Hepatitis C Virus Infection and Hepatic Steatosis

October 25, 2006

Oh, this sucks! I have type 1b, 4.3 mm RNA, and some steatosis, so I

hope the treatment even has some effect, let alone clear me! From all

the research I am reading, the postive factors I have are relative

youth, gender and a positive attitude (which I am fighting to hold

onto every single day).

>

> Hepatitis C Virus Infection and Hepatic Steatosis

>

> Question

> Considering the association of hepatitis C and the possible

> stimulatory effect of steatosis, would the glitazones represent the

> therapy of choice for diabetic patients infected with hepatitis C

> virus (HCV)? Do we need to document steatosis by ultrasonography or

> computed tomography scan to consider such therapy?

>

> Response from M. Di Bisceglie, MD, FACP

> Professor of Internal Medicine, Chief of Hepatology, Division of

> Gastroenterology and Hepatology, Saint Louis University School of

> Medicine, St. Louis, Missouri

>

> Hepatic steatosis (fatty change within the liver) is increasingly

> being recognized as a complication of obesity and the metabolic

> syndrome. The term " nonalcoholic fatty liver disease " (NAFLD) is

used

> to describe a spectrum of liver disease, ranging from simple

> steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver

> disease can occur by itself or in association with most other liver

> diseases, including hepatitis C.[1] As an aside, it is important to

> note that infection with HCV genotype 3 is associated with hepatic

> steatosis that appears to be a viral effect rather than a host

> effect, but in most cases, with other genotypes, steatosis in

> hepatitis C represents the presence of 2 separate liver conditions.

> There is growing evidence of adverse interactions between chronic

> hepatitis C and hepatic steatosis.[2] Thus, the presence of hepatic

> steatosis is associated with more severe or advanced hepatic

> fibrosis. It is interesting, too, that hepatic steatosis appears to

> impair the response to antiviral therapy with pegylated interferon

> and ribavirin.[3]

>

> The coexistence of steatosis and hepatitis C can readily be

> determined by examination of liver biopsy specimens, and it remains

> the standard of care for most patients with chronic hepatitis C to

> undergo liver biopsy to assess the severity of their liver damage.

> Ultrasound examination is not a particularly reliable means of

> diagnosing steatosis and cannot distinguish between simple

steatosis

> and steatohepatitis, which has a worse outlook. The interaction

> between hepatitis C and steatosis is somewhat complicated because

it

> is not clear whether it is steatosis or its associated factors

> (including diabetes and insulin resistance) that worsens liver

> disease and affects antiviral responses.

>

> There is no consensus regarding the choice of hypoglycemic therapy

in

> patients with hepatitis C. The PPAR (peroxisome proliferator-

> activated receptor)-gamma antagonists ( " glitazones " ) carry with

them

> concerns about hepatotoxicity, as occurred with the use of

> troglitazone, which has been withdrawn from the market. However,

> there is no evidence that having underlying liver disease, such as

> hepatitis C, increases the low rate of hepatotoxicity with the

other

> glitazones. Studies are currently under way using pioglitazone as a

> treatment for NASH. Other ongoing studies are addressing the use of

> the thiazolidinediones to improve insulin resistance profiles prior

> to attempting treatment with pegylated interferon and ribavirin.

> Thus, although there are no clear data to support their use, the

> glitazones seem a reasonable choice in patients with chronic

> hepatitis C who need oral hypoglycemic therapy.

>

October 25, 2006

I can't help believing that the latter is 99.9% of the battle, that and being in fairly good health, otherwise... You WILL make it, , just keep on BELIEVING! Many Prayers, Sheena marvindamartian05 <marvindamartian05@...> wrote: Oh, this sucks! I have type 1b, 4.3 mm RNA, and some steatosis, so I hope the treatment even has some effect, let alone clear me! From all the research I am

reading, the postive factors I have are relative youth, gender and a positive attitude (which I am fighting to hold onto every single day).>> Hepatitis C Virus Infection and Hepatic Steatosis> > Question > Considering the association of hepatitis C and the possible > stimulatory effect of steatosis, would the glitazones represent the > therapy of choice for diabetic patients infected with hepatitis C > virus (HCV)? Do we need to document steatosis by ultrasonography or > computed tomography scan to consider such therapy?> > > Response from M. Di Bisceglie, MD, FACP > Professor of Internal Medicine, Chief of Hepatology, Division of > Gastroenterology and Hepatology, Saint Louis University

School of > Medicine, St. Louis, Missouri> > > > > Hepatic steatosis (fatty change within the liver) is increasingly > being recognized as a complication of obesity and the metabolic > syndrome. The term "nonalcoholic fatty liver disease" (NAFLD) is used > to describe a spectrum of liver disease, ranging from simple > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver > disease can occur by itself or in association with most other liver > diseases, including hepatitis C.[1] As an aside, it is important to > note that infection with HCV genotype 3 is associated with hepatic > steatosis that appears to be a viral effect rather than a host > effect, but in most cases, with other genotypes, steatosis in > hepatitis C represents the presence of 2 separate liver conditions. > There is growing evidence of adverse interactions between chronic

