Welcome, Guest |
TOPIC:
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19574
Hi Hit The Road Jack
Quoting Gaj: "The main problems with us G3s seem to be related to cirrhosis, previous Tx, VL and length of Tx. I score very poorly on the first three so went into 24 week Tx knowing I only had a 80% likelihood of success based on previous studies. While I didn't achieve SVR my overall health has improved in leaps and bounds putting me in a good position to do so next time". I didn't make it over the line in the get rid of hep C race either, but then again, read the underlined bit above. I do not fully know whether the old lethargy has returned (maybe a bit of reactive depression, though I have caught a cold going around work as well), but the time on meds has seen me join the human race again and establish the habits of getting my money's worth from the gym subscriptions. Dogs and daughter appreciate my new found involvement in life too. Yours Jeff GT3a 1990 Failed Inter 1998, comb in 2000. HCC 2012 Started 24/52 Sof/Dac 27th October 2015. 1. Bloods 2 October 2015: AST - 165 (20-40), ALT - 265 (5-40), GGT 189 (5-50) 2, Bloods 20 November 2015: ALT etc normal; VL 19 3. Bloods 8 January 2016: AST - 40, ALT - 59, GGT 48 VL RNA UND 4. EOT 12 April 2016 - blood tests: all is well, CT scan: okay 5. AFP 11 June 2016: 4 ref< 11 6. VL July 2016: DET 7. Oct16 start treat - June17 UND 8. Jun 18, lfts okay, platelets a bit low. | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19781
Gaj, I was thinking (yes, I know, I think too much)...what's the one unique thing about genotype 3? The one thing that makes it different than all the others. The hepatic steatosis. So check out what I found... "Both the first and next generations of DAAs appear to be less effective against genotype 3 infections. Hepatic steatosis may be, at least in part, responsible for the persistently low rates of SVR associated with genotype 3. It may be that intrahepatic fat sequestration by the replicating virus reduces access of DAAs, thereby reducing the efficacy of these drugs." And.... "Importantly, lower baseline serum low-density lipoprotein (LDL) and lower expression of fatty acid metabolism and lipid transport genes at the end of treatment were associated with relapse, suggesting the relevance of host metabolism on treatment outcome with this DAA combination in genotype 1 HCV infection" www.ncbi.nlm.nih.gov/pmc/articles/PMC4259863/ P | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19783
So maybe losing weight at the same time as treatment may be helpful? I was already thinking this same thing. I gained a bit during treatment. Virus hiding out in fat reserves..... This email address is being protected from spambots. You need JavaScript enabled to view it. Genotype 3 VL 4,100,000 ALT 101 AST 71 Treatment Naive Started Sof/Dac Jan 12, 2016 VL= <15 4 weeks in. AST/ALT normal. VL=UNDETECTED 8 weeks in. SVR4= Virus back. 3,300,000 Started generic Epclusa Sep. 23, 2017 4 weeks in <15 *Detected. 12 weeks in <15 *Not Detected. 16 weeks in <15 *Not Detected. Finished 24 weeks treatment 3-17-18 SVR5 <15 Not Detected. SVR 20 <15 Not Detected. SVR 44 <15 Not Detected. Thank you Jesus. Thank you Dr. James | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19795
| I think I have the opposite of that, I lost too much weight, I don't absorb things properly, maybe even the meds. So too fatty or too skinny can be problematic I feel and it may well be helpful to try and keep a good balance wherever possible. There is much more written re the too fatty side, but very few articles on the skinny side and malabsorbtion / malnutrition etc ... "Liver steatosis is an accumulation of fat in the liver, making a 'fatty liver'. It corresponds to the accumulation of lipids (triglycerides) in the liver cells (hepatocytes) and may complicate alcoholic intoxication or metabolic disorders such as Type 2 diabetes, obesity, and dyslipemia. Such steatosis can either be isolated, making it a pure steatosis, or associated with hepatitis, which makes it non-alcoholic steatohepatitis (NASH). Steatosis and NASH form non-alcoholic fatty liver disease (NAFLD). These are usually asymptomatic conditions, but they are currently becoming more common because of the increasing number of overweight patients. " My Triglycerides were way too low, this turned up in a private blood test not a routine hospital one. They came under the 'cholesterol' section of testing. GT1a Dec14 F2/8.7 VL 900000-2.5M Jan16 Hepcivir-L MonkMed/Redemption Baseline: VL 913575 Alt 76 Platelets low Wk2 VL1157 Alt 23 DET Wk 8 VL 32 Alt19 'In the slow lane' June16 Fibro 5.7 F0/1 LIF 1.5 Wk 11 VL<12 Alt 13 Det/Unq Extending tx 12 wks Mylan Sofo/Dac MonkMed Wk 14 VL <12 Det/Unq Wk 16 VL UNDETECTED Wk 22 + 4 Wks Sunprevir FixHepC Wk 24 UNDETECTED Alt 13 Wk 12 post tx SVR12 Wk 26 SVR24 Thank-you Tim, Dr Debasis @ MonkMed & Dr Freeman @ Fix HepC |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19796
