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Post Info TOPIC: About contracting HBV and HCV at the same time


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RE: About contracting HBV and HCV at the same time
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Canuck wrote:

More, in regard to reactivation risks, especially for "occult" B people:

.. "The most important thing is that [HBV] be attended to before you get going with [a] course of treatment for [HCV]," Dr Chung said.

Patients with low or undetectable levels of HBV who do not meet the criteria for HBV treatment should be carefully monitored during direct-acting antiviral treatment for co-occurring HCV, the guideline recommends. Dr Chung noted that some patients have developed very serious illness as a result of reactivation, so vigilance is critical.

 

Thank you for your continued posts and updates regarding this Canuck. It just reinforces to me that my Dr. and the Hospital I went to for the second opinion were so very much on top of this considering the way I was monitored. It was like, we know we are going to cure his C but lets be very careful about the B as you probably recall. I will actually have my C viral load done this coming week. EOT+24 and I am pretty confident it will be undetected. They won't do B anymore because changes in my LFT's would indicate that should be done. Having said that, I am on certain medications now that are not liver friendly and I really need my Specialist to sort it out and watch since I am thinking they have the ability to change my LFT's as well and I don't need any confusion or scares at this point. Three weeks ago was quite enough to last me a long time * Shrugs


__________________

65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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More, in regard to reactivation risks, especially for "occult" B people:

.. "The most important thing is that [HBV] be attended to before you get going with [a] course of treatment for [HCV]," Dr Chung said.

Patients with low or undetectable levels of HBV who do not meet the criteria for HBV treatment should be carefully monitored during direct-acting antiviral treatment for co-occurring HCV, the guideline recommends. Dr Chung noted that some patients have developed very serious illness as a result of reactivation, so vigilance is critical.

"The fact of the matter is there is no substitute to being attentive if you decide not to treat or the patient doesn't warrant treatment," he said.

One issue that still hasn't been resolved is what to do with patients who are surface antigen negative for HBV and positive for anti-HBV core antibodies, Dr Chung noted. He explained that those patients are not considered chronically infected. However, there is at least one case report of HBV reactivation in such an individual...

(Dr. Chung doesn't even get to the "other", further, category - those people who are occult B with no sero-markers!). Good reason for a new standard for B DNA PCR's to be done please!

A further article: ... Occult Hepatitis B infection (OBI) is defined by the absence of HBsAg despite the presence of HBV DNA in the liver, blood serum, or peripheral blood mononuclear cells (PBMCs), irrespective of the presence of other hepatitis B viral antibodies and antigens[2]. OBI poses a significant risk to those receiving blood transfusions or tissue transplants because conventional donor screening with HBsAg and anti-HBc may yield serologically negative results despite the presence of HBV DNA[3]. It has been shown that 20% of OBI infections are negative for all HBV serological markers while HBV DNA is present[4] although the HBV viral load is often low[2]. This means detection of OBI can be challenging due to the extremely low levels of viral DNA (<200IU/mL) in infected individuals without detectable HBsAg[5]. At times, anti-HBc can be used as a less than ideal surrogate marker for identifying potential seropositive OBI[5] ... https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4357471/

My thought is that all C positives should routinely be given a B PCR.



-- Edited by Canuck on Sunday 9th of October 2016 02:07:25 PM

__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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Re: "Occult" B's

Here's a tidbit ... "The patients who developed HBV reactivation were heterogeneous in terms of HCV genotype. These patients were also heterogeneous in terms of baseline HBV disease, fitting into three general categories of patients: those with detectable HBV viral load (n=7), those with positive HBsAg and undetectable HBV viral load (n=4), and those with negative HBsAg and undetectable HBV viral load (n=3). For the remaining 10 patients, HBsAg status was either not known or baseline HBV could not be interpreted."...

This happens - (the above statement about "could not be interpreted") - the first-tier of common superficial baseline HBV assessment data can be mis-interpreted, (now, it IS RARE) but it can completely miss and not reveal an "occult" BOccult B is rare (ever wondered why!!) haha  So, "occult" B people, have been and can continue to be left out of the equation!! This has always been my big bone of contention!- they have only been warranting and doing further B PCR's based on surface and core antigen/antibody testing, or, (if you are lucky) at best, if the results show up at odds/inconclusive!! Until they start spending the big money to do B PCR's on all types- there are more than 3 divisions in my book - (acute/active, chronic, spontaneously resolved, and the people who are uninterpreted/inconclusive, and, those who show neg but could be occult)!!, how can they say they have screened you to know where you are with B! Common tests can show you to be neg (NOT chronic), and ARE most often very reliable, but, it IS "possible" for a miniscule percentage of the population who are unknown occults, because regular testing misses them, to be virtually an undiagnosed B, until confirmed by B PCR! They don't call it "occult" for nothing! For my wish list ... I believe, at minimum, anyone who has had a case of spontaneously resolved HBV, or shows inconclusive testing interpretations should automatically have a B PCR. They should really just go ahead and do B PCR's on everyone who is C pos! Oh what the hay, how 'bout we just do frequent B and C PCR's, on everybody, period!! hee hee 

