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2 Doctors, 2 Opinions - Your Opinions Please
As most of you know, I’ve been through 4 failed treatments. Within this week I saw Dr. Robert Gish, the hepatologist, and Dr. Frank Faris, the Gastroenterologist, regarding waiting or treating.
I’ve been denied both Telepravir and Bocepravir because of failed results. Dr. Gish wants me to wait and see him in one year. Dr. Faris wants me to treat now, even if it’s the double-dosing of Pegasys with Riba.
Here’s the decision part I need your opinions on: Even if I eventually get on the VX-950 trial, I may get a placebo. However, if I don’t, the success rate for hard to clear victims such as myself is 70% or better.
The double-dosing of Pegasys with 1200mg Riba is 15-20%. That doctor would treat and if I didn’t become UND in 12 weeks, he would stop treatment.
Dr. Gish eats, sleeps and lives liver problems. The Gastro is a Jack Of All Trades, Master Of None. However, he sees an urgency now that I’m at the beginning stages of Cirrhosis.
I spoke to another member on this board who knows Dr. Gish very well and has cleared. She suggests I listen to him and wait. This is a tough decision for me at this point.
On the 16th, I will begin the banding of my Esophageal Verices. This will entail 3-6 procedures. Dr. Gish examined me and said I look well and little has changed in the past year as far as blood work and progression.
For those knowledgeable:
My MELD is 7 and has remained so for years. My ALT is 85, my AST is 74, the lowest they’ve been in years. My Bilirubin is 0.3. Glucose-Fasting is 102. Platelet Count 84. Viral Load 2,900,000. Alpha-Fetoprotein 26.0
So there it is. Your opinions are highly appreciated. Wait or treat?
Magnum
I’ve been denied both Telepravir and Bocepravir because of failed results. Dr. Gish wants me to wait and see him in one year. Dr. Faris wants me to treat now, even if it’s the double-dosing of Pegasys with Riba.
Here’s the decision part I need your opinions on: Even if I eventually get on the VX-950 trial, I may get a placebo. However, if I don’t, the success rate for hard to clear victims such as myself is 70% or better.
The double-dosing of Pegasys with 1200mg Riba is 15-20%. That doctor would treat and if I didn’t become UND in 12 weeks, he would stop treatment.
Dr. Gish eats, sleeps and lives liver problems. The Gastro is a Jack Of All Trades, Master Of None. However, he sees an urgency now that I’m at the beginning stages of Cirrhosis.
I spoke to another member on this board who knows Dr. Gish very well and has cleared. She suggests I listen to him and wait. This is a tough decision for me at this point.
On the 16th, I will begin the banding of my Esophageal Verices. This will entail 3-6 procedures. Dr. Gish examined me and said I look well and little has changed in the past year as far as blood work and progression.
For those knowledgeable:
My MELD is 7 and has remained so for years. My ALT is 85, my AST is 74, the lowest they’ve been in years. My Bilirubin is 0.3. Glucose-Fasting is 102. Platelet Count 84. Viral Load 2,900,000. Alpha-Fetoprotein 26.0
So there it is. Your opinions are highly appreciated. Wait or treat?
Magnum
thanks for posting those abstracts. I had meant to track them down and then was away from computers for a bit. They seem to correspond to abstracts 1870 1891 and 168 from aasld '08, however, the Nizar Zein study Harrison is referring to doesn't seem to match 1891(Dieterich) since Zein is not one of the authors and in fact none are from Mayo; there seems to be a 4th bit of data out there.
I know you've been following this topic closely and perhaps are aware of other data, but from the above I tend to agree with Fried that whether (successfully) treating IR implies a significant improvement in SVR odds remains to be shown. The only complete data is from Conjeevaram and they did not find a benefit in SVR (though EOT was better). Perhaps, as Harrison suggests, failure to pretreat was the omission. However the 1870 (Mills) and 1891(Adler) abstracts seem *very* preliminary : the first is based on the two single injections, the 2nd on HCV/HIV co-infection and neither gives SVR data. (and the data on high-dose ifn shows that a good preliminary vl drop does not always correlate with better svr).
Based on the above, whether treating IR improves SVR still seems a reasonable hypothesis rather than fact. I'd hope the hypothesis is true, but rattling in the back of my mind are suspicions from the recent genetic signature tests showing very high ability to predict tx outcome: fixing a defective ifn response may or may not be as easy as fixing one pathway.
I know you've been following this topic closely and perhaps are aware of other data, but from the above I tend to agree with Fried that whether (successfully) treating IR implies a significant improvement in SVR odds remains to be shown. The only complete data is from Conjeevaram and they did not find a benefit in SVR (though EOT was better). Perhaps, as Harrison suggests, failure to pretreat was the omission. However the 1870 (Mills) and 1891(Adler) abstracts seem *very* preliminary : the first is based on the two single injections, the 2nd on HCV/HIV co-infection and neither gives SVR data. (and the data on high-dose ifn shows that a good preliminary vl drop does not always correlate with better svr).
Based on the above, whether treating IR improves SVR still seems a reasonable hypothesis rather than fact. I'd hope the hypothesis is true, but rattling in the back of my mind are suspicions from the recent genetic signature tests showing very high ability to predict tx outcome: fixing a defective ifn response may or may not be as easy as fixing one pathway.
My last endoscpy 18 months ago showed developng varices. Glad your banding is getting done before an occunce but sorry for your situation. I've been on a beta blocker since the endo.Did you ever get asked to take them ?. Just wondering. I'll be going for another endo soon- chris
"The final paper is an SVR-derived paper out of the University of Michigan that shows that if you start triple therapy with pioglitazone, PEG-IFN, and ribavirin together, simultaneously, SVR is not improved at the end of the day. I think the problem with that is there was no preload, there was no treating the insulin resistance beforehand to try to improve interferon signaling."
A Randomized, Double-Blind, Placebo-Controlled Study of PPAR-gamma Agonist Pioglitazone Given in Combination with Peginterferon and Ribavirin in Patients with Genotype-1 Chronic Hepatitis C.
H. Conjeevaram; C. F. Burant; B. McKenna; D. Harsh; H. Kang; A. K. Das; L. Everett; D. White; A. F. Lok
The presence of insulin resistance (IR) appears to be a key factor in the development of steatosis and disease progression in patients with hepatitis C virus (HCV) genotype 1 infection similar to that seen in NAFLD. Insulin resistance also is an independent factor for lower sustained virological response (SVR) in type 1 infection. Pioglitazine (PIO) has been shown to decrease IR and improve histologic features in NAFLD.
Aim:
To assess the effect of pioglitazine on insulin sensitivity, liver histology and SVR in treatment-naïve patients with type 1 HCV infection with insulin resistance (HOMA index > 2.0) receiving standard antiviral therapy.