> hepatitis C and hepatic steatosis.[2] Thus, the presence of hepatic > steatosis is associated with more severe or advanced hepatic > fibrosis. It is interesting, too, that hepatic steatosis appears to > impair the response to antiviral therapy with pegylated interferon > and ribavirin.[3]> > The coexistence of steatosis and hepatitis C can readily be > determined by examination of liver biopsy specimens, and it remains > the standard of care for most patients with chronic hepatitis C to > undergo liver biopsy to assess the severity of their liver damage. > Ultrasound examination is not a particularly reliable means of > diagnosing steatosis and cannot distinguish between simple steatosis > and steatohepatitis, which has a worse outlook. The interaction > between hepatitis C and steatosis is somewhat complicated because it > is not clear whether it is steatosis

or its associated factors > (including diabetes and insulin resistance) that worsens liver > disease and affects antiviral responses.> > There is no consensus regarding the choice of hypoglycemic therapy in > patients with hepatitis C. The PPAR (peroxisome proliferator-> activated receptor)-gamma antagonists ("glitazones") carry with them > concerns about hepatotoxicity, as occurred with the use of > troglitazone, which has been withdrawn from the market. However, > there is no evidence that having underlying liver disease, such as > hepatitis C, increases the low rate of hepatotoxicity with the other > glitazones. Studies are currently under way using pioglitazone as a > treatment for NASH. Other ongoing studies are addressing the use of > the thiazolidinediones to improve insulin resistance profiles prior > to attempting treatment with pegylated interferon

and ribavirin. > Thus, although there are no clear data to support their use, the > glitazones seem a reasonable choice in patients with chronic > hepatitis C who need oral hypoglycemic therapy.>

Stay in the know. Pulse on the new .com. Check it out.

October 25, 2006

Nothing is written in stone , this was just an article by one doctor . Many how have geno 1b with steatosis have cleared . But I do agree that youth , gender and attitude are factors

Re: Hepatitis C Virus Infection and Hepatic Steatosis

Oh, this sucks! I have type 1b, 4.3 mm RNA, and some steatosis, so I hope the treatment even has some effect, let alone clear me! From all the research I am reading, the postive factors I have are relative youth, gender and a positive attitude (which I am fighting to hold onto every single day).>> Hepatitis C Virus Infection and Hepatic Steatosis> > Question > Considering the association of hepatitis C and the possible > stimulatory effect of steatosis, would the glitazones represent the > therapy of choice for diabetic patients infected with hepatitis C > virus (HCV)? Do we need to document steatosis by ultrasonography or > computed tomography scan to consider such therapy?> > > Response from M. Di Bisceglie, MD, FACP > Professor of Internal Medicine, Chief of Hepatology, Division of > Gastroenterology and Hepatology, Saint Louis University School of > Medicine, St. Louis, Missouri> > > > > Hepatic steatosis (fatty change within the liver) is increasingly > being recognized as a complication of obesity and the metabolic > syndrome. The term "nonalcoholic fatty liver disease" (NAFLD) is used > to describe a spectrum of liver disease, ranging from simple > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver > disease can occur by itself or in association with most other liver > diseases, including hepatitis C.[1] As an aside, it is important to > note that infection with HCV genotype 3 is associated with hepatic > steatosis that appears to be a viral effect rather than a host > effect, but in most cases, with other genotypes, steatosis in > hepatitis C represents the presence of 2 separate liver conditions. > There is growing evidence of adverse interactions between chronic > hepatitis C and hepatic steatosis.[2] Thus, the presence of hepatic > steatosis is associated with more severe or advanced hepatic > fibrosis. It is interesting, too, that hepatic steatosis appears to > impair the response to antiviral therapy with pegylated interferon > and ribavirin.[3]> > The coexistence of steatosis and hepatitis C can readily be > determined by examination of liver biopsy specimens, and it remains > the standard of care for most patients with chronic hepatitis C to > undergo liver biopsy to assess the severity of their liver damage. > Ultrasound examination is not a particularly reliable means of > diagnosing steatosis and cannot distinguish between simple steatosis > and steatohepatitis, which has a worse outlook. The interaction > between hepatitis C and steatosis is somewhat complicated because it > is not clear whether it is steatosis or its associated factors > (including diabetes and insulin resistance) that worsens liver > disease and affects antiviral responses.> > There is no consensus regarding the choice of hypoglycemic therapy in > patients with hepatitis C. The PPAR (peroxisome proliferator-> activated receptor)-gamma antagonists ("glitazones") carry with them > concerns about hepatotoxicity, as occurred with the use of > troglitazone, which has been withdrawn from the market. However, > there is no evidence that having underlying liver disease, such as > hepatitis C, increases the low rate of hepatotoxicity with the other > glitazones. Studies are currently under way using pioglitazone as a > treatment for NASH. Other ongoing studies are addressing the use of > the thiazolidinediones to improve insulin resistance profiles prior > to attempting treatment with pegylated interferon and ribavirin. > Thus, although there are no clear data to support their use, the > glitazones seem a reasonable choice in patients with chronic > hepatitis C who need oral hypoglycemic therapy.>

October 25, 2006

I agree Sheena,, I had EVERY NEGATIVE thing going for me and I still cleared too! so the battle can be won!Sheena <mom4possums2002@...> wrote: I can't help believing that the latter is 99.9% of the battle, that and being in fairly good health, otherwise... You WILL make it, , just keep on BELIEVING! Many Prayers, Sheena marvindamartian05 <marvindamartian05 >

wrote: Oh, this sucks! I have type 1b, 4.3 mm RNA, and some steatosis, so I hope the treatment even has some effect, let alone clear me! From all the research I am reading, the postive factors I have are relative youth, gender and a positive attitude (which I am fighting to hold onto every single day).>> Hepatitis C Virus Infection and Hepatic Steatosis> > Question > Considering the association of hepatitis C and the possible > stimulatory effect of steatosis, would the glitazones represent the > therapy of choice for diabetic patients infected with hepatitis C > virus (HCV)? Do we need to document steatosis

by ultrasonography or > computed tomography scan to consider such therapy?> > > Response from M. Di Bisceglie, MD, FACP > Professor of Internal Medicine, Chief of Hepatology, Division of > Gastroenterology and Hepatology, Saint Louis University School of > Medicine, St. Louis, Missouri> > > > > Hepatic steatosis (fatty change within the liver) is increasingly > being recognized as a complication of obesity and the metabolic > syndrome. The term "nonalcoholic fatty liver disease" (NAFLD) is used > to describe a spectrum of liver disease, ranging from simple > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver > disease can occur by itself or in association with most other liver > diseases, including hepatitis C.[1] As an aside, it is important to > note that infection with HCV genotype 3 is associated with hepatic

