Just thought I'd write an update. Any information I have on MPN has been obtained from this site, which i am very grateful for. I thought that my explaining my experiences might help others.
I've been on Pegasys for about 18 months platelets were initially 530 I started on 45mcg weekly.
Went up to 60mcg weekly then up to 90mcg but I didn't get on well with that amount so back to 60mcg. Then as the platelets came down so did the dosage 45 weekly then every two weeks as platelets were in the high 300's. Now they are 305 and I'm transferring to every three weeks fingers crossed its enough to keep them stable.
Even though my numbers were good I was having some strange symptoms from about April this year - nails suddenly splitting, hair thinning, dry skin, feeling cold even in summer, breathlessness and fatigue more prevalent. Went to GP several times with these complaints. Had chest x ray all clear, given lotion for dry skin. So basically can't find anything so put up with it! I got used to feeling below par, tired, anxious and moody. I know some of these symptoms can be similar to our MPN symptoms (but they did feel a little different, lots of unrelated things) so thought ok that's as good as I'm going to feel even with low numbers.
Had a telephone appointment with my haematologist (not an MPN specialist but very good at listening, we're learning together. I do feel like the one in control and that's thanks to this site and very knowledgeable people on here). She agreed to lower Pegasys dosage also she's proactive by mentioning my thyroid TSH was high (my surgery had told me all results were within range), she suggested I needed thyroid medication which I would get from my GP. She recommended I go back to GP for more tests I had asked several times about thyroid tests but always told in range! (I had an over active thyroid about 20 years ago that had eventually cured itself) Meanwhile I was checking on thyroid Uk site for info (again someone had mentioned on here how informative they were - they are very helpful people).
So had more blood tests and GP has phoned with results and yes I have hypothyroidism (under active thyroid) with (in her words) 'sky high levels of antibodies' no wonder I wasn't feeling quite right! I'm starting on Levothyroxine tomorrow. I know some people on here are in the same situation and because I'd read they took the meds I feel more comfortable starting on them.
You just get one thing sorted and something else turns up.
Sorry to have rambled on but hope the info might help someone else in this situation.
Thanks everyone for all the valuable information and support here.
Keep well.
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Your story is a good reminder to keep track of thyroid. It is a known risk with IFN, esp for women.
In this report dose reduction or stop is suggested, but see below for medication as you're doing:
"... the importance of monitoring thyroid function before and during therapy, since the side effects of IFN-α may mimic thyroid disease. Although discontinuation of IFN-α therapy should be considered, it is possible to continue treatment."
-Most were women, which I've seen elsewhere too:
"Eight patients (seven women) developed AITD with positive thyroid peroxidase antibodies."
Endocrine toxicity has occurred in patients receiving interferon alfa products, including BESREMi. These toxicities may include worsening hypothyroidism and hyperthyroidism"
I had some negative reactions to Pegasys also, mostly g.i. issues, and have switched to Besremi. I'm tolerating it much better. You might want to inquire about it. Everyone is different so it might not be as good for you, but maybe worth a try.
Thanks for replying Orangeboykitty, I'm in the UK and don't think Besremi is prescribed for ET (I have read interesting thing about it) but I will ask at next appointment to confirm.
well done for pushing we all know our own bodies. I too faught so hard with Drs etc to get proper blood tests. It took a 6 month battle of keep going back nagging for more bloods they said we’re fine. I had ET Jak2 undiscovered for some time but how I felt told me something was wrong . Really pleased you have got there in end. I find it frustrating that the majority of Drs don’t listen . It’s Black or White with no bending.
Fortunately on my 6th visit another Dr. actually listened to me & tests done . Only the pushers get anywhere at the moment which is very sad for patients that give up pestering 👍. I am on peg but low dose due to headaches on higher .
Hi Exeter21 thanks for reply - from your user name I think we're in the same area of the country. I have found the services here are so much better than where I lived before.
I relate to your "something is wrong" I suffered from covid/long covid for most of 2020 but suddenly something is new and "not right" and I was near going to ER. The MPN was finally making its effect.