A very good OLD study was done showing the limitations of the interpretation of standard baseline B assessments, and as far as I know that study data still stands well today - they determined B PCR is the only way to know for sure if you are an occult B, as rare as being occult may be.



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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I have read (elsewhere) that certain kinds of treatments for chronic HBV may be some easier to tolerate (hold less severe adverse effects or side effects when compared to other treatments), but that importantly, some drug choices may not be quite as effective as other treatment regimes when comparing the outcome/ success rates? Now, they are speaking about a "newer" variation of Tenofovir (Viread)  with less adverse affects? (Had to edit this, as I just realized Viread IS tenofovir (TDF) - the second tenofovir (TAF), in the article below, is supposedly thought to hold less adverse effects).

 

New Tenofovir Formulation Provides Safer Hepatitis B Treatment

By Will Boggs MD - September 30, 2016

NEW YORK (Reuters Health) - A new prodrug formulation, tenofovir alafenamide, effectively treats chronic hepatitis B virus (HBV) infection with fewer bone and renal adverse effects than tenofovir disoproxil fumarate, according to two noninferiority trials.

Tenofovir disoproxil fumarate has potent antiviral activity in patients with chronic HBV infection, but long-term use has been associated with renal toxic effects and reduced bone mineral density (BMD) in some patients.

In the first study, Dr. Henry L. Y. Chan from The Chinese University of Hong Kong and colleagues from 161 centers in 19 countries compared the two formulations in 873 patients with HBeAg-positive chronic HBV infection.

In the second study, Dr. Maria Buti from Hospital Universitari Vall d'Hebron in Barcelona, Spain, and colleagues from 105 centers in 17 countries made a similar comparison in 426 patients with HBeAg-negative chronic HBV infection.

The studies were published online September 22 in The Lancet Gastroenterology & Hepatology.

Both showed that treatment with tenofovir alafenamide met the primary endpoint of noninferiority to tenofovir disoproxil fumarate with respect to the proportion of patients with HBV DNA less than 29 IU/mL at week 48 of treatment.

Among HBeAg-positive patients, BMD decreases at the hip and spine were significantly smaller with tenofovir alafenamide treatment, and patients treated with tenofovir alafenamide had significantly smaller increases in serum creatinine (although the increases were small in both groups).

Results were similar among HBeAg-negative patients.

Both formulations of tenofovir were well-tolerated, and most adverse events were mild to moderate in severity.

The authors of both studies anticipate further long-term follow-up to ascertain whether these outcomes are durable and translate into reduced incidences of bone and renal events.

"Further research and long-term and real-world clinical data are needed to be able to definitively conclude whether tenofovir alafenamide is safer than tenofovir disoproxil fumarate," writes Dr. Willem P. Brouwer from Erasmus University Medical Center Rotterdam, the Netherlands, in a related commentary. "For now, these results for tenofovir alafenamide are very exciting, but might be more of an evolution than a revolution."

Dr. Yao-Chun Hsu from China Medical University in Taichung City, Taiwan, who recently compared the effectiveness of nucleoside/nucleotide analogs in chronic HBV patients undergoing chemotherapy, told Reuters Health by email, "From this trial, we probably can argue that tenofovir alafenamide (TAF) is as efficacious as tenofovir disoproxil fumarate (TDF), at least for 48-week use. TAF potentially can replace TDF as the first-line regimen in the general chronic hepatitis B patients."

"Judging from the superior results of TAF in BMD and renal function, I'd believe that the new agent is particularly preferred in the elderly, postmenopausal women, patients with chronic kidney disease, or those vulnerable to renal injury," added Dr. Hsu, who was not involved in the new work.

But there are some limitations, he said, such as the relatively short trial length and the enrollment of mostly Asian patients.

