Aa
much concerned and need help
I have not been around for a while after failing my last trial in Miami. My liver is all scared and I'm sure much worse then 2009-2010 but now My new doctor has put me on Pegasys proclick (180) the usual Rribavirin 1200 mg a day and the new Incivek 750 mg every 8 hrs. I'm close to 70 years old and I guess this will be my last chance as he put it, so I'm very concerned with the outcome and what to expect during this 3 month although I still might be on the old medicine beyond this 3 months. I'm going on my second week on thursday and I'm not feeling too good. My urine has changed color like I never seen it before and I feel bad all over. I'm also taking pills to get this Amonia out of my system and thats one indicator I'm much worse, because I never suffered with this before. Any in-put would be helpful, and if anybody was and is in the same situation would be helpful. Thanks
Caution: Hepatitis C and Vitamin D Deficiency
In addition to dietary recommendations for liver disease, a significant portion of people with the Hepatitis C virus (HCV) take vitamins and herbs to support their liver. Despite this trend, American researchers have confirmed that living with chronic Hepatitis C is usually accompanied by a vitamin D deficiency. Worried about the consequences of a vitamin D deficiency, those with the virus may choose to supplement with this vitamin. However, vitamin D is toxic in large doses and taking too much of it could end up being more harmful than not having enough.
About Vitamin D
Vitamin D is a fat-soluble vitamin that helps the body absorb calcium and plays a crucial role in the growth and maintenance of strong, healthy bones. A lack of vitamin D causes calcium-depleted bone, which can weaken the bones and increase the risk of fractures resulting from osteoporosis. While vitamin D is probably best known for its role in bone development and maintenance, it’s also involved in the brain, immune and reproductive systems. A lack of vitamin D can cause osteomalacia in adults and rickets in children, both of which are unwelcome additions to the burden of chronic liver disease.
Vitamin D is found in food, but can also be produced in the body after exposure to ultraviolet rays from the sun. Some forms of vitamin D are relatively inactive, with a limited ability to function as a vitamin. The liver and kidney help convert vitamin D to its active hormone form. But for those with advanced liver disease from Hepatitis C, a deficiency can conceivably develop from the liver’s inability to convert vitamin D into its active form.
The Research
Presented in October 2008 at the 73rd Annual Scientific Meeting of the American College of Gastroenterology, researchers from the University of Tennessee in Memphis measured the vitamin D levels in people with chronic liver disease. Of those evaluated, 85 percent of the study participants had chronic Hepatitis C. After dividing every vitamin D deficiency into three categories (mild, moderate and severe), the investigators found the following:
92.4 percent of those with chronic liver disease had some degree of vitamin D deficiency
At least 33 percent of participants were severely deficient in vitamin D
Severe vitamin D deficiency was more common among those with cirrhosis
Lead researcher Dr. Satheesh P. Nair commented, “Since deficiency is common among these patients, Vitamin D replacement may hopefully prevent osteoporosis and other bone complications related to end stage liver disease.”
http://www.hepatitis-central.com/mt/archives/2008/10/hepatitis_c_and_11.html
I would talk to my liver doc about the recommended dosage
In addition to dietary recommendations for liver disease, a significant portion of people with the Hepatitis C virus (HCV) take vitamins and herbs to support their liver. Despite this trend, American researchers have confirmed that living with chronic Hepatitis C is usually accompanied by a vitamin D deficiency. Worried about the consequences of a vitamin D deficiency, those with the virus may choose to supplement with this vitamin. However, vitamin D is toxic in large doses and taking too much of it could end up being more harmful than not having enough.
About Vitamin D
Vitamin D is a fat-soluble vitamin that helps the body absorb calcium and plays a crucial role in the growth and maintenance of strong, healthy bones. A lack of vitamin D causes calcium-depleted bone, which can weaken the bones and increase the risk of fractures resulting from osteoporosis. While vitamin D is probably best known for its role in bone development and maintenance, it’s also involved in the brain, immune and reproductive systems. A lack of vitamin D can cause osteomalacia in adults and rickets in children, both of which are unwelcome additions to the burden of chronic liver disease.