Yes I just wish Doctors would take more notice of how we feel. Mine just looked at me & told me I was too healthy & looked well to have anything wrong 🙈 I am glad I eventually got to talk to Professor Harrison the UK MPN expert. She is extremely helpful & knowledgeable. No one knows our body & feelings like ourselves . Julia 👍
Good luck . At least this website is a godsend for information from everyone . I start on my peg again January but bigger gap between doses to hopefully tolerate it & only 45 dose . I keep you posted Julia 👍
Hi, I too am on levothyroxin and have been since my late 40's (now 74) and my surgery check the levels about every three months. I have to have a test before the prescription is reactivated, so that continues to work well. At the moment having had one done recently it is right on target, so it is good that you are getting this sorted and hopefully will sort your issues out. It pays to perservere, when we know something is wrong or out of the ordinary it is easy to be fobbed off, but as Hunter regularly says you have to stand up for what you think to be or know is right for you. As an instance, I have just had telephone referrals since my first diagnosis and hydroxy meds, although they have actually shown to be hospital attendance, they are always by phone. I have just had another "phone" follow up and queried the fact that my next one show f 2 f but then adds telephone! However as I have raised it they have now re arranged the appointment to make it a f 2 f and not telephone. Sometimes it pays to ask and query. Hope all goes well. As you say this site is invaluable for help and info.
Good to know your Levothyroxine is on target, I understand it can take a lot of tweaking to get it right. Funny you mentioned f2f I've only seen my haematologist once 2 years ago, at my last telephone appointment she actually asked if I'd like a f2f, I was stunned and said yes it would be lovely to see you!Keep well.
There were a lot of good comments above, and your case is a good reminder for all of us- especially those on IFN, that auto-immune issues can arise as part of both the common side-effects that the medications we take, and the pro-inflammatory sequelae of our disease processes can cause.
The antibodies that your GP was referring to are antithyroglobulin antibodies, that attack the thyroid-hormone-producing portions of your thyroid gland, which can initially cause hyperthyroid [release of too much thyroid hormone] as the irritated gland releases extra, but eventually, it usually leads to becoming hypothyroid d/t destruction of or damage to those cells.
This can be a result of either the pro-inflammatory part of our disease process [somewhat less likely], or as part of the pro-immune functions of IFN's causing autoimmune reactions [more likely].
I'll be back with more information, if any is wanted...
Thyroid function, autoimmunity and nodules in hematological malignancies
Abstract
Objective: Hematological malignancies encompass a large spectrum of disease entities whose treatment by chemo/radiotherapy could lead to thyroid complications. To the best of our knowledge, no study has simultaneously addressed thyroid function, autoimmunity and nodularity. Therefore, we decided to conduct one.
Materials and methods: We evaluated 82 Caucasian patients (36 women and 46 men), who were treated at our Oncology division for hematological malignancies (multiple myeloma, chronic myeloid leukemia, chronic lymphatic leukemia, non-Hodgkin lymphoma and polycythemia vera) and compared them with a control group of 104 patients. Patients who had received or were receiving external head/neck radiotherapy were excluded. All oncological patients and control individuals underwent thyroid ultrasonography and thyroid function and autoimmunity tests.
Results: A lower prevalence of enlarged thyroid and nodules were found in patients with respect to controls. The rate of thyroid nodules was the highest in multiple myeloma and polycythemia vera, and the lowest in chronic lymphatic leukemia. Non-Hodgkin lymphoma patients had the smallest thyroid nodules while men with multiple myeloma the biggest ones. No patient had hypothyroidism, while 5.6% of patients had subclinical hyperthyroidism. In contrast, within the control group the rates of hypothyroidism and hyperthyroidism, overt and subclinical, were 3.8%, 20.2%, 0% and 0% respectively. Moreover, the overall rate of thyroid autoantibody positiveness [SIC] in patients was significantly lower than controls.
Conclusion: In our experience, we found a significantly lower prevalence of thyroid abnormalities in hematologic patients who underwent chemotherapy, but not radiotherapy, with respect to controls.
So although this is a very small group study [N-82 total- ? how many were PV pts.], as might be expected given the rarity of PV, it did suggest that while an increased risk of having/developing thyroid nodule may exist with PV, there isn't a generally greater risk of overt thyroid disease. It's also of note that they didn't further characterize the thyroid nodules that they discovered as malignant or benign, or as active vs quiescent.
The predominant source of evidence that Interferon Therapy [IFN] can be implicated in the development of thyroid disease seems to come from treatment of Hepatitis [B&C] patients with IFN. E.G.:
Frequency of Thyroid Dysfunctions during Interferon Alpha Treatment of Single and Combination Therapy in Hepatitis C Virus-Infected Patients: A Systematic Review-Based Analysis
I know that a lot of this is written in pretty deep medical and scientific jargon, but it seemed worth posting anyway- and I'll be happy to translate anything requested into English.