> steatosis that appears to be a viral effect rather than a host > effect, but in most cases, with other genotypes, steatosis in > hepatitis C represents the presence of 2 separate liver conditions. > There is growing evidence of adverse interactions between chronic > hepatitis C and hepatic steatosis.[2] Thus, the presence of hepatic > steatosis is associated with more severe or advanced hepatic > fibrosis. It is interesting, too, that hepatic steatosis appears to > impair the response to antiviral therapy with pegylated interferon > and ribavirin.[3]> > The coexistence of steatosis and hepatitis C can readily be > determined by examination of liver biopsy specimens, and it remains > the standard of care for most patients with chronic hepatitis C to > undergo liver biopsy to assess the severity of their liver damage. > Ultrasound examination is not a particularly

reliable means of > diagnosing steatosis and cannot distinguish between simple steatosis > and steatohepatitis, which has a worse outlook. The interaction > between hepatitis C and steatosis is somewhat complicated because it > is not clear whether it is steatosis or its associated factors > (including diabetes and insulin resistance) that worsens liver > disease and affects antiviral responses.> > There is no consensus regarding the choice of hypoglycemic therapy in > patients with hepatitis C. The PPAR (peroxisome proliferator-> activated receptor)-gamma antagonists ("glitazones") carry with them > concerns about hepatotoxicity, as occurred with the use of > troglitazone, which has been withdrawn from the market. However, > there is no evidence that having underlying liver disease, such as > hepatitis C, increases the low rate of hepatotoxicity with the

other > glitazones. Studies are currently under way using pioglitazone as a > treatment for NASH. Other ongoing studies are addressing the use of > the thiazolidinediones to improve insulin resistance profiles prior > to attempting treatment with pegylated interferon and ribavirin. > Thus, although there are no clear data to support their use, the > glitazones seem a reasonable choice in patients with chronic > hepatitis C who need oral hypoglycemic therapy.> Stay in the know. Pulse on the new .com. Check it out. Jackie

October 25, 2006

I had every single negative risk factors for clearing too, but I did,, I was overweight, female, post menopausal, geno 1, was stage 3-4 with early cirrhosis and grade 3 inflammation... but I made itmarvindamartian05 <marvindamartian05@...> wrote: Oh, this sucks! I have type 1b, 4.3 mm RNA, and some steatosis, so I hope the treatment even has some effect, let alone clear me! From all the research I am reading, the postive factors I have are relative youth, gender and a positive attitude (which I am fighting to

hold onto every single day).>> Hepatitis C Virus Infection and Hepatic Steatosis> > Question > Considering the association of hepatitis C and the possible > stimulatory effect of steatosis, would the glitazones represent the > therapy of choice for diabetic patients infected with hepatitis C > virus (HCV)? Do we need to document steatosis by ultrasonography or > computed tomography scan to consider such therapy?> > > Response from M. Di Bisceglie, MD, FACP > Professor of Internal Medicine, Chief of Hepatology, Division of > Gastroenterology and Hepatology, Saint Louis University School of > Medicine, St. Louis, Missouri> > > > > Hepatic steatosis

(fatty change within the liver) is increasingly > being recognized as a complication of obesity and the metabolic > syndrome. The term "nonalcoholic fatty liver disease" (NAFLD) is used > to describe a spectrum of liver disease, ranging from simple > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver > disease can occur by itself or in association with most other liver > diseases, including hepatitis C.[1] As an aside, it is important to > note that infection with HCV genotype 3 is associated with hepatic > steatosis that appears to be a viral effect rather than a host > effect, but in most cases, with other genotypes, steatosis in > hepatitis C represents the presence of 2 separate liver conditions. > There is growing evidence of adverse interactions between chronic > hepatitis C and hepatic steatosis.[2] Thus, the presence of hepatic > steatosis is associated with

more severe or advanced hepatic > fibrosis. It is interesting, too, that hepatic steatosis appears to > impair the response to antiviral therapy with pegylated interferon > and ribavirin.[3]> > The coexistence of steatosis and hepatitis C can readily be > determined by examination of liver biopsy specimens, and it remains > the standard of care for most patients with chronic hepatitis C to > undergo liver biopsy to assess the severity of their liver damage. > Ultrasound examination is not a particularly reliable means of > diagnosing steatosis and cannot distinguish between simple steatosis > and steatohepatitis, which has a worse outlook. The interaction > between hepatitis C and steatosis is somewhat complicated because it > is not clear whether it is steatosis or its associated factors > (including diabetes and insulin resistance) that worsens liver > disease

and affects antiviral responses.> > There is no consensus regarding the choice of hypoglycemic therapy in > patients with hepatitis C. The PPAR (peroxisome proliferator-> activated receptor)-gamma antagonists ("glitazones") carry with them > concerns about hepatotoxicity, as occurred with the use of > troglitazone, which has been withdrawn from the market. However, > there is no evidence that having underlying liver disease, such as > hepatitis C, increases the low rate of hepatotoxicity with the other > glitazones. Studies are currently under way using pioglitazone as a > treatment for NASH. Other ongoing studies are addressing the use of > the thiazolidinediones to improve insulin resistance profiles prior > to attempting treatment with pegylated interferon and ribavirin. > Thus, although there are no clear data to support their use, the > glitazones seem a

reasonable choice in patients with chronic > hepatitis C who need oral hypoglycemic therapy.>Jackie

October 25, 2006

That's good to hear! Thanks!