Methods:
A total of 40 patients were randomly assigned to receive pioglitazine 30 mg (n, 20) or placebo (PLA) (n, 20) along with peginterferon alfa 2b + ribavirin. All pts were treated for 48 wks and followed for 24 wks. HOMA index and HCV RNA levels were measured at baseline, during therapy and follow-up. Liver biopsies at baseline and at 12 wk follow-up were assessed for steatosis, inflammation and fibrosis.
Results:
Mean age was 48.6 yrs; 22 were female and 35 Caucasian. At entry, mean HOMA index was 5.8 (2.01-12.3) and hepatic steatosis was present in 65% of patients. There was a significant reduction in HOMA index in the pioglitazine group (–1.72 and –1.88) and no change in the PLA group (+1.12 and +0.86) at wks 24 and 48 of therapy respectively (p=0.008 at both time points). The effect on insulin resistance persisted even during follow-up in the pioglitazine group (p=0.012). Mean body weight decreased on therapy in both groups; on follow-up it was no different from baseline in the pioglitazine group but remained significantly lower in the PLA group (p=0.013). In an intention-to-treat analysis, 16 patients on pioglitazine (80%) and 10 patients on PLA (50%) had undetectable HCV RNA at the end of therapy (89% vs. 56% among 36 patients who completed therapy, p=0.060); however, SVR rates were similar (45%) in both groups. Patients on pioglitazine were more likely to have reversal of steatosis compared to those on PLA (54% vs. 30%, p<0.05). Analysis of serum lipomic profiles showed a significant increase in monounsaturated fatty acids and 18:1/18:0 ratio at wk 48 compared to baseline (p<0.05) only in the pioglitazine group. Similarly, lipomic profiles from paired liver biopsies showed a decrease in relative amount of monounsaturated fatty acids and a significant increase in polyunsaturated fatty acids only in the pioglitazine group (p<0.05).
Conclusions:
Pioglitazone treatment led to a significant reduction in insulin resistance and reversal of hepatic steatosis in HCV genotype-1 patients with insulin resistance. Patients in pioglitazine group had higher rate of end of treatment response but SVR was similar in both groups. pioglitazine treatment led to increased desaturation of fatty acids, which may explain the decreased hepatic steatosis.
A Randomized, Double-Blind, Placebo-Controlled Study of PPAR-gamma Agonist Pioglitazone Given in Combination with Peginterferon and Ribavirin in Patients with Genotype-1 Chronic Hepatitis C.
H. Conjeevaram; C. F. Burant; B. McKenna; D. Harsh; H. Kang; A. K. Das; L. Everett; D. White; A. F. Lok
The presence of insulin resistance (IR) appears to be a key factor in the development of steatosis and disease progression in patients with hepatitis C virus (HCV) genotype 1 infection similar to that seen in NAFLD. Insulin resistance also is an independent factor for lower sustained virological response (SVR) in type 1 infection. Pioglitazine (PIO) has been shown to decrease IR and improve histologic features in NAFLD.
Aim:
To assess the effect of pioglitazine on insulin sensitivity, liver histology and SVR in treatment-naïve patients with type 1 HCV infection with insulin resistance (HOMA index > 2.0) receiving standard antiviral therapy.
Methods:
A total of 40 patients were randomly assigned to receive pioglitazine 30 mg (n, 20) or placebo (PLA) (n, 20) along with peginterferon alfa 2b + ribavirin. All pts were treated for 48 wks and followed for 24 wks. HOMA index and HCV RNA levels were measured at baseline, during therapy and follow-up. Liver biopsies at baseline and at 12 wk follow-up were assessed for steatosis, inflammation and fibrosis.
Results:
Mean age was 48.6 yrs; 22 were female and 35 Caucasian. At entry, mean HOMA index was 5.8 (2.01-12.3) and hepatic steatosis was present in 65% of patients. There was a significant reduction in HOMA index in the pioglitazine group (–1.72 and –1.88) and no change in the PLA group (+1.12 and +0.86) at wks 24 and 48 of therapy respectively (p=0.008 at both time points). The effect on insulin resistance persisted even during follow-up in the pioglitazine group (p=0.012). Mean body weight decreased on therapy in both groups; on follow-up it was no different from baseline in the pioglitazine group but remained significantly lower in the PLA group (p=0.013). In an intention-to-treat analysis, 16 patients on pioglitazine (80%) and 10 patients on PLA (50%) had undetectable HCV RNA at the end of therapy (89% vs. 56% among 36 patients who completed therapy, p=0.060); however, SVR rates were similar (45%) in both groups. Patients on pioglitazine were more likely to have reversal of steatosis compared to those on PLA (54% vs. 30%, p<0.05). Analysis of serum lipomic profiles showed a significant increase in monounsaturated fatty acids and 18:1/18:0 ratio at wk 48 compared to baseline (p<0.05) only in the pioglitazine group. Similarly, lipomic profiles from paired liver biopsies showed a decrease in relative amount of monounsaturated fatty acids and a significant increase in polyunsaturated fatty acids only in the pioglitazine group (p<0.05).
Conclusions:
Pioglitazone treatment led to a significant reduction in insulin resistance and reversal of hepatic steatosis in HCV genotype-1 patients with insulin resistance. Patients in pioglitazine group had higher rate of end of treatment response but SVR was similar in both groups. pioglitazine treatment led to increased desaturation of fatty acids, which may explain the decreased hepatic steatosis.
"The next study out of the Cleveland Clinic with Nizar Zein, he will be presenting data that suggest that RVRs improve if you pretreat patients with a glitazone for 12 weeks prior to initiating therapy."
