Hcc and male question

Question

For experts and studyforhope.

I would like to know some good statistics on hcc as all i see the one overall 35 percent will develop hcc from carriers so the questions are below:

1) male is dominant so out of the 35 percent hcc. male will be the most in danger. so should we say most male will develop hcc or at least 50 percent of male?

2) they say vertical transmitted so also the hcc is highest in these ppl aquired at birth 

3) male with cirrhosis is 60 percent vs 40 percent non corrhotic so for non cirrhotic is still high so why we dont treat even nonliver damage?

4) life expectancy. We say we will live long and die from something else however that contradict lot of search were they say most between 40 and 60. I don't want to sound pessimistic and sorry guys just trying to get some help with all these complicated disease.

Based on above are we saying most male who aquire at birth will develop hcc by age 50?

studyforhope · Accepted Answer

here is a meaningful extraction from two papers that try to estimate the HCC risk in general and with regard to NA treatment and then in the end to account for the particulars of a specific patient by calculating a risk score:

Please note that this topic is very complex, thats why it is recommended to read at least the abstracts of the numerous papers dealing with it.

Race and Genotype play a role as well.

 Recently published studies show that in CHB patients treated with the currently recommended first-line nucleos(t)ide analogs (NAs) entecavir or tenofovir, annual HCC incidences range from 0.01% to 1.4% in non-cirrhotic patients, and from 0.9% to 5.4% in those with cirrhosis. In Asian studies including matched untreated controls, current NA therapy consistently resulted in a significantly lower HCC incidence in patients with cirrhosis, amounting to an overall HCC risk reduction of ∼30%; in non-cirrhotic patients, HCC risk reduction was overall ∼80%, but this was only observed in some studies. 

Natural history studies in untreated patients have reported annual HCC incidences of 0.3–0.6% in non-cirrhotic patients, and 2.2–3.7% in compensated cirrhotic patients, with the highest rates observed in Asia 

Epidemiologic studies have confirmed sustained viral replication and liver injury as key risk factors for HBV-related HCC, with serum HBV DNA levels directly correlating with the future risk of HCC [8] and [9]. Specific variations in the HBV DNA sequence, such as HBV genotype C and basal core promoter (BCP) mutations have also been associated with a higher HCC risk [10], [11] and [12]. In addition to these viral factors, older age, male gender, heavy alcohol consumption, exposure to carcinogens such as aflatoxin B, a family history of HCC, and more recently, elevated levels of quantitative HBsAg (qHBsAg). Metabolic syndrome associated with obesity and diabetes mellitus have also been established as risk factors of HBV-related HCC.

Here an algorithm is given to account for a patients particulars when calculating his risk. A total score is compounded from the partial scores.

	Hazard ratio (95% CI)                                 	Risk score
Sex
Female	1•00         ..	                                        0
Male	2•2 (1•4–3•4)                                              	2
Age (years)
Per 5 years	1•64                                           	1
30–34	..	..	..	0
35–39	..	..	..	1
40–44	..	..	..	2
45–49	..	..	..	3
50–54	..	..	..	4
55–59	..	..	..	5
60–65	..	..	..	6
ALT (U/L)
<15	        1•00	                        .	                                0
15–44	1•5 	                                                                1
≥45	        2•6                                                            	2
HBeAg
Negative	1•00	                       ..	                                0
Positive	2•3                                                            	2
HBV DNA level (copies per mL)
<300 (undetectable)	1•00	                                      ..	0
300–9999	1•1                                                            	0
10 000–99 999	3•7                                                    	3
100 000–999 999	9•7                                            	5
≥106	8•1                                                                    	4*



Now the total risk score can be used in combo with the duration of the risk to calculate the time adjusted risk :

Cumulative risk score and associated 3-year, 5-year, and 10-year risk of developing hepatocellular carcinoma in patients with chronic hepatitis B
	3 years	5 years	10 years
0	0•0%	0•0%	0•0%
1	0•0%	0•0%	0•1%
2	0•0%	0•0%	0•1%
3	0•0%	0•1%	0•2%
4	0•0%	0•1%	0•3%
5	0•1%	0•2%	0•5%
6	0•1%	0•3%	0•7%
7	0•2%	0•5%	1•2%
8	0•3%	0•8%	2•0%
9	0•5%	1•2%	3•2%
10	0•9%	2•0%	5•2%
11	1•4%	3•3%	8•4%
12	2•3%	5•3%	13•4%
13	3•7%	8•5%	21•0%
14	6•0%	13•6%	32•0%
15	9•6%	21•3%	46•8%
16	15•2%	32•4%	64•4%
17	23•6%	47•4%	81•6%

Royal36 · Answer

Got it. Thanks sorte.

sorte · Answer

it's a bit different one, k2mk7 helps to move calcium from arteries to bones/teeth and Stef has written about k2mk4 which was proven to increase protection against hcc in some study.
It's good to take k2mk7 when you supplement d3, because d3 increases calcium absorbtion.

