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DDW 2007 ABSTRACTS -- Statins, Metabolic Predictors, Diabetes, , Predictive Values, and a new rectal treatment...
that I'm sure "GoofyDad" will comment on. It's Digestive Disease Week 2007 (DDW) is upon us with lots of interesting studies to examine. Wish there was an easier way to link to the studies, but for those interested, this will have to do.
1. First go here:http://www.ddw.org/
2. Then click on the word "here" in the second paragraph which reads in full" Plan or modify your DDW itinerary in advance and view accepted abstracts *here*."
3. Now click on "search" in the left-hand sidebar.
4. Click on the second heading "category" and select "viral hepatitis" near the bottom.
5. Now click on "Search" at the bottom and you will be directed to a list of the abstracts.
(For those with more time and who are more computer savvy, you can register, save a custom list of abstracts, and possibly post that list here as a single link for others.)
1. First go here:http://www.ddw.org/
2. Then click on the word "here" in the second paragraph which reads in full" Plan or modify your DDW itinerary in advance and view accepted abstracts *here*."
3. Now click on "search" in the left-hand sidebar.
4. Click on the second heading "category" and select "viral hepatitis" near the bottom.
5. Now click on "Search" at the bottom and you will be directed to a list of the abstracts.
(For those with more time and who are more computer savvy, you can register, save a custom list of abstracts, and possibly post that list here as a single link for others.)
Have any of you been able to get view of the following:
Key Oral Presentations at DDW 2007
Favorable Cross-Resistance Profile of HCV-796 and Boceprevir (SCH-503034) and Enhanced Anti-Replicon Activity Mediated By Combination Treatment; R. Ralston, Monday, May 21, 11:15 a.m., Room 206
Pharmacodynamic Analysis of the Antiviral Activity of the Non-Nucleoside Polymerase Inhibitor, HCV-796, in Combination With Peginterferon Alfa-2b in Treatment-Naive Patients With Chronic HCV; E.S. Maller, Monday, May 21, 2:15 p.m., Room 206
Phase II Study of celgosivir in combination with Peginterferon alfa-2b and ribavirin in chronic hepatitis C genotype 1 nonresponder patients; K.D. Kaita, Monday, May 21, 2:45 p.m., Room 206
Big question is "is there more help here for non-responders with Geno Type 1"?
I fear getting too sick for treatment by the VX-950, HCH-796 or SH-503034 will ever become generally available..Best I can tell none of these will get to FDA approval before 2012.
What do you think?
Reckon I'll just hnag on and hope my liver does the same.
Thanks for all the interesting info. Dr. Zhang had a paper on his website that told how to take low dose interferon under the tongue and it lowers the viral load. I don't know if it got rid of the virus. It was in the experimental stage. He has the names and addresses of the doctors that know how to do it in his office.
Jim,
Thanks for posting all that stuff.
I think I'll pass on sticking interferon up my butt! This is NOT going to happen with me. That's where I'll ABSOLUTELY draw the line.
Susan
Thanks for posting all that stuff.
I think I'll pass on sticking interferon up my butt! This is NOT going to happen with me. That's where I'll ABSOLUTELY draw the line.
Susan
Agree, GoogfyDad MUCT comment :) ... at on all the "rectal" stuff!
Thank you A LOT!!!
Thank you A LOT!!!
gee Jimbo, you must type 90 a minute while youre cuttin and pastin...anyway, thanks for all that, good reading!
METABOLIC SYNDROME IS A STRONG PREDICTOR OF TREATMENT FAILURE IN PATIENTS WITH CHRONIC HEPATITIS C
I. Hanouneh1; A. E. Feldstein1; R. Lopez1; K. B. Cesario1; A. A. Pillai1; C. O. Zein2; N. N. Zein1
1. Gastroenterology & Hepatology, Cleveland Clinic Foundation, Cleveland, OH, USA.
2. Gastroenterology & Hepatology, Case Western Reserve University, Louis Stokes VAMC, Cleveland, OH, USA.
Background: The metabolic syndrome (MS) is a unique pathophysiologic condition whose underlying mechanism is related to insulin resistance. In HCV patients undergoing therapy with Peg IFN/RBV, insulin resistance has been linked to treatment failure.
