Aa
Finally got the first "full picture" of my results... Should I start treatment?
ast 18 (ref range: 10-30 u/l)
alt 19 (ref range: 6-29 u/l)
vit d, 25-oh, total: 28 (ref range: 30-100 ng/ml)
pth intact 35 (ref range: 14-64 pg/ml)
hbsag positive
hbsab negative
hbcab positive
hbeag negative
hbeab positive
hbv dna 1311 ui/ml
hbsag count ??? ui/ml (can't do the test in the US, but I'm guessing it's going to be more than hbv dna?)
alpha fetoprotein tumor marker 2.0 (ref range: <6.1 ng/ml)
liver fibrotest score: 0.29 (F1) minimal fibrosis
acti test (assesses activity (inflammation in chb)): score 0.05 (A0) no activity.
hep a ab negative (should I get vaccinated?)
hep d co-infection negative
Ultrasound: No significant abnormality is identified.
tests pending: hbv genotype
What do you think guys am I a good candidate to start treatment? If so, what treatment plan would you advise? Is peg-Intf an option? How likely will my fibrosis progress to F2? What phase do I belong to (e.g. immunte tolrent, clearance, inactive, etc)? How often should I monitor myself? Also, would it be beneficial to get a FibroScan in addition to the FibroTest I already got?
I'm going to discuss with my gi about my treatment options this Tuesday, and also going to have a second opinion appt with a hepatologist specialist next month. I would also appreciate if you could recommend good docs in LA area.
Thanks for your help!
alt 19 (ref range: 6-29 u/l)
vit d, 25-oh, total: 28 (ref range: 30-100 ng/ml)
pth intact 35 (ref range: 14-64 pg/ml)
hbsag positive
hbsab negative
hbcab positive
hbeag negative
hbeab positive
hbv dna 1311 ui/ml
hbsag count ??? ui/ml (can't do the test in the US, but I'm guessing it's going to be more than hbv dna?)
alpha fetoprotein tumor marker 2.0 (ref range: <6.1 ng/ml)
liver fibrotest score: 0.29 (F1) minimal fibrosis
acti test (assesses activity (inflammation in chb)): score 0.05 (A0) no activity.
hep a ab negative (should I get vaccinated?)
hep d co-infection negative
Ultrasound: No significant abnormality is identified.
tests pending: hbv genotype
What do you think guys am I a good candidate to start treatment? If so, what treatment plan would you advise? Is peg-Intf an option? How likely will my fibrosis progress to F2? What phase do I belong to (e.g. immunte tolrent, clearance, inactive, etc)? How often should I monitor myself? Also, would it be beneficial to get a FibroScan in addition to the FibroTest I already got?
I'm going to discuss with my gi about my treatment options this Tuesday, and also going to have a second opinion appt with a hepatologist specialist next month. I would also appreciate if you could recommend good docs in LA area.
Thanks for your help!
Stephen does this mean people with advanced fibrosis they should take care in taking vitamin D?
of course they must take it, and when damage is very very severe even 400.000iu of vit d3 rise vitd25oh few decimals, so it does not exist a dose anyone must test vitd25oh, ipth, calcium and find his dose (it is not like for healthy persons)
http://www.vitamindwiki.com/400%2C000+IU+barely+raised+liver+transplant+candidate+vitamin+D+levels+%28no+surprise%29+%E2%80%93+March+2015
here s ho wlow vitamin d can make liver inflammation, NAFLD
http://www.vitamindwiki.com/Liver+Inflammation+%28NAFLD%29+is+prevented+by+Vitamin+D+%E2%80%93+review+May+2015
but it is not only this, it is correlated to fibrosis directly, kidneys with 50% less function, fatty liver, insulin resistance, liver cancer.few researchers proposed low vit d as a marker for liver cancer sicne they found correlation with this too
http://www.vitamindwiki.com/Liver
of course they must take it, and when damage is very very severe even 400.000iu of vit d3 rise vitd25oh few decimals, so it does not exist a dose anyone must test vitd25oh, ipth, calcium and find his dose (it is not like for healthy persons)
http://www.vitamindwiki.com/400%2C000+IU+barely+raised+liver+transplant+candidate+vitamin+D+levels+%28no+surprise%29+%E2%80%93+March+2015
here s ho wlow vitamin d can make liver inflammation, NAFLD
http://www.vitamindwiki.com/Liver+Inflammation+%28NAFLD%29+is+prevented+by+Vitamin+D+%E2%80%93+review+May+2015
but it is not only this, it is correlated to fibrosis directly, kidneys with 50% less function, fatty liver, insulin resistance, liver cancer.few researchers proposed low vit d as a marker for liver cancer sicne they found correlation with this too
http://www.vitamindwiki.com/Liver
I have no idea, but I would certainly make sure I am not deficient in my vitamin D level.
Stephen does this mean people with advanced fibrosis they should take care in taking vitamin D? How is related to fibrosis? Just curious!
"Low vitamin D serum concentration is associated with high levels of hepatitis B virus replication in chronically infected patients"
http://onlinelibrary.wiley.com/doi/10.1002/hep.26488/full
In view of the above-described data, vitamin D deficiency in liver diseases does not appear to be specific for distinct entities. Nevertheless, our study highlights an important specific feature of vitamin D metabolism in CHB, because the strong association between 25(OH)D3 and HBV DNA serum concentration is in sharp contrast to results of numerous previous studies in patients with CHC, which failed to show an association between vitamin D serum levels and HCV viral load.[17-21, 27-30] In this regard, the observed inversed seasonal fluctuations of 25(OH)D3 and HBV DNA serum levels might be considered as an important hint for a functional relationship between both variables.
