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Thyroid - Hepatitis C Treatment
It appears that my thyroid was effected during treatment and for a period of time after treatment. What causes Hepatitis C treatment to effect the thyroid?
Good articles, thanks for posting. I was also looking for information, that was when I found that HCV could affect the thyroid. I knew that the peg could I did not know about HCV
Thank you again
D
Thank you again
D
Hi Bo, I think you are right, I had the same.
I also had thyroid problems before I treated with INF so then I found the paper above that talks about the HCV and then HCV tx affecting our thyroid.
I also had problems during and after tx finished. My tsh was 17.5 after finishing tx.
I also had thyroid problems before I treated with INF so then I found the paper above that talks about the HCV and then HCV tx affecting our thyroid.
I also had problems during and after tx finished. My tsh was 17.5 after finishing tx.
http://www.wellnessresources.com/studies/hepatitis_treatment_causes_thyroid_problems/
In the study I read above, it was noted, and I believe Interferon is the culprit, as it was noted long before the PI's, but havent read a study on wether the added PI's add to the possibility of damage. The study did note factors that made Thyroid damage more likely, such as age and female gender, plus thyroid levels prior to Treating.
I also noticed that Hep C itself was associated with Thyroid problems. I notice that a lot; that the side effects of the Treatment ( i.e, joint pain, fatigue) also occur sometimes prior to us treating, and then the Interferon compounds the problem~
I know the Interferon affected my hormone levels, because prior to my Tx, I had these HORRIBLE hot flashes, which made it almost impossible for me to function, they would come about every 15 minutes, thu-out the day, and worse at night, with the sweats. Once I began my Tx, no more flashes or sweats!!!! I was like, "aha, it was the Hep C causing the sweats, and now that the virus is Und, no more flashes".....alas, no: as soon as I discontinued my meds, back came the "hormonal imbalance: that caused this sx.
Interferon is that strong, it causes changes in our hormone levels and thyroid levels, it most likely affects so many natural responses in our bodies. We are tampering with Mother Nature, by giving ourselves an increased dose of a chemical that we already have in our bodies. I am thinking (personal opinion) that the Interferon we take in the shot, may somehow train or inspire our own natural Interferon to continue on with the damage, post tx~
In the study I read above, it was noted, and I believe Interferon is the culprit, as it was noted long before the PI's, but havent read a study on wether the added PI's add to the possibility of damage. The study did note factors that made Thyroid damage more likely, such as age and female gender, plus thyroid levels prior to Treating.
I also noticed that Hep C itself was associated with Thyroid problems. I notice that a lot; that the side effects of the Treatment ( i.e, joint pain, fatigue) also occur sometimes prior to us treating, and then the Interferon compounds the problem~
I know the Interferon affected my hormone levels, because prior to my Tx, I had these HORRIBLE hot flashes, which made it almost impossible for me to function, they would come about every 15 minutes, thu-out the day, and worse at night, with the sweats. Once I began my Tx, no more flashes or sweats!!!! I was like, "aha, it was the Hep C causing the sweats, and now that the virus is Und, no more flashes".....alas, no: as soon as I discontinued my meds, back came the "hormonal imbalance: that caused this sx.
Interferon is that strong, it causes changes in our hormone levels and thyroid levels, it most likely affects so many natural responses in our bodies. We are tampering with Mother Nature, by giving ourselves an increased dose of a chemical that we already have in our bodies. I am thinking (personal opinion) that the Interferon we take in the shot, may somehow train or inspire our own natural Interferon to continue on with the damage, post tx~
Here are a couple of links to some excellent articles which explain everything in detail:
http://jcem.endojournals.org/content/89/8/3656.full
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0055364
Also, Medscape has a good article:
Interferon-alpha and Autoimmune Thyroid Disease
"There are three different types of thyroid dysfunction associated with IFN
treatment: (1) autoimmune (often subclinical) hypothyroidism; (2) destructive thyroiditis; and (3) Graves' hyperthyroidism.
These abnormalities can occur at any time during IFN therapy, from as early as 4 weeks until as late as 23 months after initiation,[6,9] and there is no clear difference between the three types, with a median date of onset of 17 weeks after start of IFN treatment.[10] Pooling of several studies shows that hypothyroidism seems to be more frequent than thyrotoxicosis ( Table 4 ).