In Chronic Hepatitis C (HCV), Pretreatment with Thiazolidinediones (TZDs) or Metformin Decreases Insulin Resistance (IR) and HCV Viral Load and Increases Early Virologic Response (EVR)
M. Adler, J.L. Matloff, A.S. Boxer, H. Han, M. Vachon, D.C. Carriero, D.T. Dieterich, , Mount Sinai School of Medicine, New York, NY; M. Vachon, D.C. Carriero, D.T. Dieterich, Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY
Background: Chronic HCV is associated with increased incidence of insulin resistance (IR), which leads to a lower rate of sustained virologic response (SVR) following treatment with peginterferon plus ribavirin (IFN + RBV). Romero-Gomez et al. reported an SVR rate of 32.8% in genotype 1-infected patients with IR (HOMA-IR > 2) compared to 60.5% in those without IR. In addition, IR is associated with increased liver fibrosis and is characterized by a higher viral load, two other independent risk factors for decreased response to treatment. A recent study showed 0/5 EVR in patients with IR who were given a TZD at initiation of IFN + RBV. It is unknown if therapeutic intervention to improve insulin sensitivity prior to anti-viral treatment increases response to HCV treatment. Aim: To evaluate the effect of treatment with TZDs or metformin on IR and viral load prior to IFN + RBV and the impact on EVR. Methods: IRB-approved, we retrospectively reviewed charts of patients with chronic HCV from a liver clinic in our center. We included patients with IR treated with either metformin or a TZD for at least 3 months prior to initiating IFN+RBV. We compared HOMA-IR, HCV viral load, liver enzymes and BMI at baseline, after treatment with an insulin sensitizer (IS), and at week 12 of HCV treatment. Results: 17 patients met inclusion criteria. 10 were co-infected with HIV. The average age was 52.2 years, and 82% of patients were genotype 1. 11 patients were treatment-naïve to IFN+RBV. The mean stage of fibrosis was 2.7 on Metavir score in 12 patients. 11 patients received a TZD and 6 received metformin. The mean HOMA-IR decreased from 7.99 to 6.06 after treatment with an IS to 4.60 at 12 weeks of IFN + RBV. There was a significant mean decrease of 0.52 log in HCV viral load on each patient after treatment with an IS (p<0.01). An EVR was achieved in 12 patients (71%). The mean ALT value decreased from 86.2 at baseline to 72.5 (p=0.02) after treatment with an IS to 34.1 IU/L (p=0.01) after 12 weeks of IFN + RBV. BMI significantly decreased from 27.9 to 26.8 kg/m2 (p=0.02) following treatment with an IS. Conclusion: The use of a TZD or metformin improved insulin sensitivity prior to treatment with IFN + RBV. The baseline viral load, a risk factor for decreased response to treatment and until now referred to as an unmodifiable factor, was also significantly lowered. This intervention allowed a 71% rate of EVR in a population of mono and co-infected patients, the majority being genotype 1. This small pilot study suggests that targeting insulin resistance prior to treatment may enhance the chance of response to traditional treatment for chronic HCV.
In Chronic Hepatitis C (HCV), Pretreatment with Thiazolidinediones (TZDs) or Metformin Decreases Insulin Resistance (IR) and HCV Viral Load and Increases Early Virologic Response (EVR)
M. Adler, J.L. Matloff, A.S. Boxer, H. Han, M. Vachon, D.C. Carriero, D.T. Dieterich, , Mount Sinai School of Medicine, New York, NY; M. Vachon, D.C. Carriero, D.T. Dieterich, Division of Liver Diseases, Mount Sinai School of Medicine, New York, NY
Background: Chronic HCV is associated with increased incidence of insulin resistance (IR), which leads to a lower rate of sustained virologic response (SVR) following treatment with peginterferon plus ribavirin (IFN + RBV). Romero-Gomez et al. reported an SVR rate of 32.8% in genotype 1-infected patients with IR (HOMA-IR > 2) compared to 60.5% in those without IR. In addition, IR is associated with increased liver fibrosis and is characterized by a higher viral load, two other independent risk factors for decreased response to treatment. A recent study showed 0/5 EVR in patients with IR who were given a TZD at initiation of IFN + RBV. It is unknown if therapeutic intervention to improve insulin sensitivity prior to anti-viral treatment increases response to HCV treatment. Aim: To evaluate the effect of treatment with TZDs or metformin on IR and viral load prior to IFN + RBV and the impact on EVR. Methods: IRB-approved, we retrospectively reviewed charts of patients with chronic HCV from a liver clinic in our center. We included patients with IR treated with either metformin or a TZD for at least 3 months prior to initiating IFN+RBV. We compared HOMA-IR, HCV viral load, liver enzymes and BMI at baseline, after treatment with an insulin sensitizer (IS), and at week 12 of HCV treatment. Results: 17 patients met inclusion criteria. 10 were co-infected with HIV. The average age was 52.2 years, and 82% of patients were genotype 1. 11 patients were treatment-naïve to IFN+RBV. The mean stage of fibrosis was 2.7 on Metavir score in 12 patients. 11 patients received a TZD and 6 received metformin. The mean HOMA-IR decreased from 7.99 to 6.06 after treatment with an IS to 4.60 at 12 weeks of IFN + RBV. There was a significant mean decrease of 0.52 log in HCV viral load on each patient after treatment with an IS (p<0.01). An EVR was achieved in 12 patients (71%). The mean ALT value decreased from 86.2 at baseline to 72.5 (p=0.02) after treatment with an IS to 34.1 IU/L (p=0.01) after 12 weeks of IFN + RBV. BMI significantly decreased from 27.9 to 26.8 kg/m2 (p=0.02) following treatment with an IS. Conclusion: The use of a TZD or metformin improved insulin sensitivity prior to treatment with IFN + RBV. The baseline viral load, a risk factor for decreased response to treatment and until now referred to as an unmodifiable factor, was also significantly lowered. This intervention allowed a 71% rate of EVR in a population of mono and co-infected patients, the majority being genotype 1. This small pilot study suggests that targeting insulin resistance prior to treatment may enhance the chance of response to traditional treatment for chronic HCV.
"references for the papers Dr. Harrison mentions were not included (aasld 07 abstracts?)"
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I'm posting the three studies they referred to.