> >

> > Hepatitis C Virus Infection and Hepatic Steatosis

> >

> > Question

> > Considering the association of hepatitis C and the possible

> > stimulatory effect of steatosis, would the glitazones represent

the

> > therapy of choice for diabetic patients infected with hepatitis

C

> > virus (HCV)? Do we need to document steatosis by

ultrasonography or

> > computed tomography scan to consider such therapy?

> >

> > Response from M. Di Bisceglie, MD, FACP

> > Professor of Internal Medicine, Chief of Hepatology, Division

of

> > Gastroenterology and Hepatology, Saint Louis University School

of

> > Medicine, St. Louis, Missouri

> >

> > Hepatic steatosis (fatty change within the liver) is

increasingly

> > being recognized as a complication of obesity and the metabolic

> > syndrome. The term " nonalcoholic fatty liver disease " (NAFLD)

is

> used

> > to describe a spectrum of liver disease, ranging from simple

> > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver

> > disease can occur by itself or in association with most other

liver

> > diseases, including hepatitis C.[1] As an aside, it is

important to

> > note that infection with HCV genotype 3 is associated with

hepatic

> > steatosis that appears to be a viral effect rather than a host

> > effect, but in most cases, with other genotypes, steatosis in

> > hepatitis C represents the presence of 2 separate liver

conditions.

> > There is growing evidence of adverse interactions between

chronic

> > hepatitis C and hepatic steatosis.[2] Thus, the presence of

hepatic

> > steatosis is associated with more severe or advanced hepatic

> > fibrosis. It is interesting, too, that hepatic steatosis

appears to

> > impair the response to antiviral therapy with pegylated

interferon

> > and ribavirin.[3]

> >

> > The coexistence of steatosis and hepatitis C can readily be

> > determined by examination of liver biopsy specimens, and it

remains

> > the standard of care for most patients with chronic hepatitis C

to

> > undergo liver biopsy to assess the severity of their liver

damage.

> > Ultrasound examination is not a particularly reliable means of

> > diagnosing steatosis and cannot distinguish between simple

> steatosis

> > and steatohepatitis, which has a worse outlook. The interaction

> > between hepatitis C and steatosis is somewhat complicated

because

> it

> > is not clear whether it is steatosis or its associated factors

> > (including diabetes and insulin resistance) that worsens liver

> > disease and affects antiviral responses.

> >

> > There is no consensus regarding the choice of hypoglycemic

therapy

> in

> > patients with hepatitis C. The PPAR (peroxisome proliferator-

> > activated receptor)-gamma antagonists ( " glitazones " ) carry with

> them

> > concerns about hepatotoxicity, as occurred with the use of

> > troglitazone, which has been withdrawn from the market.

However,

> > there is no evidence that having underlying liver disease, such

as

> > hepatitis C, increases the low rate of hepatotoxicity with the

> other

> > glitazones. Studies are currently under way using pioglitazone

as a

> > treatment for NASH. Other ongoing studies are addressing the

use of

> > the thiazolidinediones to improve insulin resistance profiles

prior

> > to attempting treatment with pegylated interferon and

ribavirin.

> > Thus, although there are no clear data to support their use,

the

> > glitazones seem a reasonable choice in patients with chronic

> > hepatitis C who need oral hypoglycemic therapy.

> >

>

October 25, 2006

Oh my God, this is so good to hear, thanks so much! I tend to be very

positive but with this new situation I feel like I have no control

(God is in control, anyway!)and I am letting " bad news " get to me. I

know I sound pathetic, but this is all so new to me...I have always

been the one that takes care of sick people, not one of the sick

people. God bless you for putting this into perspective for me, Jax!

> >

> > Hepatitis C Virus Infection and Hepatic Steatosis

> >

> > Question

> > Considering the association of hepatitis C and the possible

> > stimulatory effect of steatosis, would the glitazones represent

the

> > therapy of choice for diabetic patients infected with hepatitis C

> > virus (HCV)? Do we need to document steatosis by ultrasonography

or

> > computed tomography scan to consider such therapy?

> >

> > Response from M. Di Bisceglie, MD, FACP

> > Professor of Internal Medicine, Chief of Hepatology, Division of

> > Gastroenterology and Hepatology, Saint Louis University School of

> > Medicine, St. Louis, Missouri

> >

> > Hepatic steatosis (fatty change within the liver) is increasingly

> > being recognized as a complication of obesity and the metabolic

> > syndrome. The term " nonalcoholic fatty liver disease " (NAFLD) is

> used

> > to describe a spectrum of liver disease, ranging from simple

> > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver

> > disease can occur by itself or in association with most other

liver

> > diseases, including hepatitis C.[1] As an aside, it is important

to

> > note that infection with HCV genotype 3 is associated with

hepatic

> > steatosis that appears to be a viral effect rather than a host

> > effect, but in most cases, with other genotypes, steatosis in

> > hepatitis C represents the presence of 2 separate liver

conditions.

> > There is growing evidence of adverse interactions between chronic

> > hepatitis C and hepatic steatosis.[2] Thus, the presence of

hepatic

> > steatosis is associated with more severe or advanced hepatic

> > fibrosis. It is interesting, too, that hepatic steatosis appears

to

> > impair the response to antiviral therapy with pegylated

interferon

> > and ribavirin.[3]

> >

> > The coexistence of steatosis and hepatitis C can readily be

> > determined by examination of liver biopsy specimens, and it

remains

> > the standard of care for most patients with chronic hepatitis C

to

> > undergo liver biopsy to assess the severity of their liver

damage.