Our Aims were to estimate the prevalence of MS in HCV patients undergoing anti-viral therapy and to assess its predictive value in treatment outcome.
Methods: All HCV patients that were treated with Peg IFN/RBV between 2002 and 2004 and had clinical data to assess for MS were identified (n=251). MS was defined using the ATP III criteria. Descriptive statistics were computed for all factors. Univariate analysis was performed to compare variables of interest. A logistic regression analysis was performed to study multivariable associations. The final model contained gender, ethnicity, genotype, metabolic syndrome, fibrosis, and steatosis stage.
Results: MS was present in 71/251 (28%) patients. MS was less common in Caucasian patients compared to non-Caucasian patients [49/193 (25%) vs 22/58 (38%), p=0.063]. Overall SVR was achieved in 121/251 (48%) patients. Genotype 1 (p<0.001), non-Caucasian ethnicity (p<0.001), male gender (p=0.04), higher fibrosis stage (p=0.02), higher BMI (p=0.003), and MS (p<0.001) were significantly associated with lack of SVR. The table presents the results of the multivariable logistic regression analysis. Adjusting for ethnicity, genotype, gender, fibrosis, and steatosis stage, subjects with MS are 2.8 times (95% CI: 1.5, 5.6) more likely to fail treatment than those without MS. Conclusion: MS is frequently seen in patients with chronic HCV and is an independent predictor of lack of response to antiviral therapy. If confirmed, MS could easily be incorporated in clinical practice to identify those who are most likely to benefit from antiviral therapy in the setting of HCV infection.
Factor (Reference) OR (95% CI) P value
Genotype (1 vs. Other) 5.2 (2.5, 10.6) <0.0001
Ethnicity (Other vs. Caucasian) 4.5 (2.0, 9.8) 0.0002
Metabolic Syndrome 2.8 (1.5, 5.6) 0.002
Fibrosis (1 stage increase) 1.4 (1.1, 1.7) 0.003
Gender (Male vs. Female) 1.6 (0.89, 2.9) 0.11
Steatosis (1 stage increase) 0.63 (0.39, 1.1) 0.08
I. Hanouneh1; A. E. Feldstein1; R. Lopez1; K. B. Cesario1; A. A. Pillai1; C. O. Zein2; N. N. Zein1
1. Gastroenterology & Hepatology, Cleveland Clinic Foundation, Cleveland, OH, USA.
2. Gastroenterology & Hepatology, Case Western Reserve University, Louis Stokes VAMC, Cleveland, OH, USA.
Background: The metabolic syndrome (MS) is a unique pathophysiologic condition whose underlying mechanism is related to insulin resistance. In HCV patients undergoing therapy with Peg IFN/RBV, insulin resistance has been linked to treatment failure.
Our Aims were to estimate the prevalence of MS in HCV patients undergoing anti-viral therapy and to assess its predictive value in treatment outcome.
Methods: All HCV patients that were treated with Peg IFN/RBV between 2002 and 2004 and had clinical data to assess for MS were identified (n=251). MS was defined using the ATP III criteria. Descriptive statistics were computed for all factors. Univariate analysis was performed to compare variables of interest. A logistic regression analysis was performed to study multivariable associations. The final model contained gender, ethnicity, genotype, metabolic syndrome, fibrosis, and steatosis stage.
Results: MS was present in 71/251 (28%) patients. MS was less common in Caucasian patients compared to non-Caucasian patients [49/193 (25%) vs 22/58 (38%), p=0.063]. Overall SVR was achieved in 121/251 (48%) patients. Genotype 1 (p<0.001), non-Caucasian ethnicity (p<0.001), male gender (p=0.04), higher fibrosis stage (p=0.02), higher BMI (p=0.003), and MS (p<0.001) were significantly associated with lack of SVR. The table presents the results of the multivariable logistic regression analysis. Adjusting for ethnicity, genotype, gender, fibrosis, and steatosis stage, subjects with MS are 2.8 times (95% CI: 1.5, 5.6) more likely to fail treatment than those without MS. Conclusion: MS is frequently seen in patients with chronic HCV and is an independent predictor of lack of response to antiviral therapy. If confirmed, MS could easily be incorporated in clinical practice to identify those who are most likely to benefit from antiviral therapy in the setting of HCV infection.