Vitamin D is found in food, but can also be produced in the body after exposure to ultraviolet rays from the sun. Some forms of vitamin D are relatively inactive, with a limited ability to function as a vitamin. The liver and kidney help convert vitamin D to its active hormone form. But for those with advanced liver disease from Hepatitis C, a deficiency can conceivably develop from the liver’s inability to convert vitamin D into its active form.
The Research
Presented in October 2008 at the 73rd Annual Scientific Meeting of the American College of Gastroenterology, researchers from the University of Tennessee in Memphis measured the vitamin D levels in people with chronic liver disease. Of those evaluated, 85 percent of the study participants had chronic Hepatitis C. After dividing every vitamin D deficiency into three categories (mild, moderate and severe), the investigators found the following:
92.4 percent of those with chronic liver disease had some degree of vitamin D deficiency
At least 33 percent of participants were severely deficient in vitamin D
Severe vitamin D deficiency was more common among those with cirrhosis
Lead researcher Dr. Satheesh P. Nair commented, “Since deficiency is common among these patients, Vitamin D replacement may hopefully prevent osteoporosis and other bone complications related to end stage liver disease.”
http://www.hepatitis-central.com/mt/archives/2008/10/hepatitis_c_and_11.html
I would talk to my liver doc about the recommended dosage
Vitamin D Increases Sustained Response to Interferon-based Therapy for Hepatitis C, May Improve Liver Fibrosis
In the EASL study, S. Abu Mouch and colleagues from Israel assessed whether adding a vitamin D supplement to standard hepatitis C therapy using pegylated interferon plus ribavirin could improve rates of sustained virological response (SVR), or continued undetectable HCV viral load 24 weeks after completion of treatment.
Vitamin D is a potent immune modulator that has a direct effect on T-cells and antigen-presenting immune cells, and can directly or indirectly influence the differentiation and activity of CD4 T-cells, the researchers noted as background. They hypothesized that vitamin D has an important role in innate immune response against HCV. In addition, some studies have shown that vitamin D improves insulin sensitivity (a predictor of better treatment response) and inhibits HCV replication.
The investigators first measured vitamin D levels in a group of 157 chronic hepatitis C patients treated at their liver clinic in Israel, and found that fully 84% had low levels, and one-third had "severe deficiency."
They then performed a randomized study of 67 patients. About half were men, the average age was 48 years, and most were of Russian origin, with only a few being of Israeli or Arabic origin.
Participants were randomly assigned to receive 1.5 mcg/kg pegylated interferon alfa-2b (PegIntron) plus 1000-1200 mg/daily weight-adjusted ribavirin for 48 weeks, with or without 1000-4000 IU/day vitamin D3, enough to bring serum levels up to 32 ng/mL. By chance, patients in the vitamin D group were more difficult to treat than those in the control group, having a higher body mass index and larger percentages with high baseline viral load and advanced liver fibrosis.
Results
44% of participants receiving vitamin D achieved rapid virological response (undetectable HCV at week 4), compared with 18% in the control group (P < 0.0001).
94% of participants in the vitamin D group achieved complete early virological response (undetectable HCV at week 12), compared with 48% in the control group (P < 0.0001).
85% of patients in the vitamin D group achieved SVR, compared with 43% in the control group (P < 0.001).
Adverse events were mostly mild and were typical of those associated with pegylated interferon/ribavirin (mainly flu-like symptoms).
No serious adverse events were reported.
These findings led the investigators to conclude that adding vitamin D supplements to pegylated interferon/ribavirin therapy for treatment-naive genotype 1 patients with chronic HCV infection significantly improves SVR rates.
They further suggested that vitamin D deficiency may contribute to the strong racial/ethnic disparity observed in responses to antiviral therapy for HCV. People of African descent -- and to a lesser extent Latinos -- do not respond as well as whites and Asians to interferon-based therapy.
