Aa
Interesting Study on Insulin Resistance
J Hepatol. 2009 Apr;50(4):712-718.
Insulin resistance predicts response to peginterferon-alpha/ribavirin combination therapy in chronic hepatitis C patients.
Dai CY, Huang JF, Hsieh MY, Hou NJ, Lin ZY, Chen SC, Hsieh MY, Wang LY, Chang WY, Chuang WL, Yu ML.
Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, No. 100, Tzyou 1st Rd, Kaohsiung 807, Taiwan; Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Occupational and Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
BACKGROUND/AIMS: Insulin resistance (IR) might be associated with hepatitis C virus (HCV) infection. This study aimed to elucidate impact of IR and beta-cell function on the response to peginterferon-alpha (PEG-IFN)/ribavirin combination therapy in chronic hepatitis C (CHC) patients.
METHODS: Three hundred and thirty patients without overt diabetes were treated with combination therapy with (PEG-IFN)/ribavirin for 24 weeks. The IR and beta-cell function were evaluated by homeostasis model assessment of IR (HOMA-IR) and homeostasis model assessment of beta-cell function (HOMA-beta) before treatment.
RESULTS: HCV genotype, pretreatment HCV RNA level and pretreatment HOMA-IR, but not HOMA-beta, were independent factors associated with sustained virologic response (SVR). In 150 patients with genotype 1b infection, pretreatment HCV RNA level, HOMA-IR and age were independent predictors for SVR. The significantly lower SVR rate in high HOMA-IR patients was observed in 76 patients with high HCV RNA levels (400,000IU/mL) who were defined as 'difficult-to-treat' patients. The mean HOMA-IR of 'difficult-to-treat' patients was significantly lower in 42 sustained responders than in 34 non-responders.
CONCLUSIONS: IR was associated with SVR to (PEG-IFN)/ribavirin therapy for CHC, especially among 'difficult-to-treat' patients. These findings suggested clinical application of pretreatment HOMA-IR could enable treatment outcome to be predicted and treatment regimens to be determined.
Insulin resistance predicts response to peginterferon-alpha/ribavirin combination therapy in chronic hepatitis C patients.
Dai CY, Huang JF, Hsieh MY, Hou NJ, Lin ZY, Chen SC, Hsieh MY, Wang LY, Chang WY, Chuang WL, Yu ML.
Hepatobiliary Division, Department of Internal Medicine, Kaohsiung Medical University Hospital, No. 100, Tzyou 1st Rd, Kaohsiung 807, Taiwan; Faculty of Internal Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Occupational and Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
BACKGROUND/AIMS: Insulin resistance (IR) might be associated with hepatitis C virus (HCV) infection. This study aimed to elucidate impact of IR and beta-cell function on the response to peginterferon-alpha (PEG-IFN)/ribavirin combination therapy in chronic hepatitis C (CHC) patients.
METHODS: Three hundred and thirty patients without overt diabetes were treated with combination therapy with (PEG-IFN)/ribavirin for 24 weeks. The IR and beta-cell function were evaluated by homeostasis model assessment of IR (HOMA-IR) and homeostasis model assessment of beta-cell function (HOMA-beta) before treatment.
RESULTS: HCV genotype, pretreatment HCV RNA level and pretreatment HOMA-IR, but not HOMA-beta, were independent factors associated with sustained virologic response (SVR). In 150 patients with genotype 1b infection, pretreatment HCV RNA level, HOMA-IR and age were independent predictors for SVR. The significantly lower SVR rate in high HOMA-IR patients was observed in 76 patients with high HCV RNA levels (400,000IU/mL) who were defined as 'difficult-to-treat' patients. The mean HOMA-IR of 'difficult-to-treat' patients was significantly lower in 42 sustained responders than in 34 non-responders.
CONCLUSIONS: IR was associated with SVR to (PEG-IFN)/ribavirin therapy for CHC, especially among 'difficult-to-treat' patients. These findings suggested clinical application of pretreatment HOMA-IR could enable treatment outcome to be predicted and treatment regimens to be determined.
Thanks! I don’t know what could or can be done to ease these obstacles to those who have IR problems or are db1 or 2 and starting to look at treatment but it is better to be aware than not and am sure it will come up again.
jasper
jasper
Diabetes is a serious disease, so is treating, Bill as always your words are clear and honest! maybe a sidebar like the Occult Hep C? trihep is great about posting new articles,
Max: Is there some reason you can not post the full text?
--------------
Can't speak for the original poster, but I hear you.
A very quick search shows that full-text is not available for free online as is the case with many studies.