Factor (Reference) OR (95% CI) P value
Genotype (1 vs. Other) 5.2 (2.5, 10.6) <0.0001
Ethnicity (Other vs. Caucasian) 4.5 (2.0, 9.8) 0.0002
Metabolic Syndrome 2.8 (1.5, 5.6) 0.002
Fibrosis (1 stage increase) 1.4 (1.1, 1.7) 0.003
Gender (Male vs. Female) 1.6 (0.89, 2.9) 0.11
Steatosis (1 stage increase) 0.63 (0.39, 1.1) 0.08
Some discussion already here: http://www.medhelp.org/forums/hepatitis/messages/46494.html
Increased SVR Rate with 48 Wks
Increased SVR Rate with 48 Wks
Retrospective Analysis of the Effect of Taking a Statin Along with Peginterferon and Ribavirin (PI+R) on SVR.
T. Bader1; M. Madhoun1; S. Rizvi1
1. VA Medical Center, University of Oklahoma, Oklahoma City, OK, USA.
Methods: 104 patients taking PI+R were compared to 30 patients who by chance took triple therapy [(PI+R) plus a statin]. A modified intent to treat approach was taken whereby if any patient had a least one data point after starting therapy, he or she was included in the denominator.
Virtually all patients taking a statin were on simvastatin (n=25); 2 were on lovastatin, 2 on atorvastatin and 1 on fluvastatin.
The pooled SVR rate* for the 104 patients on standard treatment was 37%. This is the highest SVR ever reported in the medical literature for a VA based population.
The pooled SVR rate for the triple therapy group was 63%. In terms of HCV subgroups, the effect was statistically strongest for genotype one, the most difficult subgroup to treat.
Conclusion: Statins appear to be associated with a higher SVR rate of standard PI+R therapy. This observation principally occurs on the basis of a medium powered statin (simvastatin) in terms of the Ikeda experiment (Hepatology 2006;44:117-125). The only patient to take fluvastatin during the study was cured. Statins need to be studied prospectively for their effect on hepatitis C and the outcome of treatment.
SVR Rate
No Statin
(%) p value
(chi-square) Statin
(%)
Genotype 1 16/65 (25) .014 11/20
(55)
Genotype
2 20/26
(77) .43 3/5
(60)
Genotype
3 7/15
(47) .035 5/5
(100)
Pooled
Analysis* 37% .009 63%
*Pooled analysis makes the population proportion 70% genotype 1 and 30% non-genotype 1 in order to mimic the proportion of genotypes in the USA. This is the standard method of reporting SVRs.
T. Bader1; M. Madhoun1; S. Rizvi1
1. VA Medical Center, University of Oklahoma, Oklahoma City, OK, USA.
Methods: 104 patients taking PI+R were compared to 30 patients who by chance took triple therapy [(PI+R) plus a statin]. A modified intent to treat approach was taken whereby if any patient had a least one data point after starting therapy, he or she was included in the denominator.
Virtually all patients taking a statin were on simvastatin (n=25); 2 were on lovastatin, 2 on atorvastatin and 1 on fluvastatin.
The pooled SVR rate* for the 104 patients on standard treatment was 37%. This is the highest SVR ever reported in the medical literature for a VA based population.
The pooled SVR rate for the triple therapy group was 63%. In terms of HCV subgroups, the effect was statistically strongest for genotype one, the most difficult subgroup to treat.
Conclusion: Statins appear to be associated with a higher SVR rate of standard PI+R therapy. This observation principally occurs on the basis of a medium powered statin (simvastatin) in terms of the Ikeda experiment (Hepatology 2006;44:117-125). The only patient to take fluvastatin during the study was cured. Statins need to be studied prospectively for their effect on hepatitis C and the outcome of treatment.