Co
Viral Kinetic Response to 12 Week Treatment with Rosiglitazone in Chronic Hepatitis C, Genotype 1 Patients Who Are Previous Relapsers or Nonresponders to Pegylated Interferon and Ribavirin
S.J. Mills, R.J. Naus, K. Barstow, S. Harrison, Brooke Army Medical Center, San Antonio, TX;
Background: Insulin resistance (IR) is associated with CHC GT 1 virus. IR is associated with decreased SVR. The aim of this trial was to evaluate the effects rosiglitazone (rosi) on insulin sensitivity in a group of CHC, GT 1, patients who are prior nonresponders or relapsers to peg-interferon and RBV and assess viral kinetic (VK) response to interferon-alfacon-1 given before and 12 weeks after rosi was initiated. Methods: Thirty-four IR, GT 1, CHC patients, nonresponders (n=23), relapsers (n=11)to peg-interferon and RBV enrolled. Patients randomized to rosi 8mg daily and diet/exercise recs vs diet/exercise recs alone. Baseline VK obtained at time point zero, 8, 16, 24 hours, day 3, 5 and 7 after giving a 15mcg single dose of interferon-alfacon-1. Repeat VK were obtained 12 weeks later after a second dose of 15mcg of interferon-alfacon-1 was given. Results: 33 of 34 eligible patients completed the 12-week study and obtained repeat VK. Mean age:49.6 years(range 23 - 66), 45.5% female, 48.5% Cauc, 36% AA. Mean BMI:29.8, 36.4% were F3/4, mean QUICKI:0.32, logarithmic (log) mean viral load:13.29. Eighteen patients received rosi. No difference was observed between the two groups at baseline. Mean QUICKI improved from 0.32 to 0.33 in the rosi group and 0.31 to 0.32 in the diet/exercise group. Mean log value at baseline for the rosi group was 13.68, and decreased to 12.47 by the end of the first 24-hour period. A similar decline was noted with the second injection given at 12 weeks. No sig difference compared with the diet/exercise group. Patients (in either group) who improved QUICKI had a moderate corr(r=.34) with improvement in 24 hr VK. Glucose at week 12 correlated (r =-.44, p < .05) with viral load. Mean adiponectin improved from 20250.3 to 33761.5 in patients who improved their IR and adiponectin at day 97 was significantly and inversely correlated with day 97 glucose, at r =-.74, p<.05). The mean improvement for resistin was 17914.3 to 15266.8 and the resistin and insulin relationship was moderately correlated (r = .39). Within the rosi group, the mean change in insulin (-4.2) from baseline correlated with an improvement in VK response by a mean of 1.3 log (p<0.001, r=0.60). Using linear regression and the 3 variables adiponectin, QUICKI and fasting insulin, r2=0.56, suggesting a high in sample proportion of variability on outcome measures (improvement in VK). Discussion: Rosi given over 12 weeks is associated with improvement in IR and adiponectin levels in CHC, GT 1 patients. Among the patients who received rosi and improved their fasting insulin levels, there was a significant improvement in 24 hour VK response to interferon-alfacon-1 therapy.
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I'm posting the three studies they referred to.
Co
Viral Kinetic Response to 12 Week Treatment with Rosiglitazone in Chronic Hepatitis C, Genotype 1 Patients Who Are Previous Relapsers or Nonresponders to Pegylated Interferon and Ribavirin
S.J. Mills, R.J. Naus, K. Barstow, S. Harrison, Brooke Army Medical Center, San Antonio, TX;
Background: Insulin resistance (IR) is associated with CHC GT 1 virus. IR is associated with decreased SVR. The aim of this trial was to evaluate the effects rosiglitazone (rosi) on insulin sensitivity in a group of CHC, GT 1, patients who are prior nonresponders or relapsers to peg-interferon and RBV and assess viral kinetic (VK) response to interferon-alfacon-1 given before and 12 weeks after rosi was initiated. Methods: Thirty-four IR, GT 1, CHC patients, nonresponders (n=23), relapsers (n=11)to peg-interferon and RBV enrolled. Patients randomized to rosi 8mg daily and diet/exercise recs vs diet/exercise recs alone. Baseline VK obtained at time point zero, 8, 16, 24 hours, day 3, 5 and 7 after giving a 15mcg single dose of interferon-alfacon-1. Repeat VK were obtained 12 weeks later after a second dose of 15mcg of interferon-alfacon-1 was given. Results: 33 of 34 eligible patients completed the 12-week study and obtained repeat VK. Mean age:49.6 years(range 23 - 66), 45.5% female, 48.5% Cauc, 36% AA. Mean BMI:29.8, 36.4% were F3/4, mean QUICKI:0.32, logarithmic (log) mean viral load:13.29. Eighteen patients received rosi. No difference was observed between the two groups at baseline. Mean QUICKI improved from 0.32 to 0.33 in the rosi group and 0.31 to 0.32 in the diet/exercise group. Mean log value at baseline for the rosi group was 13.68, and decreased to 12.47 by the end of the first 24-hour period. A similar decline was noted with the second injection given at 12 weeks. No sig difference compared with the diet/exercise group. Patients (in either group) who improved QUICKI had a moderate corr(r=.34) with improvement in 24 hr VK. Glucose at week 12 correlated (r =-.44, p < .05) with viral load. Mean adiponectin improved from 20250.3 to 33761.5 in patients who improved their IR and adiponectin at day 97 was significantly and inversely correlated with day 97 glucose, at r =-.74, p<.05). The mean improvement for resistin was 17914.3 to 15266.8 and the resistin and insulin relationship was moderately correlated (r = .39). Within the rosi group, the mean change in insulin (-4.2) from baseline correlated with an improvement in VK response by a mean of 1.3 log (p<0.001, r=0.60). Using linear regression and the 3 variables adiponectin, QUICKI and fasting insulin, r2=0.56, suggesting a high in sample proportion of variability on outcome measures (improvement in VK). Discussion: Rosi given over 12 weeks is associated with improvement in IR and adiponectin levels in CHC, GT 1 patients. Among the patients who received rosi and improved their fasting insulin levels, there was a significant improvement in 24 hour VK response to interferon-alfacon-1 therapy.
Yes I had an Endoscopy a few months ago, which showed Esophageal Verices caused by this infernal disease. I start having them banded on the 16th. It will be 3-6 procedures according to the doctor. I'm opting to wait. It is a slow moving disease, and who knows, something may come out sooner than 2011.
I’m very vigilant in being sure my doctors do timely follow-ups and tests on me. Luckily, I have good medical insurance so I don’t have to go broke, although I had to quit my job to maintain my disability medical insurance. Only in America...
So we both wait, but we will be victorious. I have no doubt.
Magnum
I’m very vigilant in being sure my doctors do timely follow-ups and tests on me. Luckily, I have good medical insurance so I don’t have to go broke, although I had to quit my job to maintain my disability medical insurance. Only in America...
So we both wait, but we will be victorious. I have no doubt.
Magnum
I figured when she told me "all of my patients clear" , she meant the ones that last the duration of 12 weeks with svr.... well duh... .. talk about spin.
cw - I am exercising now on a treadmill that they have set up for the teachers where I teach.. even has cable tv! very cool.
my glucose is still high in the morning, 110-120, even thought the metformin has been doubled and I am exercising... maybe it takes awhile?
HI apache! yeah, i remember all that.
I am just hoping and praying that IR is the reason I failed.
As far my doctor goes... of course I am getting a new one... and am seriously thinking of trying to talk my pcp into treating me, as he is quite open to all options. I think he would probably do anything I asked as long as I can back it up with studies , etc.
It is just too hard to run around trying to find a gastro or hepa that is willing to work a little outside of the box... many seem to be content with just following standard protocol.. I guess they reluctant due to lawsuits.
My liver doc does want me to come back in , in april for an ultrasound... probably worthless, although I have had an ultrasound tech that an ultrasound will show a fatty liver as well as liver cancer.
I am going to try an wait on the polymerase/protease inhibitor combos for round 2.