The possible causal relationship between vitamin D metabolism and HBV replication, which needs to be proven by future studies, may offer attractive therapeutic opportunities for treatment of CHB. As highlighted above, the addition of relatively high doses of cholecalciferol to standard therapy was superior to the addition of placebo in the treatment of patients with lung tuberculosis.[14] In this study, as well as, for example, in studies in diabetes patients, vitamin D supplementation resulted in a profound change in serum and cellular cytokine profiles.[16, 31] For treatment of chronic hepatitis, the development of novel immunomodulatory agents appears highly relevant. Such agents might be suitable add-ons to both treatment of with Peg-IFN-α or NAs to increase the chance of long-lasting immune control of HBV infection. In this regard, it needs to be emphasized that we did not observe an association between vitamin D and HBsAg serum levels, suggesting that therapeutic administration of vitamin D alone may probably not promote the important clinical goal of HBsAg loss.
Our study has several limitations. Most important, clinical association studies cannot prove causal relationships. Thefore, a suggestive functional link between vitamin D metabolism and HBV replication remains elusive. Nevertheless, our study is of hypothesis-generating value for the design of future in vitro studies or prospective clinical interventional trials. Furthermore, the cohort investigated in our study is not representative for all phases of CHB. Especially, patients with advanced liver fibrosis and high ALT serum levels are underrepresented in our cohort. Furthermore, only few patients in our cohort were HBeAg positive. Although the majority of HBV patients treated in our center is HBeAg negative, the inclusion criterion “treatment-naïve state at time of vitamin D quantification” of our study appears to account for a selection of overall younger patients with limited degrees of liver fibrosis, as well as of HBeAg-negative patients. Yet, it appears unlikely that the profile of the present cohort affects the main finding of our study, that low 25(OH)D3 serum levels are associated with HBV DNA viral load. In addition, the number of patients in our study who received antiviral therapy after initial vitamin D quantification, and in whom vitamin D serum levels could be quantified during follow-up, appears to be too small to draw final conclusions. Although 25(OH)D3 serum levels were slightly higher during follow-up, compared to baseline, which may indicate that HBV replication affects vitamin D metabolism, this difference did not reach statistical significance. Larger studies are necessary to fully address this important question, as well as to assess the effect of other possible determinants of vitamin D serum levels, such as BMI.
In conclusion, we demonstrate a significant association between low 25(OH)D3 serum levels and high levels of HBV replication in chronically infected patients. Future studies to evaluate a therapeutic value of vitamin D and its analogs in HBV infection may be justified
http://onlinelibrary.wiley.com/doi/10.1002/hep.26488/full
In view of the above-described data, vitamin D deficiency in liver diseases does not appear to be specific for distinct entities. Nevertheless, our study highlights an important specific feature of vitamin D metabolism in CHB, because the strong association between 25(OH)D3 and HBV DNA serum concentration is in sharp contrast to results of numerous previous studies in patients with CHC, which failed to show an association between vitamin D serum levels and HCV viral load.[17-21, 27-30] In this regard, the observed inversed seasonal fluctuations of 25(OH)D3 and HBV DNA serum levels might be considered as an important hint for a functional relationship between both variables.
The possible causal relationship between vitamin D metabolism and HBV replication, which needs to be proven by future studies, may offer attractive therapeutic opportunities for treatment of CHB. As highlighted above, the addition of relatively high doses of cholecalciferol to standard therapy was superior to the addition of placebo in the treatment of patients with lung tuberculosis.[14] In this study, as well as, for example, in studies in diabetes patients, vitamin D supplementation resulted in a profound change in serum and cellular cytokine profiles.[16, 31] For treatment of chronic hepatitis, the development of novel immunomodulatory agents appears highly relevant. Such agents might be suitable add-ons to both treatment of with Peg-IFN-α or NAs to increase the chance of long-lasting immune control of HBV infection. In this regard, it needs to be emphasized that we did not observe an association between vitamin D and HBsAg serum levels, suggesting that therapeutic administration of vitamin D alone may probably not promote the important clinical goal of HBsAg loss.
Our study has several limitations. Most important, clinical association studies cannot prove causal relationships. Thefore, a suggestive functional link between vitamin D metabolism and HBV replication remains elusive. Nevertheless, our study is of hypothesis-generating value for the design of future in vitro studies or prospective clinical interventional trials. Furthermore, the cohort investigated in our study is not representative for all phases of CHB. Especially, patients with advanced liver fibrosis and high ALT serum levels are underrepresented in our cohort. Furthermore, only few patients in our cohort were HBeAg positive. Although the majority of HBV patients treated in our center is HBeAg negative, the inclusion criterion “treatment-naïve state at time of vitamin D quantification” of our study appears to account for a selection of overall younger patients with limited degrees of liver fibrosis, as well as of HBeAg-negative patients. Yet, it appears unlikely that the profile of the present cohort affects the main finding of our study, that low 25(OH)D3 serum levels are associated with HBV DNA viral load. In addition, the number of patients in our study who received antiviral therapy after initial vitamin D quantification, and in whom vitamin D serum levels could be quantified during follow-up, appears to be too small to draw final conclusions. Although 25(OH)D3 serum levels were slightly higher during follow-up, compared to baseline, which may indicate that HBV replication affects vitamin D metabolism, this difference did not reach statistical significance. Larger studies are necessary to fully address this important question, as well as to assess the effect of other possible determinants of vitamin D serum levels, such as BMI.
In conclusion, we demonstrate a significant association between low 25(OH)D3 serum levels and high levels of HBV replication in chronically infected patients. Future studies to evaluate a therapeutic value of vitamin D and its analogs in HBV infection may be justified
I am against big quantity personally take it just when there is luck after blood test
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Bringing PTH to minimum is not your target it's just signal that you have obtained your max safe vit d level when vit D has the best immunoregulation effect.