> > Ultrasound examination is not a particularly reliable means of

> > diagnosing steatosis and cannot distinguish between simple

> steatosis

> > and steatohepatitis, which has a worse outlook. The interaction

> > between hepatitis C and steatosis is somewhat complicated because

> it

> > is not clear whether it is steatosis or its associated factors

> > (including diabetes and insulin resistance) that worsens liver

> > disease and affects antiviral responses.

> >

> > There is no consensus regarding the choice of hypoglycemic

therapy

> in

> > patients with hepatitis C. The PPAR (peroxisome proliferator-

> > activated receptor)-gamma antagonists ( " glitazones " ) carry with

> them

> > concerns about hepatotoxicity, as occurred with the use of

> > troglitazone, which has been withdrawn from the market. However,

> > there is no evidence that having underlying liver disease, such

as

> > hepatitis C, increases the low rate of hepatotoxicity with the

> other

> > glitazones. Studies are currently under way using pioglitazone as

a

> > treatment for NASH. Other ongoing studies are addressing the use

of

> > the thiazolidinediones to improve insulin resistance profiles

prior

> > to attempting treatment with pegylated interferon and ribavirin.

> > Thus, although there are no clear data to support their use, the

> > glitazones seem a reasonable choice in patients with chronic

> > hepatitis C who need oral hypoglycemic therapy.

> >

>

> Jackie

>

October 25, 2006

You are right of course, and my faith has been tested before and has

not wavered. My fiance keeps telling me to give it to Him and I try

very hard to do that. Always a challenge for the type A personality -

I suppose when you mix Type A with gentoype 1b you get...a Type B

personality?

> > >

> > > Hepatitis C Virus Infection and Hepatic Steatosis

> > >

> > > Question

> > > Considering the association of hepatitis C and the possible

> > > stimulatory effect of steatosis, would the glitazones represent

> the

> > > therapy of choice for diabetic patients infected with hepatitis C

> > > virus (HCV)? Do we need to document steatosis by ultrasonography

> or

> > > computed tomography scan to consider such therapy?

> > >

> > > Response from M. Di Bisceglie, MD, FACP

> > > Professor of Internal Medicine, Chief of Hepatology, Division of

> > > Gastroenterology and Hepatology, Saint Louis University School of

> > > Medicine, St. Louis, Missouri

> > >

> > > Hepatic steatosis (fatty change within the liver) is increasingly

> > > being recognized as a complication of obesity and the metabolic

> > > syndrome. The term " nonalcoholic fatty liver disease " (NAFLD) is

> > used

> > > to describe a spectrum of liver disease, ranging from simple

> > > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver

> > > disease can occur by itself or in association with most other

> liver

> > > diseases, including hepatitis C.[1] As an aside, it is important

> to

> > > note that infection with HCV genotype 3 is associated with

> hepatic

> > > steatosis that appears to be a viral effect rather than a host

> > > effect, but in most cases, with other genotypes, steatosis in

> > > hepatitis C represents the presence of 2 separate liver

> conditions.

> > > There is growing evidence of adverse interactions between chronic

> > > hepatitis C and hepatic steatosis.[2] Thus, the presence of

> hepatic

> > > steatosis is associated with more severe or advanced hepatic

> > > fibrosis. It is interesting, too, that hepatic steatosis appears

> to

> > > impair the response to antiviral therapy with pegylated

> interferon

> > > and ribavirin.[3]

> > >

> > > The coexistence of steatosis and hepatitis C can readily be

> > > determined by examination of liver biopsy specimens, and it

> remains

> > > the standard of care for most patients with chronic hepatitis C

> to

> > > undergo liver biopsy to assess the severity of their liver

> damage.

> > > Ultrasound examination is not a particularly reliable means of

> > > diagnosing steatosis and cannot distinguish between simple

> > steatosis

> > > and steatohepatitis, which has a worse outlook. The interaction

> > > between hepatitis C and steatosis is somewhat complicated because

> > it

> > > is not clear whether it is steatosis or its associated factors

> > > (including diabetes and insulin resistance) that worsens liver

> > > disease and affects antiviral responses.

> > >

> > > There is no consensus regarding the choice of hypoglycemic

> therapy

> > in

> > > patients with hepatitis C. The PPAR (peroxisome proliferator-

> > > activated receptor)-gamma antagonists ( " glitazones " ) carry with

> > them

> > > concerns about hepatotoxicity, as occurred with the use of

> > > troglitazone, which has been withdrawn from the market. However,

> > > there is no evidence that having underlying liver disease, such

> as

> > > hepatitis C, increases the low rate of hepatotoxicity with the

> > other

> > > glitazones. Studies are currently under way using pioglitazone as

> a

> > > treatment for NASH. Other ongoing studies are addressing the use

> of

> > > the thiazolidinediones to improve insulin resistance profiles

> prior

> > > to attempting treatment with pegylated interferon and ribavirin.

> > > Thus, although there are no clear data to support their use, the

> > > glitazones seem a reasonable choice in patients with chronic

> > > hepatitis C who need oral hypoglycemic therapy.

> > >

> >

> > Jackie

> >

>

> Jackie

>

October 25, 2006

hahha,, I TOO am a type A personality,, and I truely understand how hard it is to let go of the "control" of this, but you have to and you have to trust that God KNOWS what is right for you and it will be ok,,, If you need me to remind you from time to time,, I ll be here for ya,, marvindamartian05 <marvindamartian05@...> wrote: You are right of course, and my faith has been tested before and hasnot wavered. My fiance keeps telling me to give it to Him and I tryvery hard to do that.