People with darker skin produce less vitamin D when exposed to the sun, and are therefore more likely have low levels. The 2000-2004 National Health and Nutritional Examination Survey (NHANES), for example, found that U.S. non-Hispanic whites had average vitamin D levels nearly 10 nmol/L higher than those of Mexican-Americans, who in turn had average levels more than 10 nmol/L higher than non-Hispanic blacks.
Treatment Response and Fibrosis
In the second study, published in the April 2010 issue of Hepatology, S. Petta and colleagues from Italy looked at the association between vitamin D levels and histological and virological response to interferon-based therapy.
Adding to the mechanisms described by Abu Mouch's group, the study authors noted that vitamin D also can potentially interfere with inflammatory responses and fibrogenesis (formation of fibrous scar tissue).
This study included 197 patients with genotype 1 chronic hepatitis C and 49 healthy HCV negative control subjects matched according to age and sex. Most of the hepatitis C patients (167) were treatment with pegylated interferon plus ribavirin.
Levels of 25-hydroxyvitamin D were measured using high-pressure liquid chromatography. Tissue expression of cytochrome P450 25-hydroxylating liver enzymes (CYP27A1 and CYP2R1) were assessed in 34 hepatitis patients and 8 control subjects.
Results
Serum 25-hydroxyvitamin D levels were significantly lower on average in chronic hepatitis C patients compared with healthy control subjects (25.07 vs 43.06 mcg/L; P < 0.001).
Lower vitamin D levels were independently associated with female sex and liver necro-inflammation.
Levels of CYP27A1, but not CYP2R1, were directly related to vitamin D levels and inversely correlated with necro-inflammation.
Independent predictors of severe liver fibrosis or cirrhosis (stage F3-F4) included:
Liver necro-inflammation (OR 2.235);
Older age (OR 1.043);
High ferritin (a protein that stores iron) (OR 1.003);
Low cholesterol (OR 0.981);
Low 25-hydroxyvitamin D (odds ratio [OR] 0.942).
Overall, 70 patients (41%) achieved SVR.
In a multivariate analysis, factors independently associated with poor response, or failure to achieve SVR, included;
Lower 25-hydroxyvitamin D (OR 1.039);
Lower cholesterol (OR 1.009);
Liver steatosis (fatty liver) (OR, 0.971).
Based on these findings, the study authors concluded, "Genotype 1 chronic hepatitis C patients had low [25-hydroxyvitamin D] serum levels, possibly because of reduced CYP27A1 expression."
"Low vitamin D is linked to severe fibrosis and low SVR on interferon-based therapy," they added.
http://www.hivandhepatitis.com/2010_conference/easl/docs/0518_2010_b.html
In the EASL study, S. Abu Mouch and colleagues from Israel assessed whether adding a vitamin D supplement to standard hepatitis C therapy using pegylated interferon plus ribavirin could improve rates of sustained virological response (SVR), or continued undetectable HCV viral load 24 weeks after completion of treatment.
Vitamin D is a potent immune modulator that has a direct effect on T-cells and antigen-presenting immune cells, and can directly or indirectly influence the differentiation and activity of CD4 T-cells, the researchers noted as background. They hypothesized that vitamin D has an important role in innate immune response against HCV. In addition, some studies have shown that vitamin D improves insulin sensitivity (a predictor of better treatment response) and inhibits HCV replication.
The investigators first measured vitamin D levels in a group of 157 chronic hepatitis C patients treated at their liver clinic in Israel, and found that fully 84% had low levels, and one-third had "severe deficiency."
They then performed a randomized study of 67 patients. About half were men, the average age was 48 years, and most were of Russian origin, with only a few being of Israeli or Arabic origin.
Participants were randomly assigned to receive 1.5 mcg/kg pegylated interferon alfa-2b (PegIntron) plus 1000-1200 mg/daily weight-adjusted ribavirin for 48 weeks, with or without 1000-4000 IU/day vitamin D3, enough to bring serum levels up to 32 ng/mL. By chance, patients in the vitamin D group were more difficult to treat than those in the control group, having a higher body mass index and larger percentages with high baseline viral load and advanced liver fibrosis.
