jan/2023 | N/A | 25 | N/A (Specimen hemolyzed) |
| Dec/2022 | 204,000 | 18 | 20 |
| Nov/2022 | 59,900 | 25 | 25 |
Fibroscan and Shear Wave Elastography
| Test | Value | Date |
|---|---|---|
| Previous 2023 Fibroscan | 9.2 kPa and 5.1 kPa (different areas) | 2023 |
| Shear Wave Elastography | Median: 8.53 kPa, IQR/median: 14% (good data set) | 2024 |
- Shear Wave Elastrography was preformed to compare with Fibroscan because there was a jump from F1 - F3. The internal specialist suggested it was because we were using a medium prob when she suspected a small prob was more suitable for my size. However in the past all Fibroscans were taken with a medium prob which were on average F0 - F1
According to my SWE results:
GE E10 ultrasound unit
- F1: 5.48 – 8.29 kPa
- F2: 8.29 – 9.4 kPa
- F3: 9.4 – 11.9 kPa
- F4 (cirrhosis): >11.9 kPa
Other Tests
| Test | Value | Reference Range | Date |
|---|---|---|---|
| Hemoglobin | 155 g/L | 120 - 150 g/L | 05/Jan/2024 |
| Rheumatoid Factor | > 120 IU/mL | - | 23/Feb/2023 |
| Hepatitis E Virus Ab IgM | Nonreactive | - | 13/Jan/2023 |
| Hepatitis E Virus Ab IgG | Reactive AA | - | 13/Jan/2023 |
Current Symptoms
- Intermittent fatigue, upper right quadrant pain, sore muscles and joints, and night sweats.
- I understand these symptoms could be caused by various infections but may also be associated with flare-ups and liver inflammation.
These are the question I have come up with
-
Phase Determination and Treatment Timing:
- Given that I am e-antigen negative with a viral load of 97,500 IU/mL and F2 fibrosis, how do we accurately determine whether I am in phase 3 (inactive carrier) or phase 4 (immune-active)?
- Would it be useful to test for qHBsAg levels ?
- According to the CASL guidelines:
15. HBeAg-positive (phase 2) and HBeAg-negative (phase 4) patients in whom HBV DNA is more than 2,000 IU/mL with elevated ALT (> 1 time the upper limit of normal) for 6 months should be considered for treatment. (strong recommendation; class 2, level A)
16. Patients with significant inflammation or fibrosis (above stage 1) should be considered for treatment, even if HBV DNA is lower than 2,000 IU/mL or ALT is normal. (strong recommendation; class 2, level A) (page 22 of CASL)- 5.4. qHBsAg Quantitative HBsAg (qHBsAg) is an established marker predicting infection phase and immune control, which together with HBV DNA levels guide treatment decisions. qHBsAg testing is recommended for monitoring response to treatment and establishing chronic HBeAg-negative hepatitis (phase 4) versus HBeAg-negative infection (phase 3), as discussed next and in section 6.0. Quantitative measurement of HBsAg has been standardized to an international standard, and assays are commercially available in Canada (Abbott Architect HBsAg, Abbott Diagnostics, Mississauga, Ontario; Roche Cobas Elecsys HBsAg II quant, Roche Diagnostics, Laval, Quebec) with a broad dynamic range and limits of detection to 0.05 IU/mL. Because qHBsAg can reflect the natural history of HBV infection, it allows for putative cut-off values to predict the likelihood of moderate to severe fibrosis in treatment-naïve HBeAg-positive patients, depending on HBV genotype and ALT measurements (≥7,000–25,000 IU/mL) (84). (page 13 of CASL)
- How does this apply in my case with F2 fibrosis?
-
Risk Factors for Asian Descent and Genotype C:
- Although I don’t yet know my genotype, I understand that Asian descent and genotype C (which may be more likely in my case) are associated with higher risks of liver disease progression and HCC. Given this, how should we factor these risks into treatment decisions, especially with my current viral load, fibrosis score, normal ALT and E-Antigen Negative?
- Could delaying treatment increase my risk of long-term complications?
- Would it be beneneficial to test for GenoType when determining care plan.?
- If we confirm genotype C, how does that impact the urgency of starting antiviral therapy?
- HBV/C infection is significantly associated with delayed HBeAg seroconversion (115), resulting in persistently high HBV DNA levels that, together with a higher frequency of the double basal core promoter mutation (A1762T/G1764A) (116), leads to HBV/C being an independent risk factor in the development of HCC (117). (page 15 of CASL)
-
ALT and Fibrosis Progression:
- Since my ALT levels are low (15 U/L) but I already have F2 fibrosis, should we still rely on ALT fluctuations before considering treatment? As noted in the CASL guidelines, “patients with e-antigen negative chronic Hepatitis B with high viral loads and evidence of significant fibrosis should be considered for antiviral therapy, regardless of ALT levels.” How does this influence our approach in considering HCC and liver damage risks
-
CHB as a Dynamic Disease:
- Given that chronic Hepatitis B is a dynamic disease that can evolve gradually or rapidly, what are the risks of rapid progression, especially considering my current risk score and that fibrosis has already progressed to F2?