Always a challenge for the type A personality -I suppose when you mix Type A with gentoype 1b you get...a Type Bpersonality? > > >> > > Hepatitis C Virus Infection and Hepatic Steatosis> > > > > > Question > > > Considering the association of hepatitis C and the possible > > > stimulatory effect of steatosis, would the glitazones represent > the > > > therapy of choice for diabetic patients infected with hepatitis C > > > virus (HCV)? Do we need to document steatosis by ultrasonography > or > > > computed tomography scan to consider such therapy?> > > > > > > > > Response from M. Di Bisceglie, MD, FACP > > > Professor of Internal Medicine, Chief of Hepatology, Division of > > > Gastroenterology and Hepatology, Saint Louis University

School of > > > Medicine, St. Louis, Missouri> > > > > > > > > > > > > > > Hepatic steatosis (fatty change within the liver) is increasingly > > > being recognized as a complication of obesity and the metabolic > > > syndrome. The term "nonalcoholic fatty liver disease" (NAFLD) is > > used > > > to describe a spectrum of liver disease, ranging from simple > > > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver > > > disease can occur by itself or in association with most other > liver > > > diseases, including hepatitis C.[1] As an aside, it is important > to > > > note that infection with HCV genotype 3 is associated with > hepatic > > > steatosis that appears to be a viral effect rather than a host > > > effect, but in most cases, with

other genotypes, steatosis in > > > hepatitis C represents the presence of 2 separate liver > conditions. > > > There is growing evidence of adverse interactions between chronic > > > hepatitis C and hepatic steatosis.[2] Thus, the presence of > hepatic > > > steatosis is associated with more severe or advanced hepatic > > > fibrosis. It is interesting, too, that hepatic steatosis appears > to > > > impair the response to antiviral therapy with pegylated > interferon > > > and ribavirin.[3]> > > > > > The coexistence of steatosis and hepatitis C can readily be > > > determined by examination of liver biopsy specimens, and it > remains > > > the standard of care for most patients with chronic hepatitis C > to > > > undergo liver biopsy to assess the severity of their liver

> damage. > > > Ultrasound examination is not a particularly reliable means of > > > diagnosing steatosis and cannot distinguish between simple > > steatosis > > > and steatohepatitis, which has a worse outlook. The interaction > > > between hepatitis C and steatosis is somewhat complicated because > > it > > > is not clear whether it is steatosis or its associated factors > > > (including diabetes and insulin resistance) that worsens liver > > > disease and affects antiviral responses.> > > > > > There is no consensus regarding the choice of hypoglycemic > therapy > > in > > > patients with hepatitis C. The PPAR (peroxisome proliferator-> > > activated receptor)-gamma antagonists ("glitazones") carry with > > them > > > concerns about hepatotoxicity, as

occurred with the use of > > > troglitazone, which has been withdrawn from the market. However, > > > there is no evidence that having underlying liver disease, such > as > > > hepatitis C, increases the low rate of hepatotoxicity with the > > other > > > glitazones. Studies are currently under way using pioglitazone as > a > > > treatment for NASH. Other ongoing studies are addressing the use > of > > > the thiazolidinediones to improve insulin resistance profiles > prior > > > to attempting treatment with pegylated interferon and ribavirin. > > > Thus, although there are no clear data to support their use, the > > > glitazones seem a reasonable choice in patients with chronic > > > hepatitis C who need oral hypoglycemic therapy.> > >> > > > > > > >

> > > > > > Jackie> >> > > > > > > Jackie>Jackie

October 25, 2006

Heck, I can't even let my fiance drive my car...when he drove me home

from the biopsy, I was like, " don't jam the gear shift so hard " , and

don't go that way, go this way " . I think I am going to have to get

over it. I would let God drive my car though, and I probably wouldn't

nag Him as much!

<redjaxjm@...> wrote:

>

> hahha,, I TOO am a type A personality,, and I truely understand how

hard it is to let go of the " control " of this, but you have to and you

have to trust that God KNOWS what is right for you and it will be

ok,,, If you need me to remind you from time to time,, I ll be here

for ya,,

>

> marvindamartian05 <marvindamartian05@...> wrote:

>

> You are right of course, and my faith has been tested before and has

> not wavered. My fiance keeps telling me to give it to Him and I try

> very hard to do that. Always a challenge for the type A personality -

> I suppose when you mix Type A with gentoype 1b you get...a Type B

> personality?

>

> > > >

> > > > Hepatitis C Virus Infection and Hepatic Steatosis

> > > >

> > > > Question

> > > > Considering the association of hepatitis C and the possible

> > > > stimulatory effect of steatosis, would the glitazones represent

> > the

> > > > therapy of choice for diabetic patients infected with hepatitis C

> > > > virus (HCV)? Do we need to document steatosis by ultrasonography

> > or

> > > > computed tomography scan to consider such therapy?

> > > >

> > > > Response from M. Di Bisceglie, MD, FACP

> > > > Professor of Internal Medicine, Chief of Hepatology, Division of

> > > > Gastroenterology and Hepatology, Saint Louis University School of

> > > > Medicine, St. Louis, Missouri

> > > >

> > > > Hepatic steatosis (fatty change within the liver) is increasingly

> > > > being recognized as a complication of obesity and the metabolic

> > > > syndrome. The term " nonalcoholic fatty liver disease " (NAFLD) is

> > > used

> > > > to describe a spectrum of liver disease, ranging from simple

> > > > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver

> > > > disease can occur by itself or in association with most other

> > liver

> > > > diseases, including hepatitis C.[1] As an aside, it is important

> > to

> > > > note that infection with HCV genotype 3 is associated with

> > hepatic

> > > > steatosis that appears to be a viral effect rather than a host

> > > > effect, but in most cases, with other genotypes, steatosis in

> > > > hepatitis C represents the presence of 2 separate liver

> > conditions.

