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Fatty Liver Tied to Cancer in Hepatitis C Cirrhosis
NEW YORK (Reuters Health) Jul 11 - Hepatic steatosis is associated with an increased frequency of hepatocellular carcinoma (HCC) in patients with hepatitis C-related cirrhosis, according to Massachusetts-based researchers.
"Our findings, which associated higher degrees of hepatic steatosis with HCC in patients undergoing liver transplantation for hepatitis C, implicate fatty liver as an accelerant of the development of HCC observed in these patients," senior investigator Dr. Raymond T. Chung told Reuters Health.
Dr. Chung and colleagues at General Hospital, Boston came to this conclusion after a retrospective review involving 94 patients with hepatitis C cirrhosis who underwent transplantation between 1992 and 2005.
According to their report in the June 15th issue of Cancer, 32 patients had evidence of hepatocellular cancer. In the HCC group, 69% had evidence of steatosis compared to 50% of those without HCC.
Compared with no steatosis, the odds ratio for the development of HCC ranged from 1.61 for grade 1 steatosis to 8.02 for grade 3 or 4.
The researchers conclude that steatosis is independently associated with hepatocellular cancer in these patients and may be a useful marker for identifying those at high risk.
Moreover, added Dr. Chung, the findings "suggest that measures to ameliorate fatty liver may be helpful in reducing this risk."
Cancer 2007;109:2490-2496.
"Our findings, which associated higher degrees of hepatic steatosis with HCC in patients undergoing liver transplantation for hepatitis C, implicate fatty liver as an accelerant of the development of HCC observed in these patients," senior investigator Dr. Raymond T. Chung told Reuters Health.
Dr. Chung and colleagues at General Hospital, Boston came to this conclusion after a retrospective review involving 94 patients with hepatitis C cirrhosis who underwent transplantation between 1992 and 2005.
According to their report in the June 15th issue of Cancer, 32 patients had evidence of hepatocellular cancer. In the HCC group, 69% had evidence of steatosis compared to 50% of those without HCC.
Compared with no steatosis, the odds ratio for the development of HCC ranged from 1.61 for grade 1 steatosis to 8.02 for grade 3 or 4.
The researchers conclude that steatosis is independently associated with hepatocellular cancer in these patients and may be a useful marker for identifying those at high risk.
Moreover, added Dr. Chung, the findings "suggest that measures to ameliorate fatty liver may be helpful in reducing this risk."
Cancer 2007;109:2490-2496.
Discussion
The CDD model of NASH is associated to a marked
liver injury and fibrosis development after eight to twelve
weeks of diet administration.21 The aim of the present
study was to determine if co-administration of PTX to rats
fed a CDD during eight weeks was able to attenuate CDD
induced liver damage. Our results showed that PTX failed
to improve both steatohepatitis and liver fibrosis in this
dietary model of NASH. In fact, no differences were observed
in the experimental groups (CDD and CDD+PTX)
compared to the control group with regard to weight loss,
hepatomegaly, serum levels of aminotransferases, hepatic
glutathione content, histological changes and markers of
early fibrogenesis (i.e. procollagen I and TGF-β1 overexpressiontokines and growth factors and bioavailability of the drug
in sufficient concentrations in target tissues.27 Only one
report assessing the effects of PTX in NASH has been
published.18 In this report, the authors found, in contrast
with our results, that PTX attenuated methionine-choline
deficient diet-induced steatohepatitis. Although, the latter
experimental model is similar to that used in the present
study.28,29 a variety of factors, including species and/or sex
of the animals, length of treatment [two weeks in the
study by Koope et al.18 vs 8 weeks in our protocol] may
explain the apparently conflicting results. It should be
noted that in the study of Koope et al. beneficial effects of
PTX were mainly observed in female mice indicating a
possible gender specific effect. In the present study male
rats were used with no observed benefit of PTX. Thus, the
possibility that gender influences the efficacy of PTX
therapy must be further evaluated.
In humans, two recent small pilot clinical trials have
shown that aminotransferase levels among patients with
NASH improve with administration of PTX.19,20 Larger
studies are ongoing to define if PTX could be beneficial
for patients with NASH. The results of the present study,
suggest that although an initial attenuation of liver damage
could eventually be achieved, PTX may not be able to
influence liver fibrosis development in this increasingly
important liver disease.
