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Price.
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16 June 2016 at 1:32 pm #19216
Did they measure your ALT/AST both times?
If so, how did the results compare?
m
Curehcvnow@gmail.com
http://forums.delphiforums.com/generichcvtxG 1a F-1
Started tx 10/23/15 (Meso sof & led) ALT 48 AST 28 v/l 1.6 mil
11/17/15 4 wk lab ALT 17 AST 16 <15
11/18/15 Started Harvoni
12/16/15 8 wk lab ALT: 15 AST: 13 V/l UND
1/14/16 Fin. Tx
7/07/16 UND SVR 2416 June 2016 at 1:52 pm #19219No, we didn’t do them at the time of the second VL test because I’d been ill.
GT 3a, tx naive, dx 4/12/16
4/12/16 V/L 824,000
2/03/16 AST 119 ALT 239 platelets 109
4/12/16 AST 87 ALT 164 platelets 118 (different lab)
5/5/16 FibroScan 8.9 kPa F2
5/16/16 AST 86 ALT 157
5/16/16 Fibrotest 0.6 F3 Actitest 0.79
5/31/16 VL 14,413,000 (uh… YIKES)
Y93H @ baseline
6/20/16 Started Redemption 2 Sof + Dac
7/516 QUANT VL: NOT DETECTED
7/5/16 AST 34 ALT 60 Platelets 128 (diff lab though)12/06/16 EOT VL UNDETECTED
1/03/17 EOT+4 VL 12,222,000
no new RAVs; IL28B = CC16 June 2016 at 2:10 pm #19223If it were me, I would have a liver panel. My v/l went from 4.9 million to 1.6 million in the year before I started treatment. I attribute to not drinking alcohol. During that same time period, my ALT went from 225 to 48.
We probably need an expert in this corner…
m
Curehcvnow@gmail.com
http://forums.delphiforums.com/generichcvtxG 1a F-1
Started tx 10/23/15 (Meso sof & led) ALT 48 AST 28 v/l 1.6 mil
11/17/15 4 wk lab ALT 17 AST 16 <15
11/18/15 Started Harvoni
12/16/15 8 wk lab ALT: 15 AST: 13 V/l UND
1/14/16 Fin. Tx
7/07/16 UND SVR 2416 June 2016 at 4:02 pm #19230Viral loads go up and down, but yes that’s a large change. You can’t directly compare different quantitative tests so this might have something do with it.
Viral load has very little correlation to either liver damage or SVR rate.
The best viral load to have is undetected at SVR so rather than fussing about what it is currently I would be actively seeking to make it 0
YMMV
17 June 2016 at 3:31 am #19275What are the best correlation “variables/factors” with SVR known besides length of tx? Perhaps there is a file with such a data in the forum I am missing. Thank you so much in advance.
Blood transfusion in 1992 – Diagnosed in 2007
Tx naive -G1b – F1
VL 2.270.000
ALT 40
Start tx June 4th/2016 with DAAs – Sof/Led from India
Bloods on two weeks of tx (June 18th)
AST 17 – ALT 10 – GGT 19
Virus UND
Bloods on six weeks of tx (July 16th)
AST 17 – ALT 8 – GGT 12
Virus UND
EOT on August 8th (did 9 weeks and 3 days)SVR 4 Virus UND (September 7th)
AST 13 – ALT 5SVR 14 Virus UND (November 12th)
17 June 2016 at 4:13 am #19277IIC the main factors are fibrosis level (F1-F4), genotype, previous treatment experience and presence of RAVs. I’m sure relevant data is somewhere here in the forums but can’t remember where.
M 61yo HCV+ ~ 30 yrs Gt1a F2 VL 223,000 ALT 54 AST 42 Tx start Sof/Dac 17Dec15.
SVR4 at 7Apr16 ALT 22 AST 22
SVR12 at 9Jun16 ALT 23 AST 25
Melbourne, Australia17 June 2016 at 12:58 pm #19345Past treatment (failure) is probably just another way of identifying poor levels of innate immune response to HCV – ie it picks up people with IL28 TT and probably other genes we don’t know about.
It makes sense to me that patients with high viral loads X many years = more replication cycles capable of generating resistant mutants.
Diabetes and insulin resistance is probably bad, and genotype/fibrosis.
With genotype 2 is best, 1b, 1a, then 3 last. Data for 4,5,6 is lacking. GT3 remains the problem child.
YMMV
17 June 2016 at 1:47 pm #19352 -
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