For anyone who would like to read full-text, here's a link to the study and note the "full-text" box to the right.
http://www.ncbi.nlm.nih.gov/pubmed/19231011
That will take you to one or two sites where you can download the full-text for a fee. Alternatively, some of you with professional or university access may be able to get it that way. Also, full-text is generally available for free in some public medical libraries.
When I was treating, I always ordered full-text for any study I was going to base an important treatment decision on. Abstracts often leave as many question unanswered as answered.
-- Jim
--------------
Can't speak for the original poster, but I hear you.
A very quick search shows that full-text is not available for free online as is the case with many studies.
For anyone who would like to read full-text, here's a link to the study and note the "full-text" box to the right.
http://www.ncbi.nlm.nih.gov/pubmed/19231011
That will take you to one or two sites where you can download the full-text for a fee. Alternatively, some of you with professional or university access may be able to get it that way. Also, full-text is generally available for free in some public medical libraries.
When I was treating, I always ordered full-text for any study I was going to base an important treatment decision on. Abstracts often leave as many question unanswered as answered.
-- Jim
For further interested, here is a collection of HCV/IR/Diabetes articles from the HIVandHepatitis.com web site:
http://www.hivandhepatitis.com/hep_c/hepc_news_insulin.html
"CoWriter" has also compiled a list along with commentary here:
http://www.medhelp.org/user_journals/index/568322?personal_page_id=450
--------------------------
IR and HCV tx is definitely an evolving subject and hopefully anyone with HCV, and especially about to treat, will first get tested for IR including a fasting serum glucose and serum insulin test. The fasting glucose is commonly a part of a normal HealthScreen but really don't see why a doc would refuse a serum insulin test if requested, mine didn't even though my fasting glucose values were normal.
Beyond that, study up as much as you feel comfortable with, and discuss with your medical team where relevant. Diet and exercise are the first line defense for IR but they may not work in all cases.
With tests in hand (and perhaps some supplied studies) hopefully your medical team can put your IR status in a clinical context and come up with a plan where needed. And again, if you're not seeing a hepatolgoist, I highly recommend you switch over to one if feasible. They tend to be more on top of HCV and related topics and would be best to help pull your HCV strategy together.
-- Jim
http://www.hivandhepatitis.com/hep_c/hepc_news_insulin.html
"CoWriter" has also compiled a list along with commentary here:
http://www.medhelp.org/user_journals/index/568322?personal_page_id=450
--------------------------
IR and HCV tx is definitely an evolving subject and hopefully anyone with HCV, and especially about to treat, will first get tested for IR including a fasting serum glucose and serum insulin test. The fasting glucose is commonly a part of a normal HealthScreen but really don't see why a doc would refuse a serum insulin test if requested, mine didn't even though my fasting glucose values were normal.
Beyond that, study up as much as you feel comfortable with, and discuss with your medical team where relevant. Diet and exercise are the first line defense for IR but they may not work in all cases.
With tests in hand (and perhaps some supplied studies) hopefully your medical team can put your IR status in a clinical context and come up with a plan where needed. And again, if you're not seeing a hepatolgoist, I highly recommend you switch over to one if feasible. They tend to be more on top of HCV and related topics and would be best to help pull your HCV strategy together.
-- Jim
"I am a type 2 diabetic that SVRrd. Although I had a slow response during the first treatment, the second time I cleared relatively early, and went on to achieve sustained viral response."
--------------------
I am going to take a wild guess and say that perhaps your blood sugar control was better the second time?
"Type 1 diabetes typically involves underproduction of insulin from the beta cells in the pancreas."
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Actually Bill, Type 1 means that you don't produce ANY insulin at all.
" A type 1diabetic typically requires very little exogenous insulin; they can get by with injecting small amounts."
----------------
Think about it. They don't produce any insulin at all.
"but it doesn’t *preclude* SVR"
------------------
I disagree with that, however, I do agree that IR is only one of many hurdles.
"some members on this board have become obsessed by insulin resistance"
-------------------
You can't be talking about me. I didn't just become. I've been obssessed with it for years...LOL
I find your case incredibly interesting and wish I could see what the difference was between the two times you treated (same with FlGuy) since high levels of insulin make interferon ineffective and that includes injected insulin...and you were on quite a bit of Lantus insulin.
It's fascinating. I would love it if you share more details.
Co
Dig Dis Sci. 2009 Jan 16.
Diabetes Mellitus Is Associated with Impaired Response to Antiviral Therapy in Chronic Hepatitis C Infection.
Elgouhari HM, Zein CO, Hanouneh I, Feldstein AE, Zein NN.