The CDD model of NASH is associated to a marked
liver injury and fibrosis development after eight to twelve
weeks of diet administration.21 The aim of the present
study was to determine if co-administration of PTX to rats
fed a CDD during eight weeks was able to attenuate CDD
induced liver damage. Our results showed that PTX failed
to improve both steatohepatitis and liver fibrosis in this
dietary model of NASH. In fact, no differences were observed
in the experimental groups (CDD and CDD+PTX)
compared to the control group with regard to weight loss,
hepatomegaly, serum levels of aminotransferases, hepatic
glutathione content, histological changes and markers of
early fibrogenesis (i.e. procollagen I and TGF-β1 overexpressiontokines and growth factors and bioavailability of the drug
in sufficient concentrations in target tissues.27 Only one
report assessing the effects of PTX in NASH has been
published.18 In this report, the authors found, in contrast
with our results, that PTX attenuated methionine-choline
deficient diet-induced steatohepatitis. Although, the latter
experimental model is similar to that used in the present
study.28,29 a variety of factors, including species and/or sex
of the animals, length of treatment [two weeks in the
study by Koope et al.18 vs 8 weeks in our protocol] may
explain the apparently conflicting results. It should be
noted that in the study of Koope et al. beneficial effects of
PTX were mainly observed in female mice indicating a
possible gender specific effect. In the present study male
rats were used with no observed benefit of PTX. Thus, the
possibility that gender influences the efficacy of PTX
therapy must be further evaluated.
In humans, two recent small pilot clinical trials have
shown that aminotransferase levels among patients with
NASH improve with administration of PTX.19,20 Larger
studies are ongoing to define if PTX could be beneficial
for patients with NASH. The results of the present study,
suggest that although an initial attenuation of liver damage
could eventually be achieved, PTX may not be able to
influence liver fibrosis development in this increasingly
important liver disease.
Beneficial Effects of Pentoxifylline on Hepatic Steatosis, Fibrosis and Necroinflammation in Patients With Non-alcoholic Steatohepatitis
http://www.medscape.com/viewarticle/559029_1
Posted 07/09/2007
Sanjaya K. Satapathy; Puja Sakhuja; Veena Malhotra; Barjesh C. Sharma; Shiv K. Sarin
Author Information
Information from Industry
Pentasa® (mesalamine)A convenient UC agent with a top-to-bottom delivery system.
* Important Safety Information.
* Full Prescribing Information.
Abstract and Introduction
Abstract
Background and Aim: Inhibition of tumor necrosis factor (TNF)-α is a logical approach to manage patients with non-alcoholic steatohepatitis (NASH). Pentoxifylline reduces TNF-α and alanine aminotransferase (ALT) levels in patients with NASH. The aim of the present paper was to study if pentoxifylline can improve histological injury in patients with NASH.
Methods: Nine patients (mean age 31.6 ± 7.2 years) with histologically proven NASH and with persistently elevated ALT (>1.5 times) were given pentoxyfylline at a dosage of 400 mg t.i.d. for 12 months. Besides biochemical assessment, a repeat liver biopsy was performed and the degree of inflammation and fibrosis was compared.
Results: After 12 months of therapy a significant reduction in ALT (111 ± 53 IU/L vs 45 ± 19 IU/L, P = 0.003) and aspartate aminotransferase (AST) (61 ± 27 IU/L vs 33 ± 12 IU/L, P = 0.005) levels was observed. Steatosis and lobular inflammation each reduced in 55% and six (67%) patients down-staged on Brunt's staging (P = 0.009). Four out of six patients with baseline fibrosis had reduction in their fibrosis stage.
Conclusions: Long-term pentoxyfylline therapy effectively achieves sustained biochemical improvement. This correlates well with histological resolution of the disease....
A total of nine patients fulfilled the selection criteria and were enrolled (eight from an earlier study and one new entrant). Patients were administered pentoxifylline 1200 mg/day in three divided doses over a 1-year period. A detailed clinical assessment was carried out in every patient. Patients were followed-up at monthly intervals for the initial 3 months and subsequently at 3-month intervals for the duration of the treatment. At every contact point, adverse events, concurrent medication and compliance with the study medication were assessed. Liver biochemistry was performed at 1-month intervals. Patients were classified based on their body mass index (BMI, kg/m2) according to the following Asia-Pacific cut-off values: normal, between 18.5 and 22.9 kg/m2; overweight, between 23 and 24.9 kg/m2; and obese, above ≥25 kg/m2.[7]...