SVR Rate
No Statin
(%) p value
(chi-square) Statin
(%)
Genotype 1 16/65 (25) .014 11/20
(55)
Genotype
2 20/26
(77) .43 3/5
(60)
Genotype
3 7/15
(47) .035 5/5
(100)
Pooled
Analysis* 37% .009 63%
*Pooled analysis makes the population proportion 70% genotype 1 and 30% non-genotype 1 in order to mimic the proportion of genotypes in the USA. This is the standard method of reporting SVRs.
Copy (Highlight and Ctrl "C") and Paste (Ctrl "V") only take a couple of seconds. Now if it were just that easy to copy and paste myself to Ohau this evening :)
Be well.
-- Jim
Be well.
-- Jim
How to make treatment worse? Give it rectally, I mean, come on, who thought of that? I always found a bit of pride in being able to say "I give myself my shots weekly", where is the pride in a suppository?
Good info, jmjm, the insulin resistance is of particular importance to me, my blood sugar has been a bit high and I can't seem to lose any weight. And I get tired, I mean, tired. so I have cut out a lot of sugar and am still working in the garden, mowing or walking, but doesn't seem to help much. I'm having a biopsy next week, then I'll move on to the insulin resistance. For me, I don't think it will be a problem, I need to lose 30 pounds and then all will work better, I'm sure.
Fine post, sir, and very funny too, in a twisted, Tuesday nite way.
Willow doesn't want a suppository
Good info, jmjm, the insulin resistance is of particular importance to me, my blood sugar has been a bit high and I can't seem to lose any weight. And I get tired, I mean, tired. so I have cut out a lot of sugar and am still working in the garden, mowing or walking, but doesn't seem to help much. I'm having a biopsy next week, then I'll move on to the insulin resistance. For me, I don't think it will be a problem, I need to lose 30 pounds and then all will work better, I'm sure.
Fine post, sir, and very funny too, in a twisted, Tuesday nite way.
Willow doesn't want a suppository
Interestingly, my Gluscose was 60 during the initial stages of treatment and had been normal prior to treatment. Despite requests for additional Blood/Sugar monitoring during tx because of family history risk factor, nothing was done, and then a few months post tx, diagnosis of earl diabetes is made.
Also, sx of tx is noted to be an increase risk for developing diabetes, which is why I was asking for increased level of testing.
Now it may simply be coincidental, but I am wondering if tx not only failed me but also has messed me up worse physically.
Also, sx of tx is noted to be an increase risk for developing diabetes, which is why I was asking for increased level of testing.
Now it may simply be coincidental, but I am wondering if tx not only failed me but also has messed me up worse physically.
easibility of induction by twice-daily administration of interferon-beta prior to the standard combination therapy using pegylated interferon-alpha-2b plus ribavirin
T. Nakatani 1; Y. Akashi1; H. Matsuo1; S. Takeyama1; M. Uejima1; Y. Yamane1; K. Hashimoto1; E. Kikuchi1
1. Gastroenterology, Nara Prefectural Nara Hospital, Nara, Nara, Japan.
Aims: It has been reported that longer treatment with combination therapy using pegylated interferon (IFN)-alpha-2b plus ribavirin (RIB) for patients infected with hepatitis C virus (HCV) leads to more effective viral eradication. However, in Japan where treatment period is limited, the achievement of early viral clearance should be necessary. We already confirmed the effectiveness of high dose IFN-alpha-2b induction in combination with RIB when the treatment period was limited to 24 weeks. In this study, it is evaluated whether IFN induction is also effective in the 48-week combination therapy using pegylated IFN-alpha-2b plus RIB.