"Moreover," Dr. Hsu added, "those with advanced liver disease (decompensated status or hepatocellular carcinoma) were not included. All these caveats should be kept in mind when interpreting the results."

Gilead Sciences funded both studies and employed several of the authors.

Dr. Chan and Dr. Buti did not respond to requests for comments.

SOURCE: http://bit.ly/2d868DZ and http://bit.ly/2d85AxL

Lancet Gastroenterol Hepatol 2016.

__________________________________________

Six treatments  

  • Baraclude (entecavir)
  • Epivir-HBV (lamivudine)
  • Hepsera (adefovir dipivoxil)
  • Pegasys (peginterferon alfa-2a)
  • Tyzeka (telbivudine)
  • Viread (tenofovir disoproxil fumarate)

 

 



-- Edited by Canuck on Sunday 2nd of October 2016 04:45:43 PM

__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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Dear Canuck,

you make me laugh. Words are pretty entertaining aren't they? Especially when you're playing with them Canuck. Interesting the apologising thing because I think we're a fairly self effacing bunch here too. Maybe it's something to do with being "just a colonial" although you didn't begin as a prison farm like us. It would have been very satisfying to have it out with those Brits like the US did. Maybe that's the beginning of their patriotism and pride. 

Anyway moving right on from mammary glands, colonials and back to a Hep B And C. 

Syd biggrin

ps. Rampant sexism in the titbit stakes - how about some dick bits for the ladies? ( Spell check is just not having anything to do with spelling those two words as one. Try it, duck it's every time. ) 



__________________

Contracted Hep C 1969. Genome Type 2, treatment naive. Began 12 week RIBA/sof/Dac on 12/11/15. Cirrhosis. VL before treatment 4m. Treatment extended another 12 weeks without Riba. No virus detected at 9 weeks.

Tig


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I love tit bits.... wink



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Tig

61 yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 1-4 years!

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This is Udderly silly smile



__________________

65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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I LOVE words! Especially yours syd!

What man or babe could disagree with the etymology behind "tit", a "choice morsel" or "pleasing bit of something"!

hee hee wheeee

I am a little disappointed though, that you chose not to push the envelope on this one a "bit" more thoroughly, given it's "tender" budding potential. Nipped in the bud?

No one bit on the tit thing! It could have been milked for all it was worth! Oh well. I guess there is no right or wrong when it comes to tits, just entangled differences! hahahahaha

Now, freeing my grey bits from their confines, leaving all thoughts of B's or C's behind, I reflect on this tit issue a bit with wild abandon. Using tid instead does appear more polite on paper. It does fall in line with my Canadian apologizing all the time. (eg. Sorry for saying tit, really I am. Very sorry.) Can't tits be matter pushed to fit within a B/C thing?

Now, lessee, how do I get back into this confining B/C thing, which seems to be exhaustively tits up? Alas, no more 3 letter words for me I guess? Too bad ... I was finding the bit o discussion quite titillating.

I will just let Pablo keep on apologizing, on principal, as he is just a man, and you my dear, do not have to apologize for any perceived lack of pasties.  wink C.



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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Hi guys 

re tidbits

in American and Canadian English, tidbit is the preferred spelling of the noun referring to (1)a choice morsel or (2) pleasing bit of something. Titbit is preferred everywhere else. Neither spelling is right or wrong. Titbit is older, but tidbit is etymologically justifiable ( the first syllable likely comes from the archaic colloquialism tid, meaning tender. ) and tidbit is not so new itself; it was well established in American English by he early 1800's

aarh - there's nothing quite as irritating as retired English teachers who have a tendency to become pedants. Apologies to all. Canuck, you have used the word before and I thought to myself - WTF, since when did tits become tids?    But I knew in Australia it is definitely titbits, being, as you know, rather obsessed with bits belonging to either gender. Then when I saw Pablo apologising for his xx chromosomes I had to look it up. Too dumb to cut and paste but got there in the end anyway. So now I've got my tids in a tangle, I'll back out of a sensible discussion on Hep B and C co infection. 

Syd biggrin



__________________

Contracted Hep C 1969. Genome Type 2, treatment naive. Began 12 week RIBA/sof/Dac on 12/11/15. Cirrhosis. VL before treatment 4m. Treatment extended another 12 weeks without Riba. No virus detected at 9 weeks.



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In my case had I been active with B, I was told I would just start being treated for both at the same time. The C of course expected to be cured and the B controlled since that is the best they can do right now.

