Forum Replies Created
-
AuthorPosts
-
Different labs, even different labs within the same franchise, often use different tests, instruments, and laboratory personnel and each can introduce a small amount of variability. Most labs though have a fairly reliable degree of accuracy and precision. For accuracy, consider a dart board with a dart in the centre. For precision over a number of tests using the same sample think of a dart board with a cluster of darts on the board but not necessarily in the centre. What you would prefer obviously is that a test(s) was both 100% accurate and precise, clustered darts in the centre, but it just isn’t possible. Lab results tend to be accurate and precise enough, especially if you use the same lab all the time. If they weren’t, pathology labs would lose accreditation. With most results, the important thing usually is how they change over time rather than the actual numbers themselves.
So, different labs have different ranges because they’ve factored in their equipment and their methodology, the equipment they do tests with and how they do it.
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…”James-Freeman-facebook” wrote:Yes but the reduction in Hepascore happens within days, whereas the Fibroscan results take weeks/months to fall and will remain usefully indicative.
Yes, bloods seem to react quickly, and whilst GGT can come down reasonably quickly (though probably the slowest to react) bilirubin can sometimes sharply elevate, confounding the test all over the place.
An interesting one with the AbbVie meds seems to be an almost immediate bounce in platelets, and I know they were claiming it as a sort of surrogate marker for improvement in hypertension. Seemed a ridiculous claim to me given the time frame. Mine have improved a lot from baseline though.
With normal LFTs happening rapidly the Hepascore rapidly becomes inaccurate on treatment.
In a perfect wold you get a Fibroscan before treatment but if it’s not possible and you don’t want to wait…..
Why aren’t they deployed more? I assume inexperienced users can be a problem but why have them sitting around when they are obviously so useful?
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…Gaj wrote:Single units, both 8-10mm. S5 Resect – clean.
So both stage 1. That’s good. Took segment 6 with me.
S? RFAblation – radiologist pleased & CT last week with results at monitoring visit next week and no urgent calls so sounds good. Pretty much the same comments as you. Failed Peg/riba 2013 so close monitoring. Bloods went silly this year so u/s upped to MRI and CT and confirmed #1. Came out clean so thought okay. First 3mth scan in Sept picked up the other one. Found Greg then the club the same week as doc called me and here I am.
G
Sounds like you’ve been well-handled. Cool stuff. The AbbVie meds have put my AFP into low normal range, which means no suss cells.
All the best!
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…Gaj wrote:. Resect in Jun and ablate last month.
Cluster of tumours? What sort of ablation? Did they get it? I had a HCC resected back in ’06, which was switched on by IFN/riba. Lucky it was really since AFP was high and the cancer was lurking, and when it turned feral I was being closely monitored. AFP started going exponential and they picked it up via U/S when it was about the size of a small pea. Also only a single tumour and fairly peripheral. Lucky all ’round. It was an aggro sucker though, no doubt fed by the iron in my system from riba action on my red cells.
Was so grateful to find the club in Oct and get tx. Three weeks in now and you’re right about the differences. Didn’t realise how down I was, just going through the motions so as not to worry others too much. Still a way to go but I feel alive again and ready to greet each day. Amazing what a bit of hope does.
Awesome. All the best!
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…Gaj wrote:Btw good reduction in F score Dallo. Your LFTs must have been pretty high pretreatment?
Yeah, they were, mate. AST wasn’t too bad but ALT was in the 200s and GGT about 300. I was lucky enough to get into the first AbbVie compassionate access program but there were months of red tape. The TGA had to pass individual treatment plans, something which had never been done in Australia before for HCV+. Seemed clear there’d be no problems (HIV+ had done it), but geez, it was a stressful time. And then there were some problems getting the meds from where they’d been made. It was all a really nervous time and the stress was bad. Sent my LFTs through the roof sky-high at a time when my liver seemed to be transitioning Child-Pugh A —> B. Technically that would’ve made my place in the Access dicey since they were only treating compensated cirrhosis. I lost weight. It was a bad time. I had some edema and ascite which got much worse until I restricted sodium, and numbers of key markers were mostly going south.