I just don't have much faith in the infergen, or a retreatment with riba/inf. any opinons?
thanks,
bandman
cw - I am exercising now on a treadmill that they have set up for the teachers where I teach.. even has cable tv! very cool.
my glucose is still high in the morning, 110-120, even thought the metformin has been doubled and I am exercising... maybe it takes awhile?
HI apache! yeah, i remember all that.
I am just hoping and praying that IR is the reason I failed.
As far my doctor goes... of course I am getting a new one... and am seriously thinking of trying to talk my pcp into treating me, as he is quite open to all options. I think he would probably do anything I asked as long as I can back it up with studies , etc.
It is just too hard to run around trying to find a gastro or hepa that is willing to work a little outside of the box... many seem to be content with just following standard protocol.. I guess they reluctant due to lawsuits.
My liver doc does want me to come back in , in april for an ultrasound... probably worthless, although I have had an ultrasound tech that an ultrasound will show a fatty liver as well as liver cancer.
I am going to try an wait on the polymerase/protease inhibitor combos for round 2.
I just don't have much faith in the infergen, or a retreatment with riba/inf. any opinons?
thanks,
bandman
I'm waiting for a good new trial even if it's a few years. As you know this disease can be a slow mover. Magnum you've been through double dosing before I wouldn't go there again. Just watch you're diet and health and get your mri's and sonograms done.Have you had an endoscopy? good luck giddyup
"The doc that did my first round tx, doubted me greatly when I told her i thought I was IR."
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We doubted her greatly too....when she said all her patients cleared ; )
"When I told her i had all the symptoms of IR, she said like what?? I listed them and she said, well yes, but you do not have the two most important ones.... your are not obese and you are not diabetic!"
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Family history is the most important and she forgot to ask you. I swear, your docs did all the wrong things. The hepatologist couldn't wait to get rid of you when you failed. They refused to test you for IR. When they finally agreed, they tested only the blood sugar and refused to do the insulin test. And after you insisted multiple times, they did a 2 hr GTT and misread the results! LOL
"thanks cs and cw for all your help , helping me figure this out! "
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Wed guided but you did the hard work. You should be very proud of yourself. You taught a doctor about IR and that will help his other patients.
Now that you'll have more time off you need to start getting more active. It will help lower the HOMA.
Co
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We doubted her greatly too....when she said all her patients cleared ; )
"When I told her i had all the symptoms of IR, she said like what?? I listed them and she said, well yes, but you do not have the two most important ones.... your are not obese and you are not diabetic!"
------------------
Family history is the most important and she forgot to ask you. I swear, your docs did all the wrong things. The hepatologist couldn't wait to get rid of you when you failed. They refused to test you for IR. When they finally agreed, they tested only the blood sugar and refused to do the insulin test. And after you insisted multiple times, they did a 2 hr GTT and misread the results! LOL
"thanks cs and cw for all your help , helping me figure this out! "
----------------
Wed guided but you did the hard work. You should be very proud of yourself. You taught a doctor about IR and that will help his other patients.
Now that you'll have more time off you need to start getting more active. It will help lower the HOMA.
Co
Hi Bandman,
It's amazing how much trouble I had persuading my primary care doc to test my fasting insulin. Because I'm slim like you and my fasting glucose is normal, she really dug her heels in and said there was no need. She finally agreed after I spun a very elaborate story, invoking a confused assortment of facts and white lies. She'd never heard of HOMA and I did a pretty awful job of explaining it to her. Wish Co had been with me.
I wonder when IR testing will be a routine part of the screening process, pre-tx.
It's amazing how much trouble I had persuading my primary care doc to test my fasting insulin. Because I'm slim like you and my fasting glucose is normal, she really dug her heels in and said there was no need. She finally agreed after I spun a very elaborate story, invoking a confused assortment of facts and white lies. She'd never heard of HOMA and I did a pretty awful job of explaining it to her. Wish Co had been with me.
I wonder when IR testing will be a routine part of the screening process, pre-tx.
If more Dr tried on a pair of CoWriters's IR colored glasses, there might be less non-responders and more SVR.
-----------------------------------------
No might be about it.
CS
-----------------------------------------
No might be about it.
CS
bandman54 and all
Hey bandman, how ya been ?
I remember last fall when you were treating, and on the other forum I suggested you get tested for IR after your 4wk pcr showed poor response.
The resistance you got from your DR, about IR, and how they convinced you back then that you did not have IR (without a homa2 test ?) I felt back then was a mistake and tried to tell ya. Hopefully your Dr wont make that IR mistake again. This probably happens to many people. Some Drs seem to have a resistance to insulin resistance.
Am glad to know that Now, you might have found your missing link of the non-response to inf...IR . You might have failed your first tx, but now with your IR under control, think you have a much better chance of SVR if you try again. With or with out the new PI drugs, you might have a RVR now.
If more Dr tried on a pair of CoWriters's IR colored glasses, there might be less non-responders and more SVR.
apache
Hey bandman, how ya been ?
I remember last fall when you were treating, and on the other forum I suggested you get tested for IR after your 4wk pcr showed poor response.
The resistance you got from your DR, about IR, and how they convinced you back then that you did not have IR (without a homa2 test ?) I felt back then was a mistake and tried to tell ya. Hopefully your Dr wont make that IR mistake again. This probably happens to many people. Some Drs seem to have a resistance to insulin resistance.
Am glad to know that Now, you might have found your missing link of the non-response to inf...IR . You might have failed your first tx, but now with your IR under control, think you have a much better chance of SVR if you try again. With or with out the new PI drugs, you might have a RVR now.
If more Dr tried on a pair of CoWriters's IR colored glasses, there might be less non-responders and more SVR.
apache
Yes, I agree with you. I don't know who sets these rules on how long to treat before realizing you're not going to clear with a particular regiment. Sometimes I wonder if the insurance companies aren't lending a hand towards that decision. After all, they wouldn't want us to take away money they could spend on private jest and laying on the beaches of Acapulco sipping Pina Coladas.
As for waiting. I think maintaining a healthy lifestyle and doing regular check-ups like abdominal ultra sounds and liver cancer tests every 6 months as Gish suggests, could keep you able to wait longer and longer.
Who knows, some new miracle drug may come out that will make both Telepravir and Bocepravir seem like they came from the dark ages. The polio vaccine is a great example. That turned the entire medical field upside down overnight with bewilderment and saved perhaps millions of people.
At any rate, I wish you the very best. I'm like you, I won't give up and will continue to fight until I'm victorious. As for these new drugs, where people see risks, I see opportunity...
Magnum
As for waiting. I think maintaining a healthy lifestyle and doing regular check-ups like abdominal ultra sounds and liver cancer tests every 6 months as Gish suggests, could keep you able to wait longer and longer.