The majority of patients with hypothyroidism also have TPO antibodies (87%; Table 4 ), indicating the autoimmune nature of this event. According to most studies hypothyroidism can be transient, subsiding after discontinuation of IFN. In a large Italian survey, hypothyroidism was, however, permanent in 59% of the patients.[6] A similar result was found in the review of the literature done by Koh et al.,[8] which showed that 56% of the patients had permanent hypothyroidism. In a recent long-term follow-up study, Carella et al.[18] found that 10 of 36 (28%) TPO antibody-positive patients lost their antibodies at 6 years after discontinuation. On the other hand, 26 patients remained antibody-positive at that time, and subclinical hypothyroidism was detected in seven of them. An unusual form of hypothyroidism was seen in five patients with pre-existing thyroid disease, in whom a reversible form was observed in the presence of thyrotropin (TSH) receptor autoantibodies.[19]
Only a few studies give details regarding the etiology of reported hyperthyroidism. Fattovich et al.[6] found 34 hyperthyroid patients, of whom 13 had transient thyrotoxicosis, presumably suffering from destructive thyroiditis. Twenty-one needed antithyroid drug treatment, making it likely that these suffered from Graves' disease. In the study by Kakizaki et al.,[9] all nine hyperthyroid patients had detectable TSH receptor-stimulating antibodies. In the review by Koh et al.,[8] 30% of hyperthyroid patients had a transient form of thyrotoxicosis, in agreement with a study of Hsieh et al.,[14] which reported that four of 22 hyperthyroid patients had destructive thyroiditis. In a recent study by Wong et al.[11] 10 thyrotoxic patients were identified among 321 HCV- or HBV-infected patients treated with IFN. In six of these Graves' disease was diagnosed (without eye manifestations). In three patients a typical pattern of silent thyroiditis occurred: thyrotoxicosis with reduced uptake on technetium scintigraphy followed by overt hypothyroidism. In the remaining patient, insufficient information was available to make a diagnosis.
From these data it appears that Graves' disease is the most common cause of IFN-associated hyperthyroidism. However, because destructive thyroiditis is present in about one-third of the hyperthyroid patients, adequate diagnostic procedures are indicated when this side effect occurs.
IFN is used therapeutically for its immunostimulatory and antiviral properties. The pattern of thyroid disease observed during therapy bears resemblance to the pattern observed during the "endogenous" immunostimulation occurring during the postpartum period: Circulating levels of thyroid autoantibodies tend to increase, and subjects with circulating TPO autoantibodies are at substantially increased risk of developing thyroid dysfunction. Thyroid function may normalize in some patients after withdrawal of therapy, and the subtypes of disease induced are destructive thyroiditis, Graves' disease, and autoimmune hypothyroidism. Hence IFN-induced thyroid dysfunction may to some degree be a model of postpartum thyroid dysfunction. ...............
In conclusion, IFN therapy of chronic HCV infection is associated with a risk of inducing or worsening AITD, with some resemblance to the induction or worsening of AITD often observed during the postpartum period. The risk of AITD should be evaluated before initiating IFN therapy. In high-risk patients with a strong family history of AITD, previous AITD, or subclinical AITD with circulating thyroid antibodies, thyroid function should be tested at short regular intervals, and the risks of thyroid disease balanced against the benefits of IFN
therapy. ...............
From the evidence presented above, the incidence of clinically relevant AITD is high enough to advise regular (e.g., every 2-3 months) monitoring of TSH values in females and in patients with TPO antibodies who will be treated with IFN. When hypothyroidism occurs, thyroxine therapy should be started, and there is no good reason to withdraw IFN treatment. If thyrotoxicosis is diagnosed, it is advisable to perform a thyroid scintigram. In the case of a homogeneous uptake, Graves' disease is diagnosed and should be treated accordingly, and IFN may be continued. On the other hand, if the uptake is low a diagnosis of destructive thyroiditis is made. Although this disease is usually transient, there is no effective treatment, and only in these patients discontinuation of IFN therapy may be considered."
http://www.medscape.com/nurses
You have to register for Medscape, but it is free.
http://jcem.endojournals.org/content/89/8/3656.full
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0055364
Also, Medscape has a good article:
Interferon-alpha and Autoimmune Thyroid Disease
"There are three different types of thyroid dysfunction associated with IFN
treatment: (1) autoimmune (often subclinical) hypothyroidism; (2) destructive thyroiditis; and (3) Graves' hyperthyroidism.
These abnormalities can occur at any time during IFN therapy, from as early as 4 weeks until as late as 23 months after initiation,[6,9] and there is no clear difference between the three types, with a median date of onset of 17 weeks after start of IFN treatment.[10] Pooling of several studies shows that hypothyroidism seems to be more frequent than thyrotoxicosis ( Table 4 ).