Got the drugs and felt unbelievably better within the first week. Mind fog cleared, I had more energy. depression I didn’t even know I had lifted, appetite improved, lots of other stuff. Just turned me around. Not that it really matters but I was UND by week 5. Never panicked about bloods after that because I simply knew the filth had gone. I felt too good, and having relapsed before I know how that feels.
My liver dude is really optimistic, feels that I should experience considerable regression of my situation. Having read a bunch of recent studies I’m not so sure, numbers say it’s about the toss of a coin for significant regression, but hey, I’ll take it
Cheers!
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…In the light of day with a clearer head, I withdraw the question. There’s no doubt in my mind that ALT (in HCV context) is a good surrogate marker for liver inflammation, which means that higher ALT equates probably with higher fibroscan score. However, if you remove the inflammation, or most of it, as would likely occur with a decent response to the DAAs then you might actually get a clearer picture of the true situation re fibrosis if you deploy a fibroscan, and so performing that test during Tx to decide whether liver damage warrants Tx extension is actually a reasonable idea.
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…Gaj wrote:Hi Dallo,
The inflammation and progression will slow and stop but the bridging/scarring that makes the liver stiff and is what the fibroscan measures takes much longer to heal. Similar to scars on your skin, it fades with time but it’s a slow process and probably never totally resolves.
G
I don’t think that’s correct. The inflammation adds significantly to the “stiffness” as well. It’s late here but I’ll try to find something in the Lit tomorrow. Personal anecdote: I recently treated and SVRed with the AbbVie meds (EOT January). My baseline fibroscan was 60.4. It was checked again when I had week 24 follow-up bloods done.and was 29.2. Still quite bad obviously but much, much better than baseline. Possible there was a little improvement in the histology but the only real explanation for the difference was cessation of inflammation. Same person ran both scans. 10 passes each time.
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…Assuming a decent initial response then wouldn’t fibroscan be lower also ie reduced inflammation?
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…LondonGirl, a VL drop of 2.5M to 900K is only about 0.4 of a log and isn’t significant. VL can vary quite a lot day to day, and certainly over months.
If you”boost” your immune system somehow, ie make it work better, then you are more likely to have less liver damage. It’s correct that your immune response will take out infected liver cells however a decent immune response is more likely to act like a sniper whilst a response that isn’t so good like a shotgun.
Except in special circumstances with genotype 3 (steatosis), viral load has no correlation with liver damage, and thus no correlation with ALT.
edit: reply is to a post at beginning of thread.
More on topic: Extra-hepatic manifestations of HCV: https://www.google.com.au/url?sa=t&rct=j&q=&esrc=s&source=web&cd=1&cad=rja&uact=8&ved=0ahUKEwialtPxk87JAhWE56YKHXpUA7gQFggiMAA&url=http%3A%2F%2Fhcvadvocate.org%2Fhepatitis%2Ffactsheets_pdf%2Fextrahepatic.pdf&usg=AFQjCNEwpORbaAP0t0w42oruo-g0_wq2Jg&sig2=zcAyK4XnUEiXc3dEzsCJPg
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression…SVR rates of alcoholics using IFN/riba were considerably lower though it’s considered to be an adherence issue. Afaik there’s no DDI problems with alcohol and the DAAs.
I cleared in January with AbbVie meds and didn’t drink at all during Tx. Just seemed wise to me given that side effects were a bit unpredictable.
The synergy factor with HCV + alcohol is about 10, so quite high, but from what I’ve read most of it is caused by increased reactive oxidative stress.
It’s a personal call. I’m cirrhotic but still have a drink or two occasionally. My specialist’s advice was to never have more than 2 and to ensure that I had a number of days off in-between.
Was geno 1b since 1973. SVR January 2015 (V-Pak)
Survivor primary HCC, in remission NHL (MZL)
Compensated cirrhosis. Hoping for some regression… -
AuthorPosts