> > > > There is growing evidence of adverse interactions between chronic

> > > > hepatitis C and hepatic steatosis.[2] Thus, the presence of

> > hepatic

> > > > steatosis is associated with more severe or advanced hepatic

> > > > fibrosis. It is interesting, too, that hepatic steatosis appears

> > to

> > > > impair the response to antiviral therapy with pegylated

> > interferon

> > > > and ribavirin.[3]

> > > >

> > > > The coexistence of steatosis and hepatitis C can readily be

> > > > determined by examination of liver biopsy specimens, and it

> > remains

> > > > the standard of care for most patients with chronic hepatitis C

> > to

> > > > undergo liver biopsy to assess the severity of their liver

> > damage.

> > > > Ultrasound examination is not a particularly reliable means of

> > > > diagnosing steatosis and cannot distinguish between simple

> > > steatosis

> > > > and steatohepatitis, which has a worse outlook. The interaction

> > > > between hepatitis C and steatosis is somewhat complicated because

> > > it

> > > > is not clear whether it is steatosis or its associated factors

> > > > (including diabetes and insulin resistance) that worsens liver

> > > > disease and affects antiviral responses.

> > > >

> > > > There is no consensus regarding the choice of hypoglycemic

> > therapy

> > > in

> > > > patients with hepatitis C. The PPAR (peroxisome proliferator-

> > > > activated receptor)-gamma antagonists ( " glitazones " ) carry with

> > > them

> > > > concerns about hepatotoxicity, as occurred with the use of

> > > > troglitazone, which has been withdrawn from the market. However,

> > > > there is no evidence that having underlying liver disease, such

> > as

> > > > hepatitis C, increases the low rate of hepatotoxicity with the

> > > other

> > > > glitazones. Studies are currently under way using pioglitazone as

> > a

> > > > treatment for NASH. Other ongoing studies are addressing the use

> > of

> > > > the thiazolidinediones to improve insulin resistance profiles

> > prior

> > > > to attempting treatment with pegylated interferon and ribavirin.

> > > > Thus, although there are no clear data to support their use, the

> > > > glitazones seem a reasonable choice in patients with chronic

> > > > hepatitis C who need oral hypoglycemic therapy.

> > > >

> > >

> > > Jackie

> > >

> >

> > Jackie

> >

>

> Jackie

>

October 25, 2006

hahaha,, you REALLY DO sound just like me! roflmarvindamartian05 <marvindamartian05@...> wrote: Heck, I can't even let my fiance drive my car...when he drove me homefrom the biopsy, I was like, "don't jam the gear shift so hard", anddon't go that way, go this way". I think I am going to have to getover it. I would let God drive my car though, and I probably wouldn'tnag Him as much!<redjaxjm@...> wrote:>> hahha,, I TOO am a type A personality,, and I truely understand

howhard it is to let go of the "control" of this, but you have to and youhave to trust that God KNOWS what is right for you and it will beok,,, If you need me to remind you from time to time,, I ll be herefor ya,, > > > marvindamartian05 <marvindamartian05@...> wrote:> > You are right of course, and my faith has been tested before and has> not wavered. My fiance keeps telling me to give it to Him and I try> very hard to do that. Always a challenge for the type A personality -> I suppose when you mix Type A with gentoype 1b you get...a Type B> personality? > > > > > >> > > > Hepatitis C Virus Infection and Hepatic Steatosis> > > > > > > > Question > > > > Considering the association of hepatitis C and the possible > > > > stimulatory

effect of steatosis, would the glitazones represent > > the > > > > therapy of choice for diabetic patients infected with hepatitis C > > > > virus (HCV)? Do we need to document steatosis by ultrasonography > > or > > > > computed tomography scan to consider such therapy?> > > > > > > > > > > > Response from M. Di Bisceglie, MD, FACP > > > > Professor of Internal Medicine, Chief of Hepatology, Division of > > > > Gastroenterology and Hepatology, Saint Louis University School of > > > > Medicine, St. Louis, Missouri> > > > > > > > > > > > > > > > > > > > Hepatic steatosis (fatty change within the liver) is increasingly > > > > being recognized as a complication of obesity and the metabolic > > >

> syndrome. The term "nonalcoholic fatty liver disease" (NAFLD) is > > > used > > > > to describe a spectrum of liver disease, ranging from simple > > > > steatosis to steatohepatitis (NASH) and cirrhosis. Fatty liver > > > > disease can occur by itself or in association with most other > > liver > > > > diseases, including hepatitis C.[1] As an aside, it is important > > to > > > > note that infection with HCV genotype 3 is associated with > > hepatic > > > > steatosis that appears to be a viral effect rather than a host > > > > effect, but in most cases, with other genotypes, steatosis in > > > > hepatitis C represents the presence of 2 separate liver > > conditions. > > > > There is growing evidence of adverse interactions between chronic > > > > hepatitis C

and hepatic steatosis.[2] Thus, the presence of > > hepatic > > > > steatosis is associated with more severe or advanced hepatic > > > > fibrosis. It is interesting, too, that hepatic steatosis appears > > to > > > > impair the response to antiviral therapy with pegylated > > interferon > > > > and ribavirin.[3]> > > > > > > > The coexistence of steatosis and hepatitis C can readily be > > > > determined by examination of liver biopsy specimens, and it > > remains > > > > the standard of care for most patients with chronic hepatitis C > > to > > > > undergo liver biopsy to assess the severity of their liver > > damage. > > > > Ultrasound examination is not a particularly reliable means of > > > > diagnosing steatosis and cannot distinguish