Results
44% of participants receiving vitamin D achieved rapid virological response (undetectable HCV at week 4), compared with 18% in the control group (P < 0.0001).
94% of participants in the vitamin D group achieved complete early virological response (undetectable HCV at week 12), compared with 48% in the control group (P < 0.0001).
85% of patients in the vitamin D group achieved SVR, compared with 43% in the control group (P < 0.001).
Adverse events were mostly mild and were typical of those associated with pegylated interferon/ribavirin (mainly flu-like symptoms).
No serious adverse events were reported.
These findings led the investigators to conclude that adding vitamin D supplements to pegylated interferon/ribavirin therapy for treatment-naive genotype 1 patients with chronic HCV infection significantly improves SVR rates.
They further suggested that vitamin D deficiency may contribute to the strong racial/ethnic disparity observed in responses to antiviral therapy for HCV. People of African descent -- and to a lesser extent Latinos -- do not respond as well as whites and Asians to interferon-based therapy.
People with darker skin produce less vitamin D when exposed to the sun, and are therefore more likely have low levels. The 2000-2004 National Health and Nutritional Examination Survey (NHANES), for example, found that U.S. non-Hispanic whites had average vitamin D levels nearly 10 nmol/L higher than those of Mexican-Americans, who in turn had average levels more than 10 nmol/L higher than non-Hispanic blacks.
Treatment Response and Fibrosis
In the second study, published in the April 2010 issue of Hepatology, S. Petta and colleagues from Italy looked at the association between vitamin D levels and histological and virological response to interferon-based therapy.
Adding to the mechanisms described by Abu Mouch's group, the study authors noted that vitamin D also can potentially interfere with inflammatory responses and fibrogenesis (formation of fibrous scar tissue).
This study included 197 patients with genotype 1 chronic hepatitis C and 49 healthy HCV negative control subjects matched according to age and sex. Most of the hepatitis C patients (167) were treatment with pegylated interferon plus ribavirin.
Levels of 25-hydroxyvitamin D were measured using high-pressure liquid chromatography. Tissue expression of cytochrome P450 25-hydroxylating liver enzymes (CYP27A1 and CYP2R1) were assessed in 34 hepatitis patients and 8 control subjects.
Results
Serum 25-hydroxyvitamin D levels were significantly lower on average in chronic hepatitis C patients compared with healthy control subjects (25.07 vs 43.06 mcg/L; P < 0.001).
Lower vitamin D levels were independently associated with female sex and liver necro-inflammation.
Levels of CYP27A1, but not CYP2R1, were directly related to vitamin D levels and inversely correlated with necro-inflammation.
Independent predictors of severe liver fibrosis or cirrhosis (stage F3-F4) included:
Liver necro-inflammation (OR 2.235);
Older age (OR 1.043);
High ferritin (a protein that stores iron) (OR 1.003);
Low cholesterol (OR 0.981);
Low 25-hydroxyvitamin D (odds ratio [OR] 0.942).
Overall, 70 patients (41%) achieved SVR.
In a multivariate analysis, factors independently associated with poor response, or failure to achieve SVR, included;
Lower 25-hydroxyvitamin D (OR 1.039);
Lower cholesterol (OR 1.009);
Liver steatosis (fatty liver) (OR, 0.971).
Based on these findings, the study authors concluded, "Genotype 1 chronic hepatitis C patients had low [25-hydroxyvitamin D] serum levels, possibly because of reduced CYP27A1 expression."
"Low vitamin D is linked to severe fibrosis and low SVR on interferon-based therapy," they added.
http://www.hivandhepatitis.com/2010_conference/easl/docs/0518_2010_b.html
Call your hep or gastro doctor and tell them the dosage that was recommended to you and make sure they approve of it before taking that much. I take 2,000 units per day (per my PCP) and my hepatologist is okay with that - but 50,000 is definitely in the megadose range and you really should make sure that dose is okay. Best wishes!
this came from mayo clinic---------http://www.mayoclinic.com/health/vitamin-d-toxicity/AN02008
What is vitamin D toxicity, and should I worry about it since I take supplements?
