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3 Easy Hep C Questions
Hello, I was diagnosed with Hep C in 1997 from either sharing needles approximately for the 6 month period before that or as the doctor thinks when snorting cocaine possibly 10 years earlier. I guess he thinks being diagnosed with it so quickly after sharing needles shouldn't occur especially with the viral load I had, which since it was so long ago I think it was somewhere between 2 and 4 million (genotype 1). What do you think? Further, hopefully another easy question. I had the Ribovarin/Interferon treatment done in 2004/2005 and it was successful. Lots and lots and lots of side effects but I made it through it. Unfortunately my thyroid doesnt manufacture enough hormone because of the treatment and I will be on synthroid the rest of my life. I have read also that the treatment can affect your lipid panel. Not completely sure of that, but mine is definitely screwed up as to prior to the tx it was not. What do you think? One last question. When I go to any Dr. I tell them that I have Hep C but it is in remission because my tests show no viral load. Is that the right way to refer to it as? Thank you for your time.
How and when you contracted HCV and what your Viral load was at any given time is really not at all relevant.
What IS important is that you treated and from what you say successfully so...congrats on that !
The thyroid gland being affected from HCV therapy is a fairly common occurrence and often patients are left "hypothyroid" which it sounds like you were and yes the drug "synthroid it the modality used for that(usually for life) and most often successfully .
Lipid levels may be affected "post tx" also. These levels have been seen to rise somewhat.I have copied a post I put up a few months ago(below) with some info.on that if you are interested
Again congrats on your SVR !
Will.
It is not uncommon for HCV patients to have LDL levels within normal or even slightly lower than the rest of the population.
Interesting ,however is that patients that do have elevated LDL .have somewhat better response to tx. and it is synonymous with having the preferable CC allele
I don't believe I ever read anything that signifies the meaning of the LDL lowering from "being " on tx. though.
Will
A higher plasma level of low density lipoprotein (LDL) cholesterol is an independent predictor of SVR to Peg-IFN plus RBV, both in HCV-monoinfected and in HIV/HCV- coinfected patients. Also, variations in 3’UTR of the low-density lipoprotein (LDL) receptor (LDLR) gene are associated with plasma levels of LDL cholesterol. Accordingly, a SNP in 3’UTR of LDL receptor gene (rs14158) was found to predict SVR in HCV-monoinfected patients, but these results are contradictory.
IL28B genotype is also associated with plasma levels of LDL cholesterol.
The purposes of the present study were, on the one hand, to appraise the predictive value of variations in a SNP in 3’UTR of LDLR gene for SVR
http://www.retroconference.org/2011/PDFs/481.pdf
And this:
Hepatitis C associated hypolipidemia( low LDL ) has been demonstrated in studies from Europe and Africa. In two linked studies, we evaluated the relationship between hepatitis C infection and treatment with lipid levels in an American cohort and determined the frequency of clinically significant posttreatment hyperlipidemia. First, a case-control analysis of patients with and without hepatitis C was performed. The HCV Group consisted of 179 infected patients. The Uninfected Control Group consisted of 180 age-matched controls. Fasting cholesterol, low density lipoprotein (LDL), high density lipoprotein and triglycerides were compared. Next was a retrospective cohort study (Treated Hepatitis C Group) of 87 treated hepatitis C patients with lipid data before and after therapy was performed. In the case-control analysis, the HCV Group had significantly lower LDL and cholesterol than the Uninfected Control Group. In the retrospective cohort, patients in the Treated Hepatitis C Group who achieved viral clearance had increased LDL and cholesterol from baseline compared to patients without viral clearance. These results persisted when adjusted for age, sex, and genotype. 13% of patients with viral clearance had increased LDL and 33% experienced increases in cholesterol to levels warranting lipid lowering therapy. CONCLUSION: Hepatitis C is associated with decreased cholesterol and LDL levels. This hypolipidemia resolves with successful hepatitis C treatment but persists in nonresponders. A significant portion of successfully treated patients experience LDL and cholesterol rebound to levels associated with increased coronary disease risk. Lipids should be carefully monitored in persons receiving antiviral therapy.
See: http://www.ncbi.nlm.nih.gov/pubmed/19787818?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
What IS important is that you treated and from what you say successfully so...congrats on that !
The thyroid gland being affected from HCV therapy is a fairly common occurrence and often patients are left "hypothyroid" which it sounds like you were and yes the drug "synthroid it the modality used for that(usually for life) and most often successfully .
Lipid levels may be affected "post tx" also. These levels have been seen to rise somewhat.I have copied a post I put up a few months ago(below) with some info.on that if you are interested
Again congrats on your SVR !
Will.
It is not uncommon for HCV patients to have LDL levels within normal or even slightly lower than the rest of the population.
Interesting ,however is that patients that do have elevated LDL .have somewhat better response to tx. and it is synonymous with having the preferable CC allele
I don't believe I ever read anything that signifies the meaning of the LDL lowering from "being " on tx. though.
Will
A higher plasma level of low density lipoprotein (LDL) cholesterol is an independent predictor of SVR to Peg-IFN plus RBV, both in HCV-monoinfected and in HIV/HCV- coinfected patients. Also, variations in 3’UTR of the low-density lipoprotein (LDL) receptor (LDLR) gene are associated with plasma levels of LDL cholesterol. Accordingly, a SNP in 3’UTR of LDL receptor gene (rs14158) was found to predict SVR in HCV-monoinfected patients, but these results are contradictory.
IL28B genotype is also associated with plasma levels of LDL cholesterol.
The purposes of the present study were, on the one hand, to appraise the predictive value of variations in a SNP in 3’UTR of LDLR gene for SVR
http://www.retroconference.org/2011/PDFs/481.pdf
And this:
Hepatitis C associated hypolipidemia( low LDL ) has been demonstrated in studies from Europe and Africa. In two linked studies, we evaluated the relationship between hepatitis C infection and treatment with lipid levels in an American cohort and determined the frequency of clinically significant posttreatment hyperlipidemia. First, a case-control analysis of patients with and without hepatitis C was performed. The HCV Group consisted of 179 infected patients. The Uninfected Control Group consisted of 180 age-matched controls. Fasting cholesterol, low density lipoprotein (LDL), high density lipoprotein and triglycerides were compared. Next was a retrospective cohort study (Treated Hepatitis C Group) of 87 treated hepatitis C patients with lipid data before and after therapy was performed. In the case-control analysis, the HCV Group had significantly lower LDL and cholesterol than the Uninfected Control Group. In the retrospective cohort, patients in the Treated Hepatitis C Group who achieved viral clearance had increased LDL and cholesterol from baseline compared to patients without viral clearance. These results persisted when adjusted for age, sex, and genotype. 13% of patients with viral clearance had increased LDL and 33% experienced increases in cholesterol to levels warranting lipid lowering therapy. CONCLUSION: Hepatitis C is associated with decreased cholesterol and LDL levels. This hypolipidemia resolves with successful hepatitis C treatment but persists in nonresponders. A significant portion of successfully treated patients experience LDL and cholesterol rebound to levels associated with increased coronary disease risk. Lipids should be carefully monitored in persons receiving antiviral therapy.
See: http://www.ncbi.nlm.nih.gov/pubmed/19787818?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
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