Avera Center for Liver Disease, Transplant Institute, Sanford School of Medicine, University of South Dakota, 1001 East 21st Street, Suite 303, Sioux Falls, 57105, South Dakota, USA
Insulin resistance may promote hepatic fibrosis in chronic hepatitis C (HCV) and has emerged as a cofactor in failure to achieve sustained viral response (SVR). Aims (1) To assess the association of diabetes mellitus (DM) in HCV patients to the severity of hepatic fibrosis and to the response to antiviral treatment. (2) To assess the safety of pegylated interferon and ribavirin combination therapy (Peg IFN/RBV) in diabetic HCV patients. Methods HCV diabetics (n = 61) were identified. A 2:1 matching control group was used to identify independent factors of advanced fibrosis and treatment failure. Results Compared to HCV non-diabetics, HCV diabetics were more likely to have steatosis (P < 0.0001) and advanced fibrosis (P = 0.003). Patients' age, Caucasian ethnicity, obesity, and histologic activity index were independently associated with advanced fibrosis (P < 0.05). Only 23% of HCV diabetics achieved SVR compared to 46% of HCV non-diabetics (P = 0.003). DM, genotype 1, high baseline viral load, and African-American ethnicity were independently associated with less SVR (P < 0.05). Significant adverse events were more common in HCV diabetics compared to HCV non-diabetics (P = 0.001). Side effects did not increase in patients receiving PEG IFN/RBV and insulin sensitizers. Conclusion DM was associated with impaired virologic response to PEG IFN/RBV in HCV patients. Adverse events during therapy were more frequent in diabetic compared to non-diabetic HCV patients.
http://www.ncbi.nlm.nih.gov/pubmed/19148751?ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
--------------------
I am going to take a wild guess and say that perhaps your blood sugar control was better the second time?
"Type 1 diabetes typically involves underproduction of insulin from the beta cells in the pancreas."
--------------
Actually Bill, Type 1 means that you don't produce ANY insulin at all.
" A type 1diabetic typically requires very little exogenous insulin; they can get by with injecting small amounts."
----------------
Think about it. They don't produce any insulin at all.
"but it doesn’t *preclude* SVR"
------------------
I disagree with that, however, I do agree that IR is only one of many hurdles.
"some members on this board have become obsessed by insulin resistance"
-------------------
You can't be talking about me. I didn't just become. I've been obssessed with it for years...LOL
I find your case incredibly interesting and wish I could see what the difference was between the two times you treated (same with FlGuy) since high levels of insulin make interferon ineffective and that includes injected insulin...and you were on quite a bit of Lantus insulin.
It's fascinating. I would love it if you share more details.
Co
Dig Dis Sci. 2009 Jan 16.
Diabetes Mellitus Is Associated with Impaired Response to Antiviral Therapy in Chronic Hepatitis C Infection.
Elgouhari HM, Zein CO, Hanouneh I, Feldstein AE, Zein NN.
Avera Center for Liver Disease, Transplant Institute, Sanford School of Medicine, University of South Dakota, 1001 East 21st Street, Suite 303, Sioux Falls, 57105, South Dakota, USA
Insulin resistance may promote hepatic fibrosis in chronic hepatitis C (HCV) and has emerged as a cofactor in failure to achieve sustained viral response (SVR). Aims (1) To assess the association of diabetes mellitus (DM) in HCV patients to the severity of hepatic fibrosis and to the response to antiviral treatment. (2) To assess the safety of pegylated interferon and ribavirin combination therapy (Peg IFN/RBV) in diabetic HCV patients. Methods HCV diabetics (n = 61) were identified. A 2:1 matching control group was used to identify independent factors of advanced fibrosis and treatment failure. Results Compared to HCV non-diabetics, HCV diabetics were more likely to have steatosis (P < 0.0001) and advanced fibrosis (P = 0.003). Patients' age, Caucasian ethnicity, obesity, and histologic activity index were independently associated with advanced fibrosis (P < 0.05). Only 23% of HCV diabetics achieved SVR compared to 46% of HCV non-diabetics (P = 0.003). DM, genotype 1, high baseline viral load, and African-American ethnicity were independently associated with less SVR (P < 0.05). Significant adverse events were more common in HCV diabetics compared to HCV non-diabetics (P = 0.001). Side effects did not increase in patients receiving PEG IFN/RBV and insulin sensitizers. Conclusion DM was associated with impaired virologic response to PEG IFN/RBV in HCV patients. Adverse events during therapy were more frequent in diabetic compared to non-diabetic HCV patients.
http://www.ncbi.nlm.nih.gov/pubmed/19148751?ordinalpos=19&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
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