I am hoping since I fall into the category that my B does not reactivate but I suppose there is always that possibility.

 

SF



__________________

65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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Cinnamon Girl posted about the new guidelines the other day - treat B either BEFORE or AT same time as C - an important part of the guidelines - this article speaks of it too - (perhaps this one though, leans away from the "either/or" and more suggests B should be treated prior to C)? Trouble with this recommendation (to look for HBV and do HBV pre-testing) is that it may not go far enough, what with dormant/occult HBV's, and the dependence on using standard markers that do not reveal same, there is a reluctance to spend money on B PCR's which is the sure way to reveal a truly hidden B status.
 
Medscape Medical News

Guideline: Test for HBV Before Treating Patients With HCV

Bridget M. Kuehn

September 22, 2016

 

"The most important thing is that [HBV] be attended to before you get going with [a] course of treatment for [HCV]," Dr Chung said.

Patients with low or undetectable levels of HBV who do not meet the criteria for HBV treatment should be carefully monitored during direct-acting antiviral treatment for co-occurring HCV, the guideline recommends. Dr Chung noted that some patients have developed very serious illness as a result of reactivation, so vigilance is critical.

"The fact of the matter is there is no substitute to being attentive if you decide not to treat or the patient doesn't warrant treatment," he said.

One issue that still hasn't been resolved is what to do with patients who are surface antigen negative for HBV and positive for anti-HBV core antibodies, Dr Chung noted. He explained that those patients are not considered chronically infected. However, there is at least one case report of HBV reactivation in such an individual.

There also are still many questions to be resolved, and more study is needed. For example, Dr Chung noted, it is not yet clear how often HBV reactivations occur in HCV coinfected patients during direct-acting antiviral treatment for HCV, and not all studies have documented these reactivations.

"The data are mixed, and we need much more data collection to fill in the picture, but until then use caution," Dr Chung said.

Dr. Chung reports no direct financial conflicts of interest, but he has received institutional research grants from AbbVie, Bristol-Myers Squibb, Gilead Sciences Inc, Janssen Therapeutics Inc, MassBiologics, and Merck & Co Inc. Disclosures for the full guideline panel are available online.

 

 

"HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C." American Association for the Study of Liver Diseases and the Infectious Diseases Society of America. Published online September 16, 2016. Full text



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)

Tig


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Hey C,

Thanks! The CDC has some great information. It's a great resource for anyone looking for just about anything. Our tax dollars hard at work. I have a nephew in law (lol) that is a biologist for the CDC, he loves it.

SF,

HBV is an interesting virus. The way it's selective in whom it infects, their age and if it becomes chronic. I would call that a fickle virus. I do know a woman that contracted it and like you SF, was quite ill during the acute phase. Recovered nicely too. I met her at my last hepatologist's office. There were some interesting people in those waiting rooms! 

I think having had both viruses active at the same time would certainly be enough to whip you silly. I'm glad you don't have to deal with that anymore!



__________________

Tig

61 yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 1-4 years!

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Hi Canuck,

Thank you so much for all this information. Yes, when I contracted these I was clinically ill pretty quickly although I cannot say 2 weeks, it was withing months for sure. I actually went to my doctor and told him, Hey, I have Hep to which he said looking at me .. "You're probably right"

The next seven weeks were spent in bed and I don't even want to think about those symptoms. It became clear to me this year that it had to have been the HBV that put me down, not the C since most people who contracted it never knew for decades. Of course thee is the possibility of them both doing it but I guess I will never know.

How are you?

 

SF



-- Edited by Shadowfax on Friday 26th of August 2016 04:30:20 PM

__________________

65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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Just more review about HBV:

Hepatitis B

Like hepatitis A, hepatitis B in adults produces hepatocellular enzyme level elevations (AST and ALT predominate). In adults who acquire hepatitis B, the infection almost always clears, but antibodies persist. In a few, the disease does not resolve but becomes chronic. These patients retain serum markers of viral infection. Many blood tests are available for hepatitis B antigenic determinants and their antibodies. It is best to separate testing appropriate for the acute hepatitis situation from testing for chronic liver disease caused by hepatitis B. Only a few tests need to be considered by the generalist to determine the status of a patient with possible hepatitis B. A full discussion of hepatitis B can be seen in the Disease Management chapter on Hepatitis B.