There is also a more-easily read [although still medical-professionally-oriented] discussion of the relationship to be found on Medscape, but since it's a professionals-only site, I'm going to copy it into the reply below.
Interferon- (IFN ) is the main therapeutic agent in patients infected with the hepatitis C virus (HCV). It is rather safe, but is known to induce the production of autoantibodies and can lead to the occurrence of autoimmune disease. This mini-review focuses on the induction of autoimmune thyroid disease (AITD) in HCV-infected patients treated with IFN . Females carry a higher risk to develop AITD upon IFN treatment, with a relative risk of 4.4 (95% confidence interval 3.2-5.9). The presence of thyroid peroxidase antibodies before therapy has a relative risk for AITD of 3.9 (95% confidence interval 1.9-8.1). IFN -associated AITD can consist of autoimmune primary hypothyroidism, Graves' hyperthyroidism, and destructive thyroiditis, with hypothyroidism being the most common side effect. The clear association between AITD and IFN use suggests that high endogenous IFN levels may also be associated with naturally occurring AITD. High endogenous IFN levels are seen in patients infected with certain viruses. It is concluded that IFN is one of the environmental factors capable of triggering the onset of AITD in genetically susceptible individuals.
Autoimmune thyroid diseases (AITD), like most other autoimmune disorders, have a multifactorial etiology. Genetic factors undoubtedly play a role, because AITD often runs in families and the concordance rate is higher in monozygotic as compared with dizygotic twins. Nevertheless, the concordance rate in monozygotic twins is only approximately 30%, underscoring the importance of other, environmental factors. In the case of AITD some of these factors have been identified. Stress, smoking, and iodine intake all seem to be relevant in bringing about AITD in genetically susceptible persons, but there must be many others.
In this review we will focus on a very specific factor: the apparent induction of AITD by treatment with Interferon- (IFN ) for unrelated disorders. IFN is now used in a variety of diseases, and has become the mainstay in the treatment of patients infected with the hepatitis C virus (HCV). Although IFN therapy is relatively safe, an important side effect seems to be the induction of autoantibodies and autoimmune diseases, especially AITD.
In this mini-review, we will give an overview of the incidence of IFN -induced AITD and the interplay with other risk factors for AITD. The disease pattern induced by IFN and causes for endogenous increases in IFN will be discussed because this may help to discover some of the as yet unknown environmental factors involved in the development of AITD.
Frequency of AITD in HCV-Infected Patients upon IFN
Although IFN is used as a therapeutic agent in a variety of disorders, HCV infection is by far the commonest indication for its use, and we will limit this review to this condition. In a large survey, Fattovich et al. analyzed 11,241 HCV-infected patients treated with IFN . Among the side effects recorded, thyroid dysfunction was the most frequently observed untoward effect, occurring in 71 patients (0.6%). This low rate is very likely an underestimate of the true incidence for several reasons. First, the data were collected retrospectively using a questionnaire, a method liable to recall bias. Second, the patients were not screened biochemically for thyroid dysfunction, and less symptomatic cases will therefore have been missed. Third, 2,033 patients were younger than 30 years, and the majority (64%) were males. Indeed, subsequent studies in which thyroid function was routinely assessed showed a much higher incidence of thyroid dysfunction of 6.0%.
IFN
It has been argued that HCV infection itself is associated with autoimmune thyroid disorders. Fernandez-Soto et al. reported that 27 of 134 (20%) of HCV-infected patients had antibodies against thyroid peroxidase (TPO), as opposed to only two of 41 (5%) of hepatitis B virus (HBV)-infected controls. However, the results of this study can be criticized because the HCV-infected patients had a higher likelihood to be TPO antibody-positive: They were 10 years older and more often female (43% vs. 34%) compared with the HBV-infected controls. Indeed, in a larger study Marazuela et al.[13] found that the prevalence of TPO antibodies in 95 HCV-infected (but not IFN -treated) patients was 14.7% and thus very similar to the rate found in the general population. When these authors summarized the available studies on this subject, 96 of 626 HCV-infected patients had TPO antibodies, resulting in a similar prevalence rate of 15.3%.