Hi Price, As you say, steatosis (fatty liver) is more prevalent in G3s. It certainly should be considered by anyone with this genotype. My specialist told me a couple of years ago that it isn't apparent in my case and my liver seems to be within normal range. On the other hand I do tend toward high serum triglycerides and we don't really know what I'd be like in the absence of HCV. A good reminder to check current status with him next appt. Splitdog, It's a little more complicated than just being overweight. Steatosis is retention of fat inside the liver cells, being overweight certainly doesn't help but it can occur even in skinny people. It's mostly about how your metabolism works. Along the lines of what you eat and how you process it rather than how much you eat. I believe a good diet, plenty of excercise and aiming for a healthy weight will all help. I won't suggest diets as there are others more qualified but think lean, mean and lots of energy rather than skinny, starving and weak. (Lean and mean is a bit of an ask for me these days but I try Edit: note to self - must type faster. Thanks LG. G3a since '78 - Dx '12 - F4 (2xHCC) 24wk Tx - PEG/Riba/Dac 2013 relapsed 24wk Tx - Generic Sof/Dac/Riba 2015/16 relapsed 16wk Tx - 12/01/17 -> 03/05/17 NS3/NS5a + Generic Sof SVR7 - 22/06/17 UND SRV12 - 27/07/17 UND SVR24 - 26/10/17 UND | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19798
My Dr here told me I had a fatty liver. This email address is being protected from spambots. You need JavaScript enabled to view it. Genotype 3 VL 4,100,000 ALT 101 AST 71 Treatment Naive Started Sof/Dac Jan 12, 2016 VL= <15 4 weeks in. AST/ALT normal. VL=UNDETECTED 8 weeks in. SVR4= Virus back. 3,300,000 Started generic Epclusa Sep. 23, 2017 4 weeks in <15 *Detected. 12 weeks in <15 *Not Detected. 16 weeks in <15 *Not Detected. Finished 24 weeks treatment 3-17-18 SVR5 <15 Not Detected. SVR 20 <15 Not Detected. SVR 44 <15 Not Detected. Thank you Jesus. Thank you Dr. James | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19800
Hang in Splitdog. The DAA's obviously aren't perfect, but they're damn good, and getting better with every generation. Failed Interferon 96', G1a, VL = 9 - 5.5 Million, F3/A3, AST 111, ALT 190, Generic DAA treatment Sof/Led (Mylan - India MYHEP LVIR) - 8 June, 2016 2 Week Results 20 June, 2016 AST 19, ALT 32 4 Week Results 06 July, 2016 AST 22, ALT 30, VL = 35 6 Week Results 20, July 2016 VL only = HCV RNA Detected, Non-Quantifiable <15 8 Week Results 04 August 2016, Labs, LFTs Normal, VL = UND 12 Week Results 31 August, 2016 LFTs Normal, VL = UND EOT + 4 Weeks, LFTs Normal, VL = UND, "SVR4" SVR12, 21 Nov 2016. CURED!!! | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19806
Hi Split, Sorry to hear your diagnosis. To clarify my previous statement, I was trying to say that weight while relevant isn't the defining point with NASH in case someone read this thread and thought "oh, I'm not overweight....can't happen to me". Losing excess weight will certainly help but it is also about improving your metabolism so there is less tendency for fat to accumulate in your liver. See my comments about a good diet and plenty of exercise. Many G3s do have NASH at some level (I was careful to qualify comments about myself with the words 'apparent' and 'seems') but the majority do clear HCV with DAAs, just not quite as many as other genotypes. Here is some further reading on fatty liver and HCV: hepatitiscnewdrugresearch.com/fatty-liver-and-hcv.html Good luck with the diet and excercise, neither of which are really at the top of my list of "things I'd rather be doing" G3a since '78 - Dx '12 - F4 (2xHCC) 24wk Tx - PEG/Riba/Dac 2013 relapsed 24wk Tx - Generic Sof/Dac/Riba 2015/16 relapsed 16wk Tx - 12/01/17 -> 03/05/17 NS3/NS5a + Generic Sof SVR7 - 22/06/17 UND SRV12 - 27/07/17 UND SVR24 - 26/10/17 UND | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19811
Gaj wrote: Good luck with the diet and excercise, neither of which are really at the top of my list of "things I'd rather be doing" Hi Gaj Diet & exercise is way down towards the bottom of the list of things that I'd rather be doing, however, I was advised that it should be my main priority during treatment. As it turns out, I'm thankful that I followed this advice because of the health benefits I am now enjoying. Hopefully I will achieve SVR24 and after that I will revert to living a normal life, enjoying and savouring all of its fruits on offer, but in the interim will continue living with my list of things that I'd rather be doing being inverted on it's head. It's only for a few months, and 6 months in total, so not long in the scheme of things considering the many future years that I plan to enjoy life at its fullest. Maybe you should, with all respects, re-think your priorities. I'm a former amateur boxer in my youth and rationalised my training before, during, and after treatment as being as fit as possible for my fight with HCV. Its down for the count and it didn't lay a glove on me. Respectfully GT2 1983: Hospitalised with Acute non-A, non-B Hepatitis after ICU blood transfusion 3mths earlier => HCV GT2 22/02/16: (pre-tmt) ALT 61, VL 2.48 IU/ml Hepascore 0.32 (F1/2), fatigue, brain fog, bloating (Treatment Naïve) 10/04/16: (Start tmt) Sofovir +DaclaHep (SOF + DCV) by Hetero Labs in India 09/05/16: ALT 34, VL: NOT Detected 17/6/16 FBG 5.7; PPBG (@14.22) 6.9 (@ 20.45) 7.1; BP 124/72 | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19816