Baseline liver biopsy was obtained in all patients and showed some degree of steatosis in all patients, moderate (grade II) in two, and severe (grade III) in four patients. Steatosis was predominantly centrilobular. All the patients had grade I to II lobular inflammation. Portal inflammation was mild in the majority of patients. Mallory hyaline bodies were present in a single case at presentation. Stage I fibrosis was present in three, stage II in one and stage III in two cases. After 12 months of therapy with pentoxifylline, significant overall improvement was noted in liver histology (Fig. 3). Sixty seven percent of patients had a decrease in overall grading based on Brunt's staging (P = 0.009). Fifty-five percent of the patients had a reduction in their steatosis and lobular inflammation. Four out of the six patients with baseline fibrosis had a reduction in their fibrosis stage and another two patients remained stable on follow-up biopsy. Only one patient who did not have any evidence of fibrosis on follow-up showed stage I fibrosis. Three patients had one stage reduction in fibrosis and a single patient had a two stage reduction in fibrosis. Five of the six histological responders (defined as at least one grade reduction in Brunt's histological grade) were also biochemical responders with normalization of ALT. Histological improvement in necroinflammation and fibrosis is shown in two representative patients in Figure 4 (arbitrarily named, X and Y).
http://www.medscape.com/viewarticle/559029_1
Posted 07/09/2007
Sanjaya K. Satapathy; Puja Sakhuja; Veena Malhotra; Barjesh C. Sharma; Shiv K. Sarin
Author Information
Information from Industry
Pentasa® (mesalamine)A convenient UC agent with a top-to-bottom delivery system.
* Important Safety Information.
* Full Prescribing Information.
Abstract and Introduction
Abstract
Background and Aim: Inhibition of tumor necrosis factor (TNF)-α is a logical approach to manage patients with non-alcoholic steatohepatitis (NASH). Pentoxifylline reduces TNF-α and alanine aminotransferase (ALT) levels in patients with NASH. The aim of the present paper was to study if pentoxifylline can improve histological injury in patients with NASH.
Methods: Nine patients (mean age 31.6 ± 7.2 years) with histologically proven NASH and with persistently elevated ALT (>1.5 times) were given pentoxyfylline at a dosage of 400 mg t.i.d. for 12 months. Besides biochemical assessment, a repeat liver biopsy was performed and the degree of inflammation and fibrosis was compared.
Results: After 12 months of therapy a significant reduction in ALT (111 ± 53 IU/L vs 45 ± 19 IU/L, P = 0.003) and aspartate aminotransferase (AST) (61 ± 27 IU/L vs 33 ± 12 IU/L, P = 0.005) levels was observed. Steatosis and lobular inflammation each reduced in 55% and six (67%) patients down-staged on Brunt's staging (P = 0.009). Four out of six patients with baseline fibrosis had reduction in their fibrosis stage.
Conclusions: Long-term pentoxyfylline therapy effectively achieves sustained biochemical improvement. This correlates well with histological resolution of the disease....
A total of nine patients fulfilled the selection criteria and were enrolled (eight from an earlier study and one new entrant). Patients were administered pentoxifylline 1200 mg/day in three divided doses over a 1-year period. A detailed clinical assessment was carried out in every patient. Patients were followed-up at monthly intervals for the initial 3 months and subsequently at 3-month intervals for the duration of the treatment. At every contact point, adverse events, concurrent medication and compliance with the study medication were assessed. Liver biochemistry was performed at 1-month intervals. Patients were classified based on their body mass index (BMI, kg/m2) according to the following Asia-Pacific cut-off values: normal, between 18.5 and 22.9 kg/m2; overweight, between 23 and 24.9 kg/m2; and obese, above ≥25 kg/m2.[7]...
Baseline liver biopsy was obtained in all patients and showed some degree of steatosis in all patients, moderate (grade II) in two, and severe (grade III) in four patients. Steatosis was predominantly centrilobular. All the patients had grade I to II lobular inflammation. Portal inflammation was mild in the majority of patients. Mallory hyaline bodies were present in a single case at presentation. Stage I fibrosis was present in three, stage II in one and stage III in two cases. After 12 months of therapy with pentoxifylline, significant overall improvement was noted in liver histology (Fig. 3). Sixty seven percent of patients had a decrease in overall grading based on Brunt's staging (P = 0.009). Fifty-five percent of the patients had a reduction in their steatosis and lobular inflammation. Four out of the six patients with baseline fibrosis had a reduction in their fibrosis stage and another two patients remained stable on follow-up biopsy. Only one patient who did not have any evidence of fibrosis on follow-up showed stage I fibrosis. Three patients had one stage reduction in fibrosis and a single patient had a two stage reduction in fibrosis. Five of the six histological responders (defined as at least one grade reduction in Brunt's histological grade) were also biochemical responders with normalization of ALT. Histological improvement in necroinflammation and fibrosis is shown in two representative patients in Figure 4 (arbitrarily named, X and Y).