Acute Hepatitis B

Hepatitis B surface antigen (HBsAg) emerges within 2 weeks of exposure but can often be delayed for weeks or months. This antigen is present in the blood for a variable period, usually encompassing the time during which the patient is clinically ill and most likely to seek medical attention. In patients with mild symptoms whose testing may be delayed, the HBsAg level may have already declined. In this case, a second chance to make the diagnosis comes from detection of the IgM antibody directed against the hepatitis B core (HBc) antigen, anti HBc-IgM (Table 6). Similar to the testing for acute hepatitis A, selective testing of serum IgM anti-HBc is required to establish a diagnosis of acute hepatitis B in patients whose HBsAg levels have already declined. The total anti-HBc antibody test will be positive in the presence of either anti-HBc IgG or IgM.

Table 6. Common Hepatitis B Testing Results
TestResultInterpretation
HBsAgNegativeSusceptible
Anti-HBcNegative 
Anti-HBsNegative 
HBsAgNegativeImmune due to natural infection
Anti-HBcPositive 
Anti-HBsPositive 
HBsAgNegativeImmune due to hepatitis B vaccination
Anti-HBcNegative 
Anti-HBsPositive 
HBsAgPositiveAcutely infected
Anti-HBcPositive 
IgM anti-HBcPositive 
Anti-HBsNegative 
HBsAgPositiveChronically infected
Anti-HBcPositive 
IgM anti-HBcNegative 
Anti-HBsNegative 
HBsAgNegativeInterpretation unclear 4 possibilities:
Anti-HBcPositive1. Resolved infection (most common)
Anti-HBsNegative2. False positive
  3. "Low level" chronic infection
  4. Resolving acute infection

From: Interpretation of hepatitis B serologic test results. Centers for Disease Control and Prevention website. www.cdc.gov. Accessed June 27, 2013.

In acute hepatitis B, medical attention is not sought early. In such cases the HBsAg may have already disappeared. The anti-HBs will not yet have emerged. Thus the sole viral marker may be anti-HBc. This same serologic pattern may be seen years after infection when the titer of anti-HBs is low. Sorting out the difference between late resolved hepatitis B and the period in acute hepatitis B described above can be achieved by testing for anti-HBc IgM which will be positive during this so-called "window period" of acute hepatitis B.

Chronic Hepatitis B

Chronic hepatitis B is characterized by persistence of HBsAg for a period longer than 6 months with positive anti-HBc (IgG), and negative anti-HBs. An additional antigen-antibody system plays a role in patients with chronic hepatitis B and requires mention: the hepatitis B e antigen (HBeAg) and its antibody (anti-HBe). HBeAg positivity in chronic hepatitis B usually indicates active viral replication and significant liver injury. In time, HBeAg may be lost, replaced by its antibody, anti-HBe. This transformation is often associated with lower level infection (less viral replication) or HBV DNA, lower AST and ALT values, and less (or no) hepatic inflammation.

Reactivation Hepatitis B

Hepatitis B reactivation is a sudden increase in hepatitis B virus (HBV) replication or the reappearance of active inflammatory disease of the liver in a patient with previously documented resolved HBV, or with the inactive HBsAg carrier state. Reactivation is usually triggered by immunosuppression in the host, which can occur following the use of chemotherapeutic agents for malignancy and following therapy for autoimmune diseases or organ transplantation.

Reactivation can also occur spontaneously. The extent of clinical manifestation from reactivation HBV can vary from a transient, clinically silent disease to severe or acute liver failure. A chronic infectious state can also be seen following HBV reactivation. Diagnosis of HBV reactivation depends on the HBV disease state before activation. In a patient with resolved infection (negative HBsAg and positive anti-HBs), reactivation is indicated by the decline in anti-HBs and the reappearance of HBsAg. In patients with quiescent HBV with positive HBsAg, reactivation is diagnosed by a rise in the serum HBV DNA (>1 log10 IU/mL) or a rise in the serum ALT levels (>3 times baseline). Reappearance of HBeAg in a patient with previous negative HBeAg also indicates HBV reactivation.