Who knows, some new miracle drug may come out that will make both Telepravir and Bocepravir seem like they came from the dark ages. The polio vaccine is a great example. That turned the entire medical field upside down overnight with bewilderment and saved perhaps millions of people.
At any rate, I wish you the very best. I'm like you, I won't give up and will continue to fight until I'm victorious. As for these new drugs, where people see risks, I see opportunity...
Magnum
as long as you are talking to Gish, find out if he is thinking you might get into an electoporation trial with merck. Inovio is bring their phase 3 trials state side, and you get an 99 % reduction in virus before starting SOC...might be worth a gander
http://www.prweb.com/releases/dna_vaccine/inovio_biomedical/prweb1627194.htm
http://www.prweb.com/releases/dna_vaccine/inovio_biomedical/prweb1627194.htm
I just wanted to say thanks for posting the recommendations by Dr. Gish. I'm sure that it will be helpful to many people. However, I've all but decided that I'm going to go with the Boceprevir whenever it's FDA approved because of my past experience with the Telaprevir. I base my reasons on: A: I haven't been exposed to the Boceprevir and I was exposed to Telaprevir.., therefore I'd be more likely to have resistance to it than to Boceprevir; even though technically, I was only on the Telaprevir for 6 wks and that was almost 2 yrs ago; so my hepatologist that I last saw at Shands told me that I could even try it again using all three drugs. But, I choose not to for the following reason... B: I had a horrific rash 2 weeks into my treatment on the Telaprevir. I KNOW that it was because of the Telaprevir and not the Riba since I was in the NO RIBA group. And I also know that it wasn't caused by the interferon since I've been on interferon 9 other times (not including that TX) and I'd never had a rash that bad. It literally looked like I'd put my arms into a vat of boiling water! Now, at this point, I'm up to having treated 10 times. I just feel that after all that I've been through that I should have some say so, as to what drug I want to go with, you know? And I've decided that when the time comes, I'm going with Boceprevir, Riba and Peg-Intron at the highest possible doses and hope for the best. And since it won't be within the confines of a trial, I'll use the rescue drugs rather than reduce dose. I did like your idea (Magnum) of writing all this down and presenting it to the doctor ahead of time. (Wasn't it you that did that? Or am I thinking of somebody else here on Medhelp?) I also want to have longer than just a 4 week period of time, to be allowed to clear the virus because I think that with my body, if I am even going to be able to clear (and that's a big IF) that I will need to have at the very least, up until the 12 week point to be able to have them make that decision on me, whether to continue or not. I honestly don't think that it will happen that quickly for me to clear in 4 weeks, because of my past experiences. On the past two trials, I dropped really fast and really low in the 1st 4 weeks, but still had lingering virus and I was bumped out of the trial. So, if I took until 12 weeks to clear and I did actually clear by 12 weeks, then, I'd want to continue to treat on until 48 wks past the viral clearance point; realizing of course that the later part of that would be just with SOC. Also, I've thought about it and I'd want to have a lead-in of one month of SOC before adding the BOC. This is all of course if I can get the darn doctor on board with what I want to do, you know? Does any of this sound like a doable idea? And also, for Cocksparrow (if you're reading this) I will fully investigate any Insulin Resistance that may be going on, prior to treating again.
Susan400
Susan400
Yeah I was talking about you. I knew you would know I was too.
I like using you as an example because you prove that
a. You don’t need to be overweight to be Insulin Resistant and
b. Your Glucose doesn’t need to be over 100 to be IR.
So the two main ways of diagnosing IR don’t necessarily apply to us.
Which goes some way to explaining why its so hard to get the damn tests.
Anyone who fails Tx should have a fasting glucose and Insulin test done.
CS
I like using you as an example because you prove that
a. You don’t need to be overweight to be Insulin Resistant and
b. Your Glucose doesn’t need to be over 100 to be IR.
So the two main ways of diagnosing IR don’t necessarily apply to us.
Which goes some way to explaining why its so hard to get the damn tests.
Anyone who fails Tx should have a fasting glucose and Insulin test done.
CS
the only thing Gish can be thinking is you may have one more shot at best, and the telprevir might put you over the hump in less time, which at this point, with the damage and upcoming surgeries, why beat the same dead horse...why not wait for a fresh mount so to speak.
I'd check with those who did survive double dosing, not too many do...even is the craziness doesn't get you the blood drops will.
Check out this article, it's long and deals with HIV and HCV both, but covers all the sides and complications, oxidative stress, necrosis, insulin resistance, lipidemia, DNA, cytokines and much much more. It might help you decide where and when to jump in, and what to do about insulin resistance in particular.
http://www.hcvadvocate.org/hepatitis/About_Hepatitis_pdf/1.1.1_Living_With_HepatitisC/SIDE_EFFECTS.pdf
I'd check with those who did survive double dosing, not too many do...even is the craziness doesn't get you the blood drops will.
Check out this article, it's long and deals with HIV and HCV both, but covers all the sides and complications, oxidative stress, necrosis, insulin resistance, lipidemia, DNA, cytokines and much much more. It might help you decide where and when to jump in, and what to do about insulin resistance in particular.
http://www.hcvadvocate.org/hepatitis/About_Hepatitis_pdf/1.1.1_Living_With_HepatitisC/SIDE_EFFECTS.pdf
magnum: best of luck with your decision, it seems like a good choice to me. If you have problems with ifn-based antiviral response the best option is to rely on something else. The stats for heavy-dosage/longer-duration in non-responders do generally show some improvement, but not much. Checking out the ir and adding HRs anti-fibrotic supplements are probably good steps in the interim.
badman: interesting story - thanks for posting
Here are some quotes from the panel of Drs in the CME review on medscape
http://cme.medscape.com/viewprogram/17843_pnt
that mikesimon posted a while back. This should all be current as of May'08
"Dr. Harrison: The bottom line for me is that you should be testing for insulin resistance. Baseline, when you are ordering a viral load, getting a genotype, checking the CBC, the platelet count, that sort of thing. I think throwing in a fasting insulin and a fasting glucose, but ensuring that it is a fasting glucose, and by just adding a fasting insulin, I think gives you a tremendous amount of data that could be used. Whether or not you decide to treat the patient, that is a whole other discussion about how to address the insulin resistance if you are going to treat the patient. But I think at this point there is enough compelling data with fibrosis progression, and with outcomes. If you are going to tell your patient what their probability of a response is, how can you do that if you do not know if they are insulin-resistant. The IDEAL study was recently published. It did not collect insulin, it looked at fasting glucose, showed a significant reduction in SVR with fasting glucoses greater than 100 mg/dL. You could argue that maybe just getting a fasting glucose would work, but I still think you are selling yourself short if you do not get a fasting insulin.