Royal36 · Answer

The one i have is vitK2 MK-7 a bio active form from Natto.

stef2011 · Answer

k2 mk4 is synthetic, not natural form, at least the one i use

http://www.iherb.com/Advanced-Orthomolecular-Research-AOR-Advanced-Series-Peak-K2-90-Veggie-Caps/33052

no soy, gluten...and all other rubbish contained

sorte · Answer

but k2mk4 is made from soy too, so need to wisely choose supplier

stef2011 · Answer

so difficult to be sure we dont get gmo soy...i think it is easier to use vit k2 mk4 45mg to prevent hcc

sorte · Answer

http://www.andjrnl.org/article/S2212-2672%2812%2900472-8/abstract

I'm not the big fan of soy :) any replacements ?

sorte · Answer

You mentioned something about "integration and genome disturbance". I guess it's hard to predict how many years it takes for the virus to obtain it cuz it's person dependant ? 
If integration has already happend but person will lose HBsAg and will have no replication and inflamation a risk is very low but still exists ?
I hope birinapant will pass the trials, I suppose it will solve a problem for good not like other drugs just "functional cure"

StephenCastlecrag · Answer

Good article, thanks.

stef2011 · Answer

the easiest thing is get peg and clear hbsag when vit d3 is optimum and forget about hcc then

hitman76 · Answer

Here's the link on same which has a video presentation and references as well...

http://onlinelibrary.wiley.com/enhanced/doi/10.1002/cld.158

mike9111 · Answer

Also one thing i never gets form my ultrasound report that it say "subtle coarsened liver" and everything else normal. My professor last year interpreted as "it is just and inflammation" however latest fibroscan was 4.8 kpa. I thought coarsened comes mostly in cirrhosis but i don't have cirrhosis. Maybe this time i will do MRI instead

mike9111 · Answer

Thanks studyforhope for your patient with me. My hbv dna always fluctuated even on monthly basis between as low as 300 iu/ml to as high as 20000 iu/ml. I will go to my general physician as i know he will order an ultrasound and i do really hate to go behind my professor back to do this but i have to protect myself and have kids to raise. You are doing a great job here in forum just like stef and i do appreciate you taking ur time to explain all this

studyforhope · Answer

While the risk obviously increases with time, i dont think you can say that it simply accumulates. If your risk for a car accident is 2% in one year, it does not mean that if nothing happened to you in 20 years that you are now ripe with a risk of 40%.
In your particular case, since both DNA and hbsag are low, at least now further  risk progression should be very very slow. but we dont know if you had prior episodes in which replication and inflammation were high. These could certainly prepare for later HCC.
IMO, since the ultrasound scan,  if it is done at 6 month intervals, promises a high cure rate in case of positivity, it should be done if someone can afford it. Because nobody can know all the past factors that you had existing and all the statistics find its limits in that fact.

mike9111 · Answer

thank you so much. Just a dummy question if we take the following example:

"Natural history studies in untreated patients have reported annual HCC incidences of 0.3–0.6% in non-cirrhotic patients"

So for someone at age 37 is it correct to say that since aquired at birth we take 0.6 * 37 = 22 

so the risk is 22 percent? I understand the risk score well but i'm trying to understand the annual HCC risk of 0.6 % factor

Thanks again for your quick response

mike9111 · Answer

Also how acurate in your opinion the REACH-B model to predict hcc in 5, 10 and 15 years?

mike9111 · Answer

Thank you so much for that

studyforhope · Answer

Some articles have free access to full text. I will check it later once i have time to see if a meaningful summary answer can be given, considering the various factors influencing HCC propensity.

mike9111 · Answer

I don't have access to full article. Do you have a summary of the percentages and from your experience?

studyforhope · Answer

there are many papers re HCC incidence with percentages in different  infected groups and then, within those already having HCC, in what way they distribute to the various groups. Those are quite different percentages.

Best read many of these abstracts directly in pubmed.gov. You search for HCC and hepatitis B. then restrict it to reviews, or trials.

there is no question that infection at birth with the high replication for many years gives a higher chance for integration and genome disturbance leading to cancer than an infection acquired late in adulthood.

mike9111 · Answer

Any comment?

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