Role of HBV DNA Assays, HBV Genotypes and Liver Biopsy in Chronic Hepatitis B

HBV DNA level plays several important roles in chronic hepatitis B. It is the most important factor for predicting the progression to cirrhosis, helps to determine the need for treatment in HBeAg negative patients, and also plays a crucial role in estimating the response to treatment. Up to 8 HBV genotypes, labeled from A to H, have been identified. Recent studies have shown that some genotypes are associated with early HBeAg seroconversion, less progression to cirrhosis and hepatocellular carcinoma, and may also predict the response to treatment with interferon. These concepts and exceptions are discussed more fully in the Hepatitis B chapter. A clinical practice guideline on viral hepatitis B has provided additional information on laboratory testing in various contexts of hepatitis B infection.7

Resolved Hepatitis B and Immunization Status

As indicated in Table 6, an individual with resolved hepatitis B infection almost always has anti-HBc and anti-HBs. An individual successfully immunized against hepatitis B expresses only anti-HBs. Confusion may occasionally arise in the interpretation of hepatitis B tests in a patient who has recovered from hepatitis B many years ago and who has a low or absent level of measurable anti-HBc.



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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Pablito wrote:

Canuck - as always, you are a fountain of knowledge.

Further, I never knew "tidbit" was spelt thus; for most of my life I have been offending one half of the planet whenever I've used that word....for this I can only apologise to my XX chromosome compadres and blame it on my ignorance.  


Hee hee - Pablito, sometimes you (and Cheddy) just kill me!! Tit-bits, lady-bits, wife units, Cheddy's old girlfriend and her entertainment employment improvements, looking for the go-to guy for yeast in all the wrong places. Wheee, where's syd, she's missin out on some inspiration here!

Your phonetic "tit-bits" reminds me of another word I LONG held (since childhood) ... until (fairly recently) when I saw it spelled out one day - I always thought those heightened cold temp warnings they refer to, to make you respect decisions about heading out on trips over some blizzardy windy highway, was "the windshield effect".  



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)



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Loopy Lisa wrote:

I know that you can only contract Hep D if you have B. But it actually kinda sucks. One is dominant over the other, until the other is resolved. So, you treat one to get the full force of the other if it hasn't spontaneously cleared by the immune system. I do hope they can find a decent cure for Hep B. I was suprized hep B is much more contagious than C, yet they chose to cure C first. The mind boggles, although of course I am happy there is a cure. It is interesting all these interactions, although it must be worrisome for dual infected.....



-- Edited by Loopy Lisa on Tuesday 2nd of August 2016 07:17:44 AM


 Exactly right Lisa because when I was at the hospital for my consultation regarding Hep B and starting Harvoni, I specifically asked the specialist (and these are the leaders in the world at this hospital) about being tested for Hep D. I was told that it cannot exist without B being active and since it seemed I may have cleared it, there was no reason to investigate at that time. Still waiting to hear about my C and B status. It will be 14 days this Tuesday that I had my labs done. I will start calling since my appointment is not until the end of August. I am just not waiting that long. In my mind, they are both gone.

SF



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65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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I know that you can only contract Hep D if you have B. But it actually kinda sucks. One is dominant over the other, until the other is resolved. So, you treat one to get the full force of the other if it hasn't spontaneously cleared by the immune system. I do hope they can find a decent cure for Hep B. I was suprized hep B is much more contagious than C, yet they chose to cure C first. The mind boggles, although of course I am happy there is a cure. It is interesting all these interactions, although it must be worrisome for dual infected.....



-- Edited by Loopy Lisa on Tuesday 2nd of August 2016 07:17:44 AM

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VL.�over 15, 000 000

Failed TX 2014: Interferon/Riba.

Cured using Sof/Dak combination.

I can eat cake again! <3 



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Can't really say with any authority RC, all I know is that ALL HEPATITIS is BAD (by B, by C, by both, or by any other "letter" or causative reason for the inflammation and the consequences of long term damage and dysfunction)!! We all know that after packing HCV for a couple decades we are all at higher risk for HCC, same applies to B. And, B and C (together) can be quite a different animal - seems it's complicated!

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047495/

http://www.ncbi.nlm.nih.gov/pubmed/20483498

 

... "There are suggestions that the presence of hepatitis B virus (HBV) gene in patients with chronic HCV-associated liver injury appears to promote hepatocarcinogenesis.[33] Similar to most types of cancer, hepatocarcinogenesis is a multistep process involving different genetic alterations that ultimately lead to the malignant transformation of the hepatocyte.[34] In most patients with HCV-related HCC, the tumors are more likely to be solitary, smaller sized, and encapsulated, whereas, HBV-related HCC are more commonly infiltrative and multinodular.[35] " ...

There are just TONS of studies out there, about the downsides of having ANY kind of hepatitis, B/C or combo's there of. B and C primarily being blamed for HCC. The one study above shows less incidence of  HCC developing as a consequence of having your chronic B treated/controlled, much like what we are trying to achieve by treating our chronic C. 