Oops, sorry! It appears that my attempt at self depreciating humour was misinterpreted. I fully agree and support the importance of good diet and exercise during treatment to the extent that I have been able to adjust my favourite belt in by several holes and bought half a new wardrobe since commencing treatment. In recognition of the impact on my health and lifestyle I fully intend to continue the process into the future including after achieving SVR. I have always eaten reasonably well in the past but often too much and while I quite enjoy exercise in the right situation I can be a lazy bastard if I allow myself and/or the weather is inclement (or too nice) thus the aside about "rather be doing". (NOT) Gaj's approved training program. G3a since '78 - Dx '12 - F4 (2xHCC) 24wk Tx - PEG/Riba/Dac 2013 relapsed 24wk Tx - Generic Sof/Dac/Riba 2015/16 relapsed 16wk Tx - 12/01/17 -> 03/05/17 NS3/NS5a + Generic Sof SVR7 - 22/06/17 UND SRV12 - 27/07/17 UND SVR24 - 26/10/17 UND | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19821
Hi Gaj Thanks for clarifying that … it’s just another exercise in pragmatic competence, which was touched upon with the discussion of semantics on another thread. For those of us who have suffered serious head injuries, pragmatics can be an issue. I too have needed to adjust my belt by several holes and will now have to buy some new jeans as they are hanging off me. I’m innately lazy, it's the default human condition for most I think, but I always get the job done by any means that are needed … like swimming over here at the moment during winter in an outdoor heated pool while it is raining … it’s better than it sounds, as it’s warmer in the pool than out, and you virtually have the pool to yourself. 1983: Hospitalised with Acute non-A, non-B Hepatitis after ICU blood transfusion 3mths earlier => HCV GT2 22/02/16: (pre-tmt) ALT 61, VL 2.48 IU/ml Hepascore 0.32 (F1/2), fatigue, brain fog, bloating (Treatment Naïve) 10/04/16: (Start tmt) Sofovir +DaclaHep (SOF + DCV) by Hetero Labs in India 09/05/16: ALT 34, VL: NOT Detected 17/6/16 FBG 5.7; PPBG (@14.22) 6.9 (@ 20.45) 7.1; BP 124/72 | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19830
I have been really busy at work and not online much. I came here and saw your news - I have logged on to say I'm sorry to hear it and wish you all the very best in finding the right cure. | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19844
Split dog, if you have genotype 1 which is associated with having insulin resistance and you're overweight, then lowering your weight BEFORE you start treatment should help. Londongirl, thin people can also be insulin resistant and steatosis but obviously if you're underweight then loosing weight would not be recommended. But diet can always be improved. I would concentrate on having less carbs and more protein if ok with your doc (since he's the one familiar with your case). | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19846
G1a dx'd in 1992, Biopsy F2 VL 8mill +. Tried tx with Interferon/Riba, back in 2008 didn't last long it felt horribly ugly!! I stopped tx, after 5 weeks!! Started tx 6/1/16 with Harvoni. 12 Month Labs= UND | |
Hard to treat Gt3 - Another stage of the journey 7 years 9 months ago #19863
Gaj, "For people with genotype 3 though, the link between steatosis and the virus has now been definitively established. Up to 80% of people with genotype 3 have moderate to severe steatosis. It seems that that there is a complex interaction between the core protein of the genotype 3 strand of the virus and liver cells that leads to steatosis. This interaction is not seen in other genotypes. It also seems that the severity of steatosis in these patients is directly related to their viral load. The higher the viral load the greater the amount of steatosis." Plus, the steatosis is around the portal areas, rather than in the middle of the lobules of the liver like the usual steatosis. hepatitiscnewdrugresearch.com/fatty-liver-and-hcv.html Reducing dietary saturated fat is associated with an increase in LDL-receptor abundance (which helps the virus multiply) of magnitude similar to the decrease in serum LDL-cholesterol (which is what happens with geno 3). So it looks like your new diet will have to include restriction of PUFAs in favor of big fat steaks, and eggs and bacon for breakfast instead of cereal, butter, coconut oil P | |
Time to create page: 0.370 seconds