between simple > > > steatosis > > > > and steatohepatitis, which has a worse outlook. The interaction > > > > between hepatitis C and steatosis is somewhat complicated because > > > it > > > > is not clear whether it is steatosis or its associated factors > > > > (including diabetes and insulin resistance) that worsens liver > > > > disease and affects antiviral responses.> > > > > > > > There is no consensus regarding the choice of hypoglycemic > > therapy > > > in > > > > patients with hepatitis C. The PPAR (peroxisome proliferator-> > > > activated receptor)-gamma antagonists ("glitazones") carry with > > > them > > > > concerns about hepatotoxicity, as occurred with the use of > > > > troglitazone, which has been withdrawn from

the market. However, > > > > there is no evidence that having underlying liver disease, such > > as > > > > hepatitis C, increases the low rate of hepatotoxicity with the > > > other > > > > glitazones. Studies are currently under way using pioglitazone as > > a > > > > treatment for NASH. Other ongoing studies are addressing the use > > of > > > > the thiazolidinediones to improve insulin resistance profiles > > prior > > > > to attempting treatment with pegylated interferon and ribavirin. > > > > Thus, although there are no clear data to support their use, the > > > > glitazones seem a reasonable choice in patients with chronic > > > > hepatitis C who need oral hypoglycemic therapy.> > > >> > > > > > > > > > >

> > > > > > > > > > Jackie> > >> > > > > > > > > > > > > > Jackie> >> > > > > > > Jackie>Jackie

October 26, 2006

Ask the Experts about Liver Disease

From Medscape Gastroenterology

Hepatitis C Virus Infection and Hepatic Steatosis

Question

Considering the association of hepatitis C and the possible stimulatory

effect of steatosis, would the glitazones represent the therapy of choice

for diabetic patients infected with hepatitis C virus (HCV)? Do we need to

document steatosis by ultrasonography or computed tomography scan to

consider such therapy?

Response from M. Di Bisceglie, MD, FACP

Professor of Internal Medicine, Chief of Hepatology, Division of

Gastroenterology and Hepatology, Saint Louis University School of Medicine,

St. Louis, Missouri

Hepatic steatosis (fatty change within the liver) is increasingly being

recognized as a complication of obesity and the metabolic syndrome. The term

" nonalcoholic fatty liver disease " (NAFLD) is used to describe a spectrum of

liver disease, ranging from simple steatosis to steatohepatitis (NASH) and

cirrhosis. Fatty liver disease can occur by itself or in association with

most other liver diseases, including hepatitis C.[1] As an aside, it is

important to note that infection with HCV genotype 3 is associated with

hepatic steatosis that appears to be a viral effect rather than a host

effect, but in most cases, with other genotypes, steatosis in hepatitis C

represents the presence of 2 separate liver conditions. There is growing

evidence of adverse interactions between chronic hepatitis C and hepatic

steatosis.[2] Thus, the presence of hepatic steatosis is associated with

more severe or advanced hepatic fibrosis. It is interesting, too, that

hepatic steatosis appears to impair the response to antiviral therapy with

pegylated interferon and ribavirin.[3]

The coexistence of steatosis and hepatitis C can readily be determined by

examination of liver biopsy specimens, and it remains the standard of care

for most patients with chronic hepatitis C to undergo liver biopsy to assess

the severity of their liver damage. Ultrasound examination is not a

particularly reliable means of diagnosing steatosis and cannot distinguish

between simple steatosis and steatohepatitis, which has a worse outlook. The

interaction between hepatitis C and steatosis is somewhat complicated

because it is not clear whether it is steatosis or its associated factors

(including diabetes and insulin resistance) that worsens liver disease and

affects antiviral responses.

There is no consensus regarding the choice of hypoglycemic therapy in

patients with hepatitis C. The PPAR (peroxisome proliferator-activated

receptor)-gamma antagonists ( " glitazones " ) carry with them concerns about

hepatotoxicity, as occurred with the use of troglitazone, which has been

withdrawn from the market. However, there is no evidence that having

underlying liver disease, such as hepatitis C, increases the low rate of

hepatotoxicity with the other glitazones. Studies are currently under way

using pioglitazone as a treatment for NASH. Other ongoing studies are

addressing the use of the thiazolidinediones to improve insulin resistance

profiles prior to attempting treatment with pegylated interferon and

ribavirin. Thus, although there are no clear data to support their use, the

glitazones seem a reasonable choice in patients with chronic hepatitis C who

need oral hypoglycemic therapy.

Posted 10/19/2006

--------------------------------------------------------------------------------

References

Brunt EM, Ramrahkiani S, Cordes BG, et al. Concurrence of histologic

features of steatohepatitis with other forms of chronic liver disease. Mod

Pathol. 2003;16:49-56.

Adinolfi LE, Gambardella M, na A, Tripodi MF, Utili R, Ruggiero G.

Steatosis accelerates the progression of liver damage of chronic hepatitis C

patients and correlates with specific HCV genotype and visceral obesity.

Hepatology. 2001;33:1358-1364.

on SA, Brunt EM, Qazi RA, et al. Effect of significant histologic

steatosis or steatohepatitis on response to antiviral therapy in patients

with chronic hepatitis C. Clin Gastroenterol Hepatol. 2005;3:604-609.

M. Di Bisceglie, MD, FACP, has disclosed that he has received

research support from Schering-Plough, Roche, Gilead Sciences, Idenix,

SciClone Pharmaceuticals, and Vertex, and has served as an advisor or

consultant to Roche, Idenix, SciClone Pharmaceuticals, Chiron, Novartis,

Vertex, Bristol-Myers Squibb, Abbott, and Pharmasset. Dr. Di Bisceglie has

also disclosed that he has served on the speaker's bureau for Roche, Gilead

Sciences, and Bristol-Myers Squibb.

http://www.medscape.com/viewarticle/545849?src=mp

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