-- Edited by Canuck on Tuesday 2nd of August 2016 05:08:57 AM



-- Edited by Canuck on Tuesday 2nd of August 2016 05:13:03 AM

__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

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Knowing that both B&C are not good, is one worse than the other?  RC



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 M-61 (3 Treatments)( SOF-RIBA 2014)(SOF-RIBA-PEG 2016)(HCC 2016) (LIVER TRANSPLANT 8-2017)(VOSEVI-RIBA 2017) On my way to SVR.    SVR-12. 3-13-18



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Canuck - as always, you are a fountain of knowledge.

Further, I never knew "tidbit" was spelt thus; for most of my life I have been offending one half of the planet whenever I've used that word....for this I can only apologise to my XX chromosome compadres and blame it on my ignorance.  



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44 y.o. male, HCV G4 since 1996, F-scan score 9, F2, Failed prior I/R, finished sof/vel/vox 8 weeks 5/16, pre-treatment VL 2 million, EOT UND, EOT+4 UND, EOT+12 UND.

Tig


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Good stuff you two! It's good to have a thread and discussion on the HBV and HCV coinfection that can be researched and will expand our knowledge base. There's a lot of technical information and studies involved in these reports, but those interested will always glean some useful information by reviewing them. It helps to connect the dots. Thanks for your continuing efforts to educate the masses!



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Tig

61 yo GT1A - 5 Mil - A2/F3 - (1996) Intron A - Non Responder, (2013) Peg/Riba/Vic SOT:05/23/13 EOT:12/04/13 SVR 1-4 years!

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I found my original thread and will post it here and at least one older article regarding this subject. I am sure there is a lot more information in this thread as it was discussed and some of the related problems that could come up.

 

http://www.healio.com/gastroenterology/curbside-consultation/%7B5453133c-3fa4-443d-abb1-81fbae9047e1%7D/how-do-i-treat-a-patient

Now below is my coinfection thread!

[/url]http://hepcfriends.activeboard.com/t61453315/hbvhcv-coinfection/?page=1&sort=newestFirst[/url]

 

SF

 



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65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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Excellent!

Thanks Canuck and Shadowfax, sharing what you've learned regarding the co-infection of Hep B & C is greatly appreciated.

Thanks for ALL that you both do on a regular basis ... it's appreciated!!

 

Dave



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63yy,HCV,2b,F3-A1, Sof/Riba,12wks Tx   SOT: 1/20/16, HCV-RNA 9,816,581, ALT 56, Hb 14.6

4wk: HCV-RNA <15 Detected, ALT 15, AST 17, Hb 13.6 EOT: 4/12/16, ALT 18 , Hb 12.9176a2f85d05d9c965eafe199f2ba9ba5.jpg SVR Achieved 7/8/16

 



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Interesting information Canuck. I will look through the forum to find anything that I had found in the early year and posted. I do know when I introduced myself, I did talk about B and C and did post some studies that I had found. We did have a thread buried deep somewhere on B and C co-infections.

Thank you for sharing this and finally I found something you did :)

Sf



__________________

65 yo, GT1A, , Cirrhosis, F-Scan F4 33.5, TX Naive Harvoni 12 wks

SOT 2/9/16 / ALT 187 AST 114 VL 2.3M.    POSTS

EOT 5/2/16  ALT 35/ AST/25  platlets 126 C/B VL UND

EOT +12 7/26/16  ALT 25 /AST 22/ ALP 83  platlets 129 C/B VL UND

EOT + 24 10/18/16 ALT 27/ AST 20/ ALP 71 platlets 153 C UND

 * SVR *



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Relating to having contracted HBV and HCV infections (at the same time).

Shadowfax and I hold a particular interest, in those of us who contracted both HBV AND HCV at the same time (whether we subsequently spontaneously "naturally" resolved our B, or not), and just continued on having chronic C, or, whether we continued on, to harbor both chronic B and C.

He and I have shared quite a few studies and info relating to this subject. We should have been posting them, all along, in a thread, for possible interest by others who are being treated for HCV now (and perhaps had HBV in the past), or, for those who currently are chronic B and C. I lament now that we did not start a thread way back then on this subject, as so many of these studies would be hard to dredge up again.

