Well, it certainly indicates that your doc keeps up with the new research and literature! When my husband started treatment 2 years ago, none of that was "ordered," but over the course of treatment, he added 2,000 IU of Vitamin D (after clearing with his doc that it was ok, of course).
My "carrot in front of the horse" during treatment was my pass through the Starbucks drive up on my way to work. Couldn't stand paying $5 for a cup of coffee but it actually was a small price to pay to keep me going to work. :)
Vit D...yes, my Endocrinologist is a fan of Vit D (and calcium).
Wow, good for you two! I don't know how you can stand to drink coffee on tx but my hats off to ya'!
I take 2000u vit.D on advice of hepa when started tx. No coffee advice,drink 2 cups anyway!
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.