Risk Factors for IFN
The factors that increase the risk for thyroid autoimmune disease during IFN therapy appear to be the same as in the general population. Thus, females carry a higher risk to develop thyroid dysfunction during IFN treatment than males. In a compilation of data from different studies, females have a 4.4 times higher risk than males . Another risk factor is the pretreatment presence of TPO autoantibodies, which increases the risk for thyroid dysfunction 3.9-fold. Twenty-one percent of TPO antibody-positive patients developed thyroid dysfunction, as opposed to only 5% of the antibody-negative patients. This figure is almost certainly an underestimate of the true risk, because antibody positivity is often seen as a relative contraindication to the use of IFN .
On the other hand, in three studies including 421 patients without TPO antibodies prior to treatment, TPO antibodies occurred de novo in 40 of 421 (9.5%) patients of whom 23 (58%) developed clinically overt thyroid dysfunction.
Type of Thyroid Dysfunction Induced by IFN
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, and there is no clear difference between the three types, with a median date of onset of 17 weeks after start of IFN treatment. Pooling of several studies shows that hypothyroidism seems to be more frequent than thyrotoxicosis .
The majority of patients with hypothyroidism also have TPO antibodies (87%), 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. A similar result was found in the review of the literature done by Koh et al., which showed that 56% of the patients had permanent hypothyroidism. In a recent long-term follow-up study, Carella et al. 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.
Only a few studies give details regarding the etiology of reported hyperthyroidism. Fattovich et al. found 34 hyperthyroid patients, of whom 13 had transient thyrotoxicosis, presumably suffering from destructive thyroiditis. Twenty-one needed anti-thyroid drug treatment, making it likely that these suffered from Graves' disease. In the study by Kakizaki et al., all nine hyperthyroid patients had detectable TSH receptor-stimulating antibodies. In the review by Koh et al., 30% of hyperthyroid patients had a transient form of thyrotoxicosis, in agreement with a study of Hsieh et al., which reported that four of 22 hyperthyroid patients had destructive thyroiditis. In a recent study by Wong et al. 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 immuno-stimulatory and antiviral properties. The pattern of thyroid disease observed during therapy bears resemblance to the pattern observed during the "endogenous" immuno-stimulation 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 addition it is interesting to speculate if high endogenous IFN may be involved in triggering AITD in genetically susceptible individuals. The most prominent reason for high levels of IFN are certain viral infections. The importance of this was recently stressed by a study in 56 patients with type 1 diabetes mellitus, another autoimmune disease that can be triggered by the use of IFN . Chehadah et al. found that IFN could be detected in 70% of patients with diabetes of recent onset, as compared with none of 37 controls. In 50% of these patients, Coxsackie B virus, a virus implicated as a cause of type 1 diabetes mellitus, could be detected.
These findings suggest that viral infections capable of inducing an IFN response in the host may be one of the environmental factors implicated in the development of AITD in genetically predisposed individuals. In vitro studies have shown that IFN up-regulates major histocompatibility complex class I and II expression on xeno-grafted thyroid tissues from Graves' patients, in parallel with an increase in anti-TPO antibodies. This, however, only happens if local infiltrating lymphocytes remain present in the graft, suggesting that Interferon- may be capable of aggravating an immune response only in predisposed subjects with some degree of pre-existing thyroiditis. Viral infections have been suspected to be such a triggering factor, but clinical studies linking certain viruses to the development of AITD are lacking. We suspect that this is due to the large number of different viruses that may affect humans. The data presented above suggest that it is worthwhile to focus on viruses known to induce an IFN response.
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.
It may be hypothesized that environmental factors, such as certain viral infections, by inducing an increase in IFN generation may be involved in triggering seemingly spontaneous AITD in genetically susceptible individuals.
Clinical Implications
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 [should] be considered.
As far as I am concerned, the possibility of developing thyroid problems [which many people have w/o IFN therapy, and is [usually] easily treated] is worth the potential benefits of IFN therapy.
This article also points out that Type 1 Diabetes [autoimmune antibody-mediated destruction of pancreatic islet cells causing absolute endogenous insulin deficiency] can be associated with [triggered by] IFN therapy.
Happy days! [That's going to be my next research project- once I catch my breath from this one... 😇
"You just get one thing sorted and something else turns up."
In my experience, through a weird and wooly life [so far] Your sentence os the essential definition of life.
Or as, Rosanna Rosanna Danna [one of Gilda Radner's more famous alter egos] often said: "Well, Jane, it just goes to show you, it’s always something! If it’s not one thing, it’s another!"
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ET, JAK+ scared
Jak 2 positive ET
Good News: Pegasys finally working! Bad News: Pulmonary embolus!
ET :Hydroxy to Pegasys
Pegasys working too well?