The majority of patients with hypothyroidism also have TPO antibodies (87%; Table 4 ), indicating the autoimmune nature of this event. According to most studies hypothyroidism can be transient, subsiding after discontinuation of IFN. In a large Italian survey, hypothyroidism was, however, permanent in 59% of the patients.[6] A similar result was found in the review of the literature done by Koh et al.,[8] which showed that 56% of the patients had permanent hypothyroidism. In a recent long-term follow-up study, Carella et al.[18] found that 10 of 36 (28%) TPO antibody-positive patients lost their antibodies at 6 years after discontinuation. On the other hand, 26 patients remained antibody-positive at that time, and subclinical hypothyroidism was detected in seven of them. An unusual form of hypothyroidism was seen in five patients with pre-existing thyroid disease, in whom a reversible form was observed in the presence of thyrotropin (TSH) receptor autoantibodies.[19]
Only a few studies give details regarding the etiology of reported hyperthyroidism. Fattovich et al.[6] found 34 hyperthyroid patients, of whom 13 had transient thyrotoxicosis, presumably suffering from destructive thyroiditis. Twenty-one needed antithyroid drug treatment, making it likely that these suffered from Graves' disease. In the study by Kakizaki et al.,[9] all nine hyperthyroid patients had detectable TSH receptor-stimulating antibodies. In the review by Koh et al.,[8] 30% of hyperthyroid patients had a transient form of thyrotoxicosis, in agreement with a study of Hsieh et al.,[14] which reported that four of 22 hyperthyroid patients had destructive thyroiditis. In a recent study by Wong et al.[11] 10 thyrotoxic patients were identified among 321 HCV- or HBV-infected patients treated with IFN. In six of these Graves' disease was diagnosed (without eye manifestations). In three patients a typical pattern of silent thyroiditis occurred: thyrotoxicosis with reduced uptake on technetium scintigraphy followed by overt hypothyroidism. In the remaining patient, insufficient information was available to make a diagnosis.
From these data it appears that Graves' disease is the most common cause of IFN-associated hyperthyroidism. However, because destructive thyroiditis is present in about one-third of the hyperthyroid patients, adequate diagnostic procedures are indicated when this side effect occurs.
IFN is used therapeutically for its immunostimulatory and antiviral properties. The pattern of thyroid disease observed during therapy bears resemblance to the pattern observed during the "endogenous" immunostimulation occurring during the postpartum period: Circulating levels of thyroid autoantibodies tend to increase, and subjects with circulating TPO autoantibodies are at substantially increased risk of developing thyroid dysfunction. Thyroid function may normalize in some patients after withdrawal of therapy, and the subtypes of disease induced are destructive thyroiditis, Graves' disease, and autoimmune hypothyroidism. Hence IFN-induced thyroid dysfunction may to some degree be a model of postpartum thyroid dysfunction. ...............
In conclusion, IFN therapy of chronic HCV infection is associated with a risk of inducing or worsening AITD, with some resemblance to the induction or worsening of AITD often observed during the postpartum period. The risk of AITD should be evaluated before initiating IFN therapy. In high-risk patients with a strong family history of AITD, previous AITD, or subclinical AITD with circulating thyroid antibodies, thyroid function should be tested at short regular intervals, and the risks of thyroid disease balanced against the benefits of IFN
therapy. ...............
From the evidence presented above, the incidence of clinically relevant AITD is high enough to advise regular (e.g., every 2-3 months) monitoring of TSH values in females and in patients with TPO antibodies who will be treated with IFN. When hypothyroidism occurs, thyroxine therapy should be started, and there is no good reason to withdraw IFN treatment. If thyrotoxicosis is diagnosed, it is advisable to perform a thyroid scintigram. In the case of a homogeneous uptake, Graves' disease is diagnosed and should be treated accordingly, and IFN may be continued. On the other hand, if the uptake is low a diagnosis of destructive thyroiditis is made. Although this disease is usually transient, there is no effective treatment, and only in these patients discontinuation of IFN therapy may be considered."
http://www.medscape.com/nurses
You have to register for Medscape, but it is free.
Hi I found this article that talks about HCV and tx for HCV and the swinging thyroid.
I don't know if it will help you but evidently there are problems before, during and sometimes after. I hope this helps. This is from 2009, I am trying to
find something more recent.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029615/
I don't know if it will help you but evidently there are problems before, during and sometimes after. I hope this helps. This is from 2009, I am trying to
find something more recent.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3029615/
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