Dr. Jensen: Michael, is this standard of care?
Dr. Fried: No, it is not standard of care. I look at it selectively, particularly in my previous nonresponders or relapsers who looked like they have some features in metabolic syndrome and things. I will look at that as a potentially treatable factor, but I do not think it is standard of care at this point. We just do not have enough prospective data that when you treat the insulin resistance, you have clearly improved sustained virologic response rates. I think the data are very conflicting.
Dr. Nelson: I think that that is the key. I agree with Steve that, in general, you would like to know: are patients that you are evaluating just upfront during an initial evaluation? Are they someone who is at more risk for more rapid progression of their fibrosis? But the issue is: are you going to use it prior to treating someone with PEG-IFN. Before you are willing to adopt that as standard of care, you have to have answered the other part that you brought up - if you find it, how are you going to adjust therapy. Currently, there are a number of trials being presented here at this meeting, and my summary of what I have seen so far is that it does not look like treating insulin resistance, either before or during therapy, has so far made a convincing difference. I think that the checking of insulin resistance is another prognostic factor for how the person's going to do, but I struggle then when I see insulin resistance. What am I going to do about it in the setting of antiviral therapy?
Dr. Harrison: There are 3 abstracts being presented here that address the issue of response to therapy if you mitigate or you improve insulin resistance. So let's separate out fibrosis progression and whether or not you are going to test based on that, and look at what we do if we have insulin resistance to improve SVR. There is one abstract that looks at just improving insulin resistance and seeing what happens with a dose of interferon. What happens is there is a dramatic improvement in first-phase viral kinetics of about 1.3 log and so that is provocative. The next study out of the Cleveland Clinic with Nizar Zein, he will be presenting data that suggest that RVRs improve if you pretreat patients with a glitazone for 12 weeks prior to initiating therapy.
The final paper is an SVR-derived paper out of the University of Michigan that shows that if you start triple therapy with pioglitazone, PEG-IFN, and ribavirin together, simultaneously, SVR is not improved at the end of the day. I think the problem with that is there was no preload, there was no treating the insulin resistance beforehand to try to improve interferon signaling. Granted, these are all very early studies, they are small numbers. There are a lot more data that need to be derived and those studies are ongoing and hopefully we will have that data before too long. But I agree, we do not have end-of-treatment data, we do not have SVR data. I still think it is very helpful to have, to inform my patients how they are likely to respond once I start them on interferon therapy."
references for the papers Dr. Harrison mentions were not included (aasld 07 abstracts?) overall it looks like there's
clearer consensus that IR is worth identifying than on whether its treatment improves svr.
badman: interesting story - thanks for posting
Here are some quotes from the panel of Drs in the CME review on medscape
http://cme.medscape.com/viewprogram/17843_pnt
that mikesimon posted a while back. This should all be current as of May'08
"Dr. Harrison: The bottom line for me is that you should be testing for insulin resistance. Baseline, when you are ordering a viral load, getting a genotype, checking the CBC, the platelet count, that sort of thing. I think throwing in a fasting insulin and a fasting glucose, but ensuring that it is a fasting glucose, and by just adding a fasting insulin, I think gives you a tremendous amount of data that could be used. Whether or not you decide to treat the patient, that is a whole other discussion about how to address the insulin resistance if you are going to treat the patient. But I think at this point there is enough compelling data with fibrosis progression, and with outcomes. If you are going to tell your patient what their probability of a response is, how can you do that if you do not know if they are insulin-resistant. The IDEAL study was recently published. It did not collect insulin, it looked at fasting glucose, showed a significant reduction in SVR with fasting glucoses greater than 100 mg/dL. You could argue that maybe just getting a fasting glucose would work, but I still think you are selling yourself short if you do not get a fasting insulin.
Dr. Jensen: Michael, is this standard of care?
Dr. Fried: No, it is not standard of care. I look at it selectively, particularly in my previous nonresponders or relapsers who looked like they have some features in metabolic syndrome and things. I will look at that as a potentially treatable factor, but I do not think it is standard of care at this point. We just do not have enough prospective data that when you treat the insulin resistance, you have clearly improved sustained virologic response rates. I think the data are very conflicting.
Dr. Nelson: I think that that is the key. I agree with Steve that, in general, you would like to know: are patients that you are evaluating just upfront during an initial evaluation? Are they someone who is at more risk for more rapid progression of their fibrosis? But the issue is: are you going to use it prior to treating someone with PEG-IFN. Before you are willing to adopt that as standard of care, you have to have answered the other part that you brought up - if you find it, how are you going to adjust therapy. Currently, there are a number of trials being presented here at this meeting, and my summary of what I have seen so far is that it does not look like treating insulin resistance, either before or during therapy, has so far made a convincing difference. I think that the checking of insulin resistance is another prognostic factor for how the person's going to do, but I struggle then when I see insulin resistance. What am I going to do about it in the setting of antiviral therapy?
Dr. Harrison: There are 3 abstracts being presented here that address the issue of response to therapy if you mitigate or you improve insulin resistance. So let's separate out fibrosis progression and whether or not you are going to test based on that, and look at what we do if we have insulin resistance to improve SVR. There is one abstract that looks at just improving insulin resistance and seeing what happens with a dose of interferon. What happens is there is a dramatic improvement in first-phase viral kinetics of about 1.3 log and so that is provocative. The next study out of the Cleveland Clinic with Nizar Zein, he will be presenting data that suggest that RVRs improve if you pretreat patients with a glitazone for 12 weeks prior to initiating therapy.
The final paper is an SVR-derived paper out of the University of Michigan that shows that if you start triple therapy with pioglitazone, PEG-IFN, and ribavirin together, simultaneously, SVR is not improved at the end of the day. I think the problem with that is there was no preload, there was no treating the insulin resistance beforehand to try to improve interferon signaling. Granted, these are all very early studies, they are small numbers. There are a lot more data that need to be derived and those studies are ongoing and hopefully we will have that data before too long. But I agree, we do not have end-of-treatment data, we do not have SVR data. I still think it is very helpful to have, to inform my patients how they are likely to respond once I start them on interferon therapy."
references for the papers Dr. Harrison mentions were not included (aasld 07 abstracts?) overall it looks like there's
clearer consensus that IR is worth identifying than on whether its treatment improves svr.
"Here is somebodies Glucose level it was 97. Normal in other words
No matter how hard he tried he could not convince his hepatologist to run an Insulin test.
Why would he his glucose was normal.
Eventually he talked his normal Dr to run an Insulin test.
The result came back 18. This gave him a HOM-IR score of 4.48.