From my knowlege it is available here and Europe but use for NASH would likely be off label and you would probably have to educate or propagandize your doctor before he would prescribe it. With the US insurance here it would likely have to be paid for by the patient but if it works it might be worth it to me if I thought it would help. It is still in the investigation stage so you'd be out on a limb. Check the rx site for side effects and warnings before thinking too much about this approach.
From: http://www.rxlist.com/cgi/generic/pentox_ids.htm
TRENTAL is indicated for the treatment of patients with intermittent claudication on the basis of chronic occlusive arterial disease of the limbs. TRENTAL can improve function and symptoms but is not intended to replace more definitive therapy, such as surgical bypass, or removal of arterial obstructions when treating peripheral vascular disease.
DOSAGE AND ADMINISTRATION
The usual dosage of TRENTAL in controlled-release tablet form is one tablet (400 mg) three times a day with meals.
While the effect of TRENTAL may be seen within 2 to 4 weeks, it is recommended that treatment be continued for at least 8 weeks. Efficacy has been demonstrated in double-blind clinical studies of 6 months duration.
Digestive and central nervous system side effects are dose related. If patients develop these effects it is recommended that the dosage be lowered to one tablet twice a day (800 mg/day). If side effects persist at this lower dosage, the administration of TRENTAL should be discontinued.
HOW SUPPLIED
TRENTAL (pentoxifylline) is available for oral administration as 400 mg pink film-coated oblong tablets imprinted Trental®; supplied in bottles of 100 (NDC 0039-0078-10), and Unit Dose Packs of 100 (NDC 0039-0078-11). Store between 59 and 86° F (15 and 30° C). Dispense in well-closed, light-resistant containers. Protect blisters from light.
Rx only.
Rev. May 2003
US Patents 3,737,433 & 4,189,469
US Patent 3,737,433 patent term has been extended.
Manufactured by:
Patheon Pharmaceuticals Inc.
Cincinnati, OH 45215 USA
Manufactured for:
Aventis Pharmaceuticals NJ
Bridgewater, NJ 08807 USA
©2002 Aventis Pharmaceuticals Inc.
TRE-MAY03-F-A
Revised April 2005
From: http://www.rxlist.com/cgi/generic/pentox_ids.htm
TRENTAL is indicated for the treatment of patients with intermittent claudication on the basis of chronic occlusive arterial disease of the limbs. TRENTAL can improve function and symptoms but is not intended to replace more definitive therapy, such as surgical bypass, or removal of arterial obstructions when treating peripheral vascular disease.
DOSAGE AND ADMINISTRATION
The usual dosage of TRENTAL in controlled-release tablet form is one tablet (400 mg) three times a day with meals.
While the effect of TRENTAL may be seen within 2 to 4 weeks, it is recommended that treatment be continued for at least 8 weeks. Efficacy has been demonstrated in double-blind clinical studies of 6 months duration.
Digestive and central nervous system side effects are dose related. If patients develop these effects it is recommended that the dosage be lowered to one tablet twice a day (800 mg/day). If side effects persist at this lower dosage, the administration of TRENTAL should be discontinued.
HOW SUPPLIED
TRENTAL (pentoxifylline) is available for oral administration as 400 mg pink film-coated oblong tablets imprinted Trental®; supplied in bottles of 100 (NDC 0039-0078-10), and Unit Dose Packs of 100 (NDC 0039-0078-11). Store between 59 and 86° F (15 and 30° C). Dispense in well-closed, light-resistant containers. Protect blisters from light.
Rx only.
Rev. May 2003
US Patents 3,737,433 & 4,189,469
US Patent 3,737,433 patent term has been extended.
Manufactured by:
Patheon Pharmaceuticals Inc.
Cincinnati, OH 45215 USA
Manufactured for:
Aventis Pharmaceuticals NJ
Bridgewater, NJ 08807 USA
©2002 Aventis Pharmaceuticals Inc.