Answer
from Katherine Zeratsky, R.D., L.D.
Vitamin D toxicity, also called hypervitaminosis D, is a rare but potentially serious condition that occurs when you have excessive amounts of vitamin D in your body.
Vitamin D toxicity is usually caused by megadoses of vitamin D supplements — not by diet or sun exposure. That's because your body regulates the amount of vitamin D produced by sun exposure, and even fortified foods don't contain large amounts of vitamin D.
The main consequence of vitamin D toxicity is a buildup of calcium in your blood (hypercalcemia), which can cause symptoms such as poor appetite, nausea and vomiting. Weakness, frequent urination and kidney problems also may occur. Treatment includes the stopping of excessive vitamin D intake. Your doctor may also prescribe intravenous fluids and medications, such as corticosteroids or bisphosphonates.
Taking 50,000 international units (IU) a day of vitamin D for several months has been shown to cause toxicity. This level is many times higher than the recommended dietary allowance (RDA) for most adults of 600 IU of vitamin D a day. Doses higher than the RDA are sometimes used to treat medical problems such as vitamin D deficiency, but these are given only under the care of a doctor and only for a short time.
Although vitamin D toxicity is uncommon even among people who take supplements, you may be at greater risk if you have health problems, such as liver or kidney conditions, or if you take thiazide-type diuretics. As always, talk to your doctor before taking vitamin and mineral supplements---------
What is vitamin D toxicity, and should I worry about it since I take supplements?
Answer
from Katherine Zeratsky, R.D., L.D.
Vitamin D toxicity, also called hypervitaminosis D, is a rare but potentially serious condition that occurs when you have excessive amounts of vitamin D in your body.
Vitamin D toxicity is usually caused by megadoses of vitamin D supplements — not by diet or sun exposure. That's because your body regulates the amount of vitamin D produced by sun exposure, and even fortified foods don't contain large amounts of vitamin D.
The main consequence of vitamin D toxicity is a buildup of calcium in your blood (hypercalcemia), which can cause symptoms such as poor appetite, nausea and vomiting. Weakness, frequent urination and kidney problems also may occur. Treatment includes the stopping of excessive vitamin D intake. Your doctor may also prescribe intravenous fluids and medications, such as corticosteroids or bisphosphonates.
Taking 50,000 international units (IU) a day of vitamin D for several months has been shown to cause toxicity. This level is many times higher than the recommended dietary allowance (RDA) for most adults of 600 IU of vitamin D a day. Doses higher than the RDA are sometimes used to treat medical problems such as vitamin D deficiency, but these are given only under the care of a doctor and only for a short time.
Although vitamin D toxicity is uncommon even among people who take supplements, you may be at greater risk if you have health problems, such as liver or kidney conditions, or if you take thiazide-type diuretics. As always, talk to your doctor before taking vitamin and mineral supplements---------
I am taking one 50000 units vit D once per week
I never heard my GP saying anything aginst it. Liver specialist did not say anything against vit D either although we did not discucc the dose
As far as I know it is good. What makes you say that might not be ok? I mean if you gve me couple of references I could discuss them with the specialist
I never heard my GP saying anything aginst it. Liver specialist did not say anything against vit D either although we did not discucc the dose
As far as I know it is good. What makes you say that might not be ok? I mean if you gve me couple of references I could discuss them with the specialist
Well I was doing well but now I went to the VA and they find I'm in bad shape with lack of VIT D. Oh by the way all my blood work from my hep c doctor is almost the same and I'm anemic because of the med.Getting back to this VIT D problem I asked my doctor if its ok to take VIT D and she said its OK but I just found out I need to take 50000 units for 8 weeks and when looking it up, doesn't sound too good for the liver. Any input on this because I think I need to explain this to my hep doctor. Thanks
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