Methods: Forty patients chronically infected with genotype 1b HCV were divided into 2 groups. Thirty-two patients underwent standard 48-week combination therapy using 1.5
T. Nakatani 1; Y. Akashi1; H. Matsuo1; S. Takeyama1; M. Uejima1; Y. Yamane1; K. Hashimoto1; E. Kikuchi1
1. Gastroenterology, Nara Prefectural Nara Hospital, Nara, Nara, Japan.
Aims: It has been reported that longer treatment with combination therapy using pegylated interferon (IFN)-alpha-2b plus ribavirin (RIB) for patients infected with hepatitis C virus (HCV) leads to more effective viral eradication. However, in Japan where treatment period is limited, the achievement of early viral clearance should be necessary. We already confirmed the effectiveness of high dose IFN-alpha-2b induction in combination with RIB when the treatment period was limited to 24 weeks. In this study, it is evaluated whether IFN induction is also effective in the 48-week combination therapy using pegylated IFN-alpha-2b plus RIB.
Methods: Forty patients chronically infected with genotype 1b HCV were divided into 2 groups. Thirty-two patients underwent standard 48-week combination therapy using 1.5
Rectal administration of low dose interferon alpha for patients with chronic hepatitis C led to elevation of platelet count and serum albumin level as well as suppression of viral replication.
Y. Haruna1; A. Inoue1
1. Dept. of Gastroenterology and Hepatology, Osaka Prefectural Medical Center, Osaka, Japan.
(Aim) It was suggested that rectally administered interferon (IFN) is transferred into the lymphatic system via rectal mucous membrane in animal study. We reported that administration of low dose IFN suppository could suppress hepatitis C virus (HCV) replication in patients with chronic hepatitis C. In this study, we focused on examining the long-term biological effects after the therapy. (Methods) Fourteen patients with chronic hepatitis C participated in the study. The IFN suppository, which was made in the Department of Pharmacy of Osaka Prefectural Medical Center, contained 1000 units of lymphoblastoid IFN alpha. The patients had administration of one IFN suppository daily for 24 weeks. Serum HCV viral loads, liver function and blood cell count were tested every 4 weeks during the treatment and until 72 weeks after the end of the treatment. The CD4/CD8 ratio and 2
Y. Haruna1; A. Inoue1
1. Dept. of Gastroenterology and Hepatology, Osaka Prefectural Medical Center, Osaka, Japan.
(Aim) It was suggested that rectally administered interferon (IFN) is transferred into the lymphatic system via rectal mucous membrane in animal study. We reported that administration of low dose IFN suppository could suppress hepatitis C virus (HCV) replication in patients with chronic hepatitis C. In this study, we focused on examining the long-term biological effects after the therapy. (Methods) Fourteen patients with chronic hepatitis C participated in the study. The IFN suppository, which was made in the Department of Pharmacy of Osaka Prefectural Medical Center, contained 1000 units of lymphoblastoid IFN alpha. The patients had administration of one IFN suppository daily for 24 weeks. Serum HCV viral loads, liver function and blood cell count were tested every 4 weeks during the treatment and until 72 weeks after the end of the treatment. The CD4/CD8 ratio and 2
Background: Previous epidemiologic studies using the NHANES database have revealed a higher than expected prevalence of DM in patients infected with HCV. It has been hypothesized that insulin resistance may be the etiologic link although a precise cause and effect relationship remains unclear. This study's aim was to clarify the relationship between HCV and diabetes using the most recent iteration of the NHANES survey (2003-2004).
Methods: Demographic, physical exam, and laboratory data from the 2003-04 NHANES survey were combined into a single database using SPSS v.14.0. HCV status was determined using an ELISA, confirmed by RIBA. DM status was classified based on the subject's self-reported medical history. Cases coded as missing or indeterminate for either disorder were censored.
Results: The final database included 7,283 persons; 87 (1.2%) had HCV and 486 (6.7%) were diagnosed with DM. Mean age was 35.7
Methods: Demographic, physical exam, and laboratory data from the 2003-04 NHANES survey were combined into a single database using SPSS v.14.0. HCV status was determined using an ELISA, confirmed by RIBA. DM status was classified based on the subject's self-reported medical history. Cases coded as missing or indeterminate for either disorder were censored.
Results: The final database included 7,283 persons; 87 (1.2%) had HCV and 486 (6.7%) were diagnosed with DM. Mean age was 35.7
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