TRE-MAY03-F-A
Revised April 2005
Hi there
I've got steatosis also and I wonder if this pentoxifylline is OTC?. Can anyone without concurrent conidtions take it? Anyone knows?
I' afraid that if I bring this medscape article to my hep doc I'm gonna get the same "stop googling stuff" look. The fact is that I finished TX 2 months ago and I feel fine now (with a slight pain in the URQ) I don't know if I'm UND but I do feel like I am and I wouldn't mind using this pentoxifylline for a year. I guess it is used for something else right? Do u know the SX? or effects long term??
My doc told me just last week that exercise and low fat diet was my only option :-(
Thanks Mike for this valuable information
You big, me small
scuba
I've got steatosis also and I wonder if this pentoxifylline is OTC?. Can anyone without concurrent conidtions take it? Anyone knows?
I' afraid that if I bring this medscape article to my hep doc I'm gonna get the same "stop googling stuff" look. The fact is that I finished TX 2 months ago and I feel fine now (with a slight pain in the URQ) I don't know if I'm UND but I do feel like I am and I wouldn't mind using this pentoxifylline for a year. I guess it is used for something else right? Do u know the SX? or effects long term??
My doc told me just last week that exercise and low fat diet was my only option :-(
Thanks Mike for this valuable information
You big, me small
scuba
Yeh, i got the transplant bit but you dont get steatosis after cirrhosis do you. I though it disappeared then actually. I also think we need to be aware of this, it makes you think.
CS
CS
In case you didn't see my other thread I will repost it here: It certainly looks promising in my opinion.
From: http://www.medscape.com/viewarticle/559029_1
Discussion
"In the present study, we demonstrated significant histological improvement and normalization of aminotranferases at the end of 12 months of pentoxifylline treatment in patients with NASH.
NASH could progress to cirrhosis in up to 20-30% of patients.[2-4] No effective therapy for preventing disease progression or amelioration of this disease currently exists. The improvement in liver enzymes in the present study was associated with histological resolution of NASH. Sixty-seven percent of the patients in the present study had at least one grade improvement in Brunt's grading. Five of the six histological responders also had persistent normalization of their aminotransferases. Histological response was noted in steatosis, necroinflammation and fibrosis stage. Fibrosis could be down-staged in four out of six patients with baseline fibrosis. Most importantly, worsening of the fibrosis was observed in only one patient at the end of 12 months of treatment. Pentoxifylline thus could prove useful as an antifibrotic drug in NASH in addition to improving necroinflammation. However, in view of the small number of patients included in the study and because it was not a randomized controlled study, the possibility of sampling error in liver biopsy cannot be entirely excluded. Ratziu et al. recently found that histological lesions of NASH are unevenly distributed throughout the liver parenchyma, which might account for sampling error of liver leading to staging inaccuracies.[9] Although we agree to this theoretical possibility, the sustained biochemical improvement over the entire 12-month period and histological improvement in almost two-thirds of the patients is unlikely to be due to be a result of sampling error.....
In conclusion, pentoxifylline leads to a significant reduction in the AST and ALT levels in patients with NASH. This improvement correlates with histological resolution of steatosis, inflammation and fibrosis stage. Randomized controlled trials with long-term pentoxyfylline treatment with histological follow-up are justified."
Mike
From: http://www.medscape.com/viewarticle/559029_1
Discussion
"In the present study, we demonstrated significant histological improvement and normalization of aminotranferases at the end of 12 months of pentoxifylline treatment in patients with NASH.
NASH could progress to cirrhosis in up to 20-30% of patients.[2-4] No effective therapy for preventing disease progression or amelioration of this disease currently exists. The improvement in liver enzymes in the present study was associated with histological resolution of NASH. Sixty-seven percent of the patients in the present study had at least one grade improvement in Brunt's grading. Five of the six histological responders also had persistent normalization of their aminotransferases. Histological response was noted in steatosis, necroinflammation and fibrosis stage. Fibrosis could be down-staged in four out of six patients with baseline fibrosis. Most importantly, worsening of the fibrosis was observed in only one patient at the end of 12 months of treatment. Pentoxifylline thus could prove useful as an antifibrotic drug in NASH in addition to improving necroinflammation. However, in view of the small number of patients included in the study and because it was not a randomized controlled study, the possibility of sampling error in liver biopsy cannot be entirely excluded. Ratziu et al. recently found that histological lesions of NASH are unevenly distributed throughout the liver parenchyma, which might account for sampling error of liver leading to staging inaccuracies.[9] Although we agree to this theoretical possibility, the sustained biochemical improvement over the entire 12-month period and histological improvement in almost two-thirds of the patients is unlikely to be due to be a result of sampling error.....