Damn near diabetic.
When he was on Tx he managed to only get a 0.5 log drop by week 12. "
Hey CS, you talkin about me??? sounds like it.
My HOMA came down to 3.3 on the lowest dose of metformin... the doc has now doubled it to 1000 mg. 2x per day.
The doc that did my first round tx, doubted me greatly when I told her i thought I was IR. I think she didnt want me to blame her for failing tx... which I do.
When I told her i had all the symptoms of IR, she said like what?? I listed them and she said, well yes, but you do not have the two most important ones.... your are not obese and you are not diabetic!" I could have slapped her What an idiot.
Anyway, skinny as a rail AND I.R., no doubt about it.
And yes, to all, please fast before your glucose and insulin test are done and they the blood taken for both shouldl be on the same day. I had to give my doc the HOMA formula... he was unaware, but very cooperative and wiling to learn.
thanks cs and cw for all your help , helping me figure this out!
bandman
No matter how hard he tried he could not convince his hepatologist to run an Insulin test.
Why would he his glucose was normal.
Eventually he talked his normal Dr to run an Insulin test.
The result came back 18. This gave him a HOM-IR score of 4.48.
Damn near diabetic.
When he was on Tx he managed to only get a 0.5 log drop by week 12. "
Hey CS, you talkin about me??? sounds like it.
My HOMA came down to 3.3 on the lowest dose of metformin... the doc has now doubled it to 1000 mg. 2x per day.
The doc that did my first round tx, doubted me greatly when I told her i thought I was IR. I think she didnt want me to blame her for failing tx... which I do.
When I told her i had all the symptoms of IR, she said like what?? I listed them and she said, well yes, but you do not have the two most important ones.... your are not obese and you are not diabetic!" I could have slapped her What an idiot.
Anyway, skinny as a rail AND I.R., no doubt about it.
And yes, to all, please fast before your glucose and insulin test are done and they the blood taken for both shouldl be on the same day. I had to give my doc the HOMA formula... he was unaware, but very cooperative and wiling to learn.
thanks cs and cw for all your help , helping me figure this out!
bandman
Echo what Port said.
Even with the recommended dosage of Infergen I could not do it. Those who have treated with it or currently treating are the ultimate warriors.
The PI's by all indications will be added to the next generation of SOC ensuring greater odds of SVR. With Dr. Gish in charge and the addition of a PI, I see successful SVR in your future. All good things come to those who wait. I wish you only the best.
Trin
Even with the recommended dosage of Infergen I could not do it. Those who have treated with it or currently treating are the ultimate warriors.
The PI's by all indications will be added to the next generation of SOC ensuring greater odds of SVR. With Dr. Gish in charge and the addition of a PI, I see successful SVR in your future. All good things come to those who wait. I wish you only the best.
Trin
That seems like the soundest decision to make, as long as you stay on Dr. Gish's radar screen until the PI's come off trial.
All the best,
Port
All the best,
Port
I was right about the Glucose test being high and suggesting to Dr. Gish I had a problem. I was supposed to fast, but it was not written on the order. Therefore, I have to do it again with fasting. This is what happens when people don't know what they're doing when writing orders. A little less partying the night before would be a good idea for them.
Thanks to all for your input and suggestions. I'm electing to wait for VX-950 as Dr. Gish suggested. He will know at what point things get to where I will have to treat instead of waiting...
Magnum
Thanks to all for your input and suggestions. I'm electing to wait for VX-950 as Dr. Gish suggested. He will know at what point things get to where I will have to treat instead of waiting...
Magnum
Nasty, powerful stuff that Infergen. Nearly put me in my grave. However, I was overdosing at 24mcg daily as opposed to the typical 15mcg. For you it may be fine. Only your doctor knows for sure. I can say this, during the overdosing, it did bring my viral count from 3.2000,000 to 6200 in 12 weeks, but it was killing me at that dose. I'm electing to wait for VX-950, as Dr. Gish suggested.
Magnum
Magnum
I would never counsel against an IR test - I think that's always a prudent course.
That being said, if you ate any significant carbohydrates with a few hours of your test then a glucose level of 103 would look very good to me. If you didn't ingest any carbs or if the test was more than 4 hours after you ate then 103 wouldn't look so good.
One thing your gastro said that just seems wrong is that if you are undetectable at week 12 then he would advise continuing treatment. I think that an undetectable reading at week 4 should be the determining factor. You've failed 4 times and though I don't know your treatment regimens I assume they were within guidelines. I don't recall if and when you became undetectable or how long you treated. But again I assume you must have had reason to re-treat. I think it is clear that you haven't responded well and if I was going to consider enduring treatment again I would want to see some very strong positive predictor and that for me would be undetectable at week 4. So, I might treat but not longer than 4 weeks if not undetectable by then.
Your bilirubin looks great to me and if it is "Total Bilirubin". If your number refers to your "Direct" or "Conjugated Bilirubin" then I think it's OK. Different labs have different reference range but .3 is high normal on some and if the range tops out at .2 a result of .3 is still nothing alarming. I wouldn't think twice about it.
I'd ask Gish about the double treatment and ask him whether if you did treat and became undetectable by week 4 would he see a reason to continue. If he says "no" or "you'll never be undetectable at week 4" then I would take his advice and wait for the PI. He if said "yes" or "perhaps" then I might take a shot.
Mike
That being said, if you ate any significant carbohydrates with a few hours of your test then a glucose level of 103 would look very good to me. If you didn't ingest any carbs or if the test was more than 4 hours after you ate then 103 wouldn't look so good.
One thing your gastro said that just seems wrong is that if you are undetectable at week 12 then he would advise continuing treatment. I think that an undetectable reading at week 4 should be the determining factor. You've failed 4 times and though I don't know your treatment regimens I assume they were within guidelines. I don't recall if and when you became undetectable or how long you treated. But again I assume you must have had reason to re-treat. I think it is clear that you haven't responded well and if I was going to consider enduring treatment again I would want to see some very strong positive predictor and that for me would be undetectable at week 4. So, I might treat but not longer than 4 weeks if not undetectable by then.
Your bilirubin looks great to me and if it is "Total Bilirubin". If your number refers to your "Direct" or "Conjugated Bilirubin" then I think it's OK. Different labs have different reference range but .3 is high normal on some and if the range tops out at .2 a result of .3 is still nothing alarming. I wouldn't think twice about it.
I'd ask Gish about the double treatment and ask him whether if you did treat and became undetectable by week 4 would he see a reason to continue. If he says "no" or "you'll never be undetectable at week 4" then I would take his advice and wait for the PI. He if said "yes" or "perhaps" then I might take a shot.
Mike
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