At best, holistically, I find it a daunting task to fully understand "the basics" on HBV (and then, add to that, all of HBV's nuances, idiosyncrasies and co-relationships) - they are weighty, complex, convoluted and gangley subjects to absorb. There are MANY articles/studies out there, on many aspects of HBV, but the ones that BEST interest me are the ones which dwell on or relate to (1) occult versus overt HBV, (2) those of us who were simultaneously infected with HBV/HCV, and (3) various combinations of HCV accompanied by active/chronic, "dormant" HBV, or "supposedly" spontaneously passively resolved HBV.

Shadowfax and I noted some interesting theories about the birth of B and C "co-infections". There is an interesting "initial" co-existence moment the 2 viruses share at the start of infection/replication, and then, many studies lean to and support the theory about C becoming the "dominant infection" over B.

Without any of the background thread info on HBV, I just jump ahead to the most recent tidbit I found on HBV (it's a meaty read). But this study did NOT really draw my interest in it's HCC perspective, rather , it was the one skinny comment it contained which lead me back to the theory of B, or C, being "dominant" over the other that piqued my interest ... the tidbit comment dumps the C dominance theory backward on it's head for a change! This B/C dominance theory seems to be batted back and forth like a tennis match! The study did also draw my attention just because they were considering and doing comparables between "occult and overt" B people. (Occult B is very interesting subject to me all in itself, and far as I have read, having occult B cannot be ascertained by any other means other than by having a B DNA PCR done).

 

Occult, overt HBV coinfection predictive of outcomes from HCV-associated HCC

Chang M-L. PloS One. 2013;doi:10.1371/journal.pone.0064891.

July 16, 2013

Disease-free survival after surgical treatment of hepatitis C-associated hepatocellular carcinoma was significantly influenced by occult or overt hepatitis B coinfection in a recent study.

Researchers evaluated liver tissue from 115 patients with HCV-associated hepatocellular carcinoma (HCC) who underwent total surgical removal of tumors between July 1998 and August 2001 at Chang Gung Memorial Hospital in Linko, Taiwan. All tissue was collected from the noncancerous parts of the removed HCC.

Chau-Ting Yeh

"Theoretically, occult HBV-infected patients can have negative serum HBV DNA and negative serum HBsAg, but positive liver tissue HBV DNA," researcher Chau-Ting Yeh, MD, PhD, director of the Liver Research Center at the hospital, told Healio.com. "[However,] it is very difficult to identify such patients. Using surgically removed HCC tissue, we have an excellent opportunity to look into this issue."

Overt hepatitis B coinfection (HBVCI) was observed in 35 patients, and occult coinfection was observed in 16 patients. These groups had similar HCV RNA levels or HCV genotype. Among 12 patients with positive anti-HCV but negative serum and tissue HCV RNA, nine patients had overt and one had occult HBVCI, suggesting that HBV repressed HCV replication, Yeh said.

Significant associations were observed between poor disease-free survival and occult HBV infection (adjusted HR=2.708; 95% CI, 1.317-5.566) and lack of overt HBVCI (aHR=2.216; 95% CI, 1.15-4.269), along with alpha-fetoprotein levels above 8 ng/mL (aHR=5.976; 95% CI, 2.007-17.794), albumin levels of 4 g/dL or lower (aHR=2.539; 95% CI, 1.399-4.606), ALT of greater than 50 U/L (aHR=1.086; 95% CI, 1.006-1.172) and tumors greater than 3 cm (aHR=2.079; 95% CI, 1.149-3.761).

Compared with patients with overt HBVCI , those with occult infection had shorter overall (P=.026) and disease-free survival (P=.002), higher bilirubin levels (P=.003) and were more likely to have precore G1896A mutations (P=.006.

"In HCV-associated hepatocellular carcinoma, patients with overt HBV coinfection had a better postoperative prognosis, whereas patients with occult HBV coinfection had a poorer postoperative prognosis", Yeh said. "A significant proportion of patients had occult HBV infection, and these patients had a higher bilirubin level, suggesting a poorer functional reserve. This observation is consistent with the fact that such patients had a poorer postoperative outcome. Intriguingly, patients with overt HBV coinfection actually had a better postoperative outcome."

 

 

 



__________________

HCV/HBV 1973. HBV resolved. HCV undiagnosed to 2015. 63 y.o. F. Canada.

GT3a, Fibroscan F3/12 kPa - F4/12.6 kPa, VL log 7.01 (10,182,417), steatosis, high iron load.

SOF/VEL with/without GS-9857 trial - NCT02639338.

SOT March 10 - EOT May 5, 2016 - SOF/VEL/VOX 8 week trial.

 

(SEE UPDATES IN BIO)

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