In conclusion, pentoxifylline leads to a significant reduction in the AST and ALT levels in patients with NASH. This improvement correlates with histological resolution of steatosis, inflammation and fibrosis stage. Randomized controlled trials with long-term pentoxyfylline treatment with histological follow-up are justified."
Mike
I have NASH on top of HCV. My GI didn't even mention my NASH. Now that I'm being tx out of the Mayo Clinic , they are concerned. They recommended exercise and a low fat diet as stated above.
Thanks for posting Mike.
If people get that scared, they should google the topics and educate themselves.
Thanks for posting Mike.
If people get that scared, they should google the topics and educate themselves.
Sparrow, Mike - forgive me for asking but you do realize my previous post was my misguided attempt at humor right ? The statement I made is contradictory by nature.
ie. stats -->meaningless, 7 out of 10 know that (use of a statistic)
sfw - I'm doing ok I guess, probably be better to keep my big yap shut.
ie. stats -->meaningless, 7 out of 10 know that (use of a statistic)
sfw - I'm doing ok I guess, probably be better to keep my big yap shut.
Keep in mind that this article was based on a liver transplant population and thus may not be as relevant to the non transplant patient population.
"Dr. Chung and colleagues at General Hospital, Boston came to this conclusion after a retrospective review involving 94 patients with hepatitis C cirrhosis who underwent transplantation between 1992 and 2005."
I thought it was an interesting article but there really isn't much more than a conclusion based on 94 liver transplants.
"The researchers conclude that steatosis is independently associated with hepatocellular cancer in THESE PATIENTS and may be a useful marker for identifying those at high risk. "
I didn't meant to scare anyone but I did think it is something that we should be aware of. Transplantation carries with it some distinguishing factors and until we see similar evidence in the non transplant population I wouldn't worry too much about this article.
Mike
"Dr. Chung and colleagues at General Hospital, Boston came to this conclusion after a retrospective review involving 94 patients with hepatitis C cirrhosis who underwent transplantation between 1992 and 2005."
I thought it was an interesting article but there really isn't much more than a conclusion based on 94 liver transplants.
"The researchers conclude that steatosis is independently associated with hepatocellular cancer in THESE PATIENTS and may be a useful marker for identifying those at high risk. "
I didn't meant to scare anyone but I did think it is something that we should be aware of. Transplantation carries with it some distinguishing factors and until we see similar evidence in the non transplant population I wouldn't worry too much about this article.
Mike
Yes diet and excersize can reduce Fatty Liver, even for G3s like me, where steatosis is at least partly viral. HCV must play a part with steatosis in all genotypes as people with HepC have higher rates of fatty liver than the general population. Sorry CrazyTrain thats another statisic.
CS
CS
Thanks just what i needed to know - NOT. Does it apply to all genotypes, I wonder.
sfwandwow
Its not meant to scare new comers, merely stating facts, as hard as they are to take sometimes.
I've got steatosis, but that goes with being G3 and I am glad it was posted.
Orleans
There are many studies that state that INF Tx reduces HCC rates.
sfwandwow
Its not meant to scare new comers, merely stating facts, as hard as they are to take sometimes.
I've got steatosis, but that goes with being G3 and I am glad it was posted.
Orleans
There are many studies that state that INF Tx reduces HCC rates.
welli agree with that one.. why put things on here that scare people.. i think people should be alittle more positive in many ways.. especially to new comers..well how are u crazytrain?
so the best result for fatty liver is low fat diet and exercise to the maximum..drink lots of water,is this correct.... Alot of people here have fatty liver i think? but excercise what i read and diet change can change it all.. May GOD BLESS U ALL
About tx cutting your chance of getting HHC by half, Any studies to back that. thanks,jm
i have slightly fatty liver.. iam losing weight and excercising ,plus i take milk thistle
I don't think I like this news. I see the N.P. next week and will have her explain where I stand. How I understand my "Non-alchoholic steatosis hepatitis' (NASH) lose weight and exercise are recommended. Is there annother way to "ameliorate fatty liver. My Dr. seemed to feel It was a "heredity" factor for me. Also I must say with a Hemoglobin at 11, going to